subject:(N cadherin)

Universiteit Utrecht

1. Pilzecker, B. The E- and N-cadherin switch in Epithelial to Mesenchymal Transition and metastasis. Potential drug targets?.

Degree: 2013, Universiteit Utrecht

URL: http://dspace.library.uu.nl:8080/handle/1874/287101

► Carcinomas are most prevalent type of cancers and arise from an epithelial layer. Epithelial layers have a strict organization; cells are tightly linked through different… (more)

▼ Carcinomas are most prevalent type of cancers and arise from an epithelial layer. Epithelial layers have a strict organization; cells are tightly linked through different junctions. The Epithelial to Mesenchymal Transition (EMT) developmental program enables epithelial cells to transform into mesenchymal cells and break free from neighboring epithelial cells in order to migrate though the body. Also in carcinomas, EMT enables cells to invade into healthy tissue. EMT also aids cancer progression in other manners by suppressing senescence, anoikis, apoptosis, oncogene addiction and modulating the immune response. Furthermore, EMT can lead to the formation of mesenchymal cancer stem cells. Mesenchymal cancer stem cells seem to be more resistant to chemotherapy than epithelial cancer cells. All of these traits increase the chance of an invading cancer cell being successful in setting up a metastatic niche. The cadherin switch from E-cadherin to N-cadherin is considered a mark of EMT. Cadherins are cell-cell adhesion proteins. E-cadherin inhibits invasion by protecting epithelial integrity and N-cadherin increases invasion. It seems that a part of carcinomas has an E- to N-cadherin switch during EMT. However, other carcinomas show other cadherin switches and E- and N-cadherin expression is not always mutually exclusive. In the HMLE cancer cell line E-cadherin knockdown is enough to induce EMT. By knocking out E-cadherin and p53 in a tissue specific manner they show an increase of invasion and metastases. In gastric carcinoma model E-cadherin and p53 knockout leads to EMT, however, in an invasive lobular carcinoma model EMT has not been observed. If EMT could be inhibited in carcinomas, the chance of metastasis would decrease and the formation of new cancer stem cells would be inhibited. Since chemotherapy mainly targets epithelial cancer cells, combining an EMT inhibitor might lead to more efficient chemotherapy. There are some compounds capable of inhibiting EMT or promoting the reverse process Mesenchymal to Epithelial Transition (MET). The identified compounds either inhibit a pathway which induces EMT or lead regaining epithelial identity and re-expression of E-cadherin. These compounds need to be further tested using in vivo models. Antibodies targeting mesenchymal marker proteins are being developed as well. An anti N-cadherin antibody shows a decrease of tumor growth and metastases in mice, perhaps by targeting mesenchymal cancer stem cells. Since chemotherapy does not efficiently target cancer stem cells, screens were performed to find compounds that target cancer stem cells. In the future, there may be a combined anticancer therapy developed which inhibits EMT and targets cancer stem cells. This type of therapy could be combined with chemo-, radiotherapy or surgery to treat carcinomas more efficiently. Advisors/Committee Members: Bos, Prof. Dr. J.L..

Subjects/Keywords: Carcinomas; Epithelial to Mesenchymal Transition (EMT); E-cadherin; N-cadherin

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Pilzecker, B. (2013). The E- and N-cadherin switch in Epithelial to Mesenchymal Transition and metastasis. Potential drug targets?. (Masters Thesis). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/287101

Chicago Manual of Style (16^th Edition):

Pilzecker, B. “The E- and N-cadherin switch in Epithelial to Mesenchymal Transition and metastasis. Potential drug targets?.” 2013. Masters Thesis, Universiteit Utrecht. Accessed January 27, 2021. http://dspace.library.uu.nl:8080/handle/1874/287101.

MLA Handbook (7^th Edition):

Pilzecker, B. “The E- and N-cadherin switch in Epithelial to Mesenchymal Transition and metastasis. Potential drug targets?.” 2013. Web. 27 Jan 2021.

Vancouver:

Pilzecker B. The E- and N-cadherin switch in Epithelial to Mesenchymal Transition and metastasis. Potential drug targets?. [Internet] [Masters thesis]. Universiteit Utrecht; 2013. [cited 2021 Jan 27]. Available from: http://dspace.library.uu.nl:8080/handle/1874/287101.

Council of Science Editors:

Pilzecker B. The E- and N-cadherin switch in Epithelial to Mesenchymal Transition and metastasis. Potential drug targets?. [Masters Thesis]. Universiteit Utrecht; 2013. Available from: http://dspace.library.uu.nl:8080/handle/1874/287101

2. Nore, Andrea Marie. Regulation Of Vectorial Active Transport In Human Proximal Tubule Cells By MT-3: The Role Of The C-Terminal Domain On E-And N-Cadherin Expression And The Confirmation Of Protein-Protein Interactions.

Degree: PhD, Biomedical Sciences, 2015, University of North Dakota

URL: https://commons.und.edu/theses/1938

► The proximal tubule of the kidney is particularly susceptible to toxicant-induced damage and cell cultures of human proximal tubule cells are widely utilized to… (more)

▼ The proximal tubule of the kidney is particularly susceptible to toxicant-induced damage and cell cultures of human proximal tubule cells are widely utilized to study the role of epithelial-mesenchymal transition (EMT) in renal disease. Cadmium is a toxic metal ion that is known to produce renal tubular necrosis and accumulate in the proximal tubule. This metal binds to a family of cysteine rich metal binding proteins known as metallothioneins (MT) that are found in abundance in the kidney. Previous studies from our laboratory have shown that the third isoform of metallothionein (MT-3) is expressed in the epithelial cells of the human kidney, including those of the proximal tubule. An immortalized proximal tubule cell line does not express MT-3 and does not demonstrate vectorial active transport. Transfection of the MT-3 gene into the HK-2 cells restores vectorial active transport as evidenced by dome formation. This suggests that MT-3 is involved in mesenchymal to epithelial transition (MET), the reverse of EMT, and promotes and epithelial phenotype. The goals of the present study were to examine the role of growth media composition on classic EMT responses, quantitatively evaluate the expression levels of E- and N-cadherin, define the functional epitope of MT-3 that mediates MET in HK-2 cells, and identify proteins that interact with MT-3 to promote epithelial features in the proximal tubule. It was shown that both E- and N-cadherin mRNA and protein are expressed in the human renal proximal tubule. Based on the pattern of cadherin expression, vectorial active transport, and transepithelial resistance, it seems that the HK-2 cell line has already undergone many of the early features associated with EMT. Our data indicates the unique, six amino acid C-terminal sequence of MT-3 is required to induce MET in HK-2 cells. A combination of co-immunoprecipitation and western blotting indicate that MT-3 interacts with myosin-IIa, β-actin, enolase-1, tropomyosin-3, and aldolase-a in vitro. Together, the data suggests the HK-2 cell line can be an effective model to study later stages in the conversion of the renal epithelial cell to a mesenchymal cell and when transfected with MT-3 it may be an effective model to study the process of MET. MT-3 protein-protein interactions provide insight into the potential mechanism by which MT-3 promotes cytoskeletal organization in non-diseased epithelial proximal tubule cells and offers the opportunity to investigate these interactions under pathological conditions. Advisors/Committee Members: Scott H. Garrett.

Subjects/Keywords: Cadmium; E-cadherin; Kidney Disease; MT-3; N-cadherin; Proximal Tubule

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Nore, A. M. (2015). Regulation Of Vectorial Active Transport In Human Proximal Tubule Cells By MT-3: The Role Of The C-Terminal Domain On E-And N-Cadherin Expression And The Confirmation Of Protein-Protein Interactions. (Doctoral Dissertation). University of North Dakota. Retrieved from https://commons.und.edu/theses/1938

Chicago Manual of Style (16^th Edition):

Nore, Andrea Marie. “Regulation Of Vectorial Active Transport In Human Proximal Tubule Cells By MT-3: The Role Of The C-Terminal Domain On E-And N-Cadherin Expression And The Confirmation Of Protein-Protein Interactions.” 2015. Doctoral Dissertation, University of North Dakota. Accessed January 27, 2021. https://commons.und.edu/theses/1938.

MLA Handbook (7^th Edition):

Nore, Andrea Marie. “Regulation Of Vectorial Active Transport In Human Proximal Tubule Cells By MT-3: The Role Of The C-Terminal Domain On E-And N-Cadherin Expression And The Confirmation Of Protein-Protein Interactions.” 2015. Web. 27 Jan 2021.

Vancouver:

Nore AM. Regulation Of Vectorial Active Transport In Human Proximal Tubule Cells By MT-3: The Role Of The C-Terminal Domain On E-And N-Cadherin Expression And The Confirmation Of Protein-Protein Interactions. [Internet] [Doctoral dissertation]. University of North Dakota; 2015. [cited 2021 Jan 27]. Available from: https://commons.und.edu/theses/1938.

Council of Science Editors:

Nore AM. Regulation Of Vectorial Active Transport In Human Proximal Tubule Cells By MT-3: The Role Of The C-Terminal Domain On E-And N-Cadherin Expression And The Confirmation Of Protein-Protein Interactions. [Doctoral Dissertation]. University of North Dakota; 2015. Available from: https://commons.und.edu/theses/1938

3. Sandquist, Elizabeth. N-Cadherin Expression And EMT Progression In Arsenic- And Cadmium-Transformed Urotsa.

Degree: PhD, Biomedical Sciences, 2015, University of North Dakota

URL: https://commons.und.edu/theses/1830

► Environmental agents are common causes of bladder cancer. Specifically, arsenic (As3+) and cadmium (Cd2+) are known carcinogens implicated in the development of bladder cancer.… (more)

▼ Environmental agents are common causes of bladder cancer. Specifically, arsenic (As3+) and cadmium (Cd2+) are known carcinogens implicated in the development of bladder cancer. Previous studies from our laboratory have shown that As3+ and Cd2+ can cause malignant transformation of normal immortalized bladder urothelial cells, which can form tumors when injected subcutaneous or intraperitoneal into nude mice. Microarray analysis of repeated metal transformation in parallel revealed that N-cadherin was the most upregulated gene in As3+ transformants, and a top induced gene in Cd2+-transformed cells. The switch from E-cadherin to N-cadherin is a well-known indicator of the epithelial-to-mesenchymal transition occurring in bladder cancer. Further, N-cadherin upregulation is correlated with tumor stage, increased recurrence, and decreased survival in patients. While the factors mediating the decrease in E-cadherin expression are well-established, little is known of the factors regulating the increase in N-cadherin expression. The goal of the present study was to determine how As3+ and Cd2+ regulate N-cadherin expression, whether this expression is maintained in heterotransplant models, and if N-cadherin is promoting the epithelial-to-mesenchymal transition in As3+- and Cd2+-transformed UROtsa cells in vitro. This work has demonstrated that N-cadherin is induced in As3+- and Cd2+-transformed UROtsa cell lines, and that the expression is maintained in intraperitoneal, but not subcutaneous, tumor xenografts. Further, tumor-initiating cells derived from transformed UROtsa cells did not express N-cadherin. This suggests that tumor microenvironment and heterogeneity of cell populations are important factors for the use of animal models in cancer research. The As3+ and Cd2+ UROtsa cell lines represent the initial phases of EMT in bladder cancer, and may demonstrate a unique EMT pathway specific to heavy metal carcinogens. Transcriptional regulation of N-cadherin, which is mostly unknown, may be elucidated by the investigation of the transcription factor Twist and epigenetic regulation, particularly histone acetylation. Advisors/Committee Members: Scott H. Garrett.

Subjects/Keywords: arsenic; bladder cancer; cadmium; N-cadherin; UROtsa

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Sandquist, E. (2015). N-Cadherin Expression And EMT Progression In Arsenic- And Cadmium-Transformed Urotsa. (Doctoral Dissertation). University of North Dakota. Retrieved from https://commons.und.edu/theses/1830

Chicago Manual of Style (16^th Edition):

Sandquist, Elizabeth. “N-Cadherin Expression And EMT Progression In Arsenic- And Cadmium-Transformed Urotsa.” 2015. Doctoral Dissertation, University of North Dakota. Accessed January 27, 2021. https://commons.und.edu/theses/1830.

MLA Handbook (7^th Edition):

Sandquist, Elizabeth. “N-Cadherin Expression And EMT Progression In Arsenic- And Cadmium-Transformed Urotsa.” 2015. Web. 27 Jan 2021.

Vancouver:

Sandquist E. N-Cadherin Expression And EMT Progression In Arsenic- And Cadmium-Transformed Urotsa. [Internet] [Doctoral dissertation]. University of North Dakota; 2015. [cited 2021 Jan 27]. Available from: https://commons.und.edu/theses/1830.

Council of Science Editors:

Sandquist E. N-Cadherin Expression And EMT Progression In Arsenic- And Cadmium-Transformed Urotsa. [Doctoral Dissertation]. University of North Dakota; 2015. Available from: https://commons.und.edu/theses/1830

4. APRILE, PAOLA. Unravelling the role of mechanical cues on the chondrogenic differentiation of stem cells.

Degree: School of Engineering. Discipline of Mechanical & Manuf. Eng, 2019, Trinity College Dublin

URL: http://hdl.handle.net/2262/91120

► The inability of adult articular cartilage to regenerate has motivated the development of tissue engineering strategies to repair cartilage defects before they progress to osteoarthritis.… (more)

▼ The inability of adult articular cartilage to regenerate has motivated the development of tissue engineering strategies to repair cartilage defects before they progress to osteoarthritis. Common cell based strategies employing autologous chondrocytes to treat cartilage lesions, often fail to promote hyaline cartilage repair. Mesenchymal stem cells / stromal cells (MSC) represent a promising cell type for cartilage tissue engineering, due to their relative ease of isolation, ability to proliferate extensively in vitro and differentiate along multiple pathways1-3. MSC differentiation can be influenced by the mechanical properties of their environment4. The objective of this dissertation was to examine the influence of intrinsic and extrinsic mechanical cues on the initiation of chondrogenesis of MSC seeded on top (2-Dimension) or encapsulated within (3-Dimension) hydrogels of defined stiffness. The development of an Interpenetrating Network (IPN) hydrogel system able to support cell growth in 2D and 3D, enabled the independent control of substrate rigidity (2D and 3D) and cell morphology (3D). A softer environment (2D and 3D) was correlated to enhanced upregulation of key chondrogenic markers and cell condensation. Contrary to the expectations, allowing the cells to spread in a soft 3D context greatly improved this chondrogenic response. Finally, the effect of biomaterial's mechanical properties and external forces was combined to the application of a physiological magnitude of Hydrostatic Pressure (HP) to mimic the physiological environment of a loaded knee joint. In this case, the chondrogenic differentiation of HP-stimulated cells resulted enhanced to a greater extent, when the mechanical perturbation was applied after the initiation of their chondrogenic commitment. Mechanical forces and local morphogen gradients greatly influence cartilage development, hence biomimetic cartilage repair strategies aiming to recapitulate the complex interplay of biophysical and biochemical cues, would open new possibilities for cartilage tissue regeneration5,6. The results described in this work evidenced the fundamental role of biophysical cues in regulating MSC biology and the importance of this information to inspire new biomimetic strategies for stem cell based cartilage regeneration procedures. REFERENCES 1. Johnstone, B., Hering, T. M., Caplan, A. I., Goldberg, V. M. & Yoo, J. U. In VitroChondrogenesis of Bone Marrow-Derived Mesenchymal Progenitor Cells. Exp. Cell Res. 238, 265-272 (1998). 2. Caplan, A. I. Mesenchymal stem cells. J. Orthop. Res. 9, 641-650 (1991). 3. Badylak, S. F., Weiss, D. J., Caplan, A. & Macchiarini, P. Engineered whole organs and complex tissues. Lancet 379, 943-52 (2012). 4. Engler, A. J., Sen, S., Sweeney, H. L. & Discher, D. E. Matrix Elasticity Directs Stem Cell Lineage Specification. Cell 126, 677-689 (2006). 5. Ingber, D. E. et al. Tissue Engineering and Developmental Biology: Going Biomimetic. Tissue Eng. 12, 3265-3283 (2007). 6. Mammoto, T., Mammoto, A. & Ingber, D. E. Mechanobiology and… Advisors/Committee Members: Kelly, Daniel.

Subjects/Keywords: Hydrostatic pressure; Mechanobiology; YAP; N-cadherin

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

APRILE, P. (2019). Unravelling the role of mechanical cues on the chondrogenic differentiation of stem cells. (Thesis). Trinity College Dublin. Retrieved from http://hdl.handle.net/2262/91120

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

APRILE, PAOLA. “Unravelling the role of mechanical cues on the chondrogenic differentiation of stem cells.” 2019. Thesis, Trinity College Dublin. Accessed January 27, 2021. http://hdl.handle.net/2262/91120.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

APRILE, PAOLA. “Unravelling the role of mechanical cues on the chondrogenic differentiation of stem cells.” 2019. Web. 27 Jan 2021.

Vancouver:

APRILE P. Unravelling the role of mechanical cues on the chondrogenic differentiation of stem cells. [Internet] [Thesis]. Trinity College Dublin; 2019. [cited 2021 Jan 27]. Available from: http://hdl.handle.net/2262/91120.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

APRILE P. Unravelling the role of mechanical cues on the chondrogenic differentiation of stem cells. [Thesis]. Trinity College Dublin; 2019. Available from: http://hdl.handle.net/2262/91120

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Colorado State University

5. Chernyavskaya, Yelena. Voltage gated calcium channel β2 protein is required in the heart for control of cell proliferation and heart tube integrity, The.

Degree: PhD, Biology, 2011, Colorado State University

URL: http://hdl.handle.net/10217/70435

► L-type calcium channels regulate calcium (LTCC) entry into cardiomyocytes. CACNB2 (β2) LTCC auxiliary subunits traffic the pore-forming CACNA subunit to the membrane and modulate channel… (more)

Subjects/Keywords: cardiac; development; LTCC; N-cadherin; adhesion; zebrafish

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Chernyavskaya, Y. (2011). Voltage gated calcium channel β2 protein is required in the heart for control of cell proliferation and heart tube integrity, The. (Doctoral Dissertation). Colorado State University. Retrieved from http://hdl.handle.net/10217/70435

Chicago Manual of Style (16^th Edition):

Chernyavskaya, Yelena. “Voltage gated calcium channel β2 protein is required in the heart for control of cell proliferation and heart tube integrity, The.” 2011. Doctoral Dissertation, Colorado State University. Accessed January 27, 2021. http://hdl.handle.net/10217/70435.

MLA Handbook (7^th Edition):

Chernyavskaya, Yelena. “Voltage gated calcium channel β2 protein is required in the heart for control of cell proliferation and heart tube integrity, The.” 2011. Web. 27 Jan 2021.

Vancouver:

Chernyavskaya Y. Voltage gated calcium channel β2 protein is required in the heart for control of cell proliferation and heart tube integrity, The. [Internet] [Doctoral dissertation]. Colorado State University; 2011. [cited 2021 Jan 27]. Available from: http://hdl.handle.net/10217/70435.

Council of Science Editors:

Chernyavskaya Y. Voltage gated calcium channel β2 protein is required in the heart for control of cell proliferation and heart tube integrity, The. [Doctoral Dissertation]. Colorado State University; 2011. Available from: http://hdl.handle.net/10217/70435

University of Illinois – Urbana-Champaign

6. Qin, Ellen C. Engineered N-cadherin substrates for stem cell differentiation.

Degree: MS, Chemical Engineering, 2016, University of Illinois – Urbana-Champaign

URL: http://hdl.handle.net/2142/92878

► In the case of injury, aging, or disease, tissues in the body may have a limited capability to regenerate. As a result, great interest have… (more)

Subjects/Keywords: N-cadherin; Hydrogel; Stiffness; Bone marrow stromal cell

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Qin, E. C. (2016). Engineered N-cadherin substrates for stem cell differentiation. (Thesis). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/92878

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Qin, Ellen C. “Engineered N-cadherin substrates for stem cell differentiation.” 2016. Thesis, University of Illinois – Urbana-Champaign. Accessed January 27, 2021. http://hdl.handle.net/2142/92878.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Qin, Ellen C. “Engineered N-cadherin substrates for stem cell differentiation.” 2016. Web. 27 Jan 2021.

Vancouver:

Qin EC. Engineered N-cadherin substrates for stem cell differentiation. [Internet] [Thesis]. University of Illinois – Urbana-Champaign; 2016. [cited 2021 Jan 27]. Available from: http://hdl.handle.net/2142/92878.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Qin EC. Engineered N-cadherin substrates for stem cell differentiation. [Thesis]. University of Illinois – Urbana-Champaign; 2016. Available from: http://hdl.handle.net/2142/92878

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

7. Bard, Lucie. Dynamique des interactions protéiques lors de la maturation synaptique : etude du trafic de surface des récepteurs NMDA : Valorization of Mexican agriculture by preservation and drying by instant autovaporization : case of green pepper.

Degree: Docteur es, Sciences, technologie, santé. Neurosciences, 2009, Université de Bordeaux Segalen

URL: http://www.theses.fr/2009BOR21640

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Les synapses se forment selon plusieurs étapes comprenant la synaptogenèse, la maturation et la plasticité synaptique. Les molécules d’adhésion et les récepteurs ionotropiques du glutamate… (more)

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Les synapses se forment selon plusieurs étapes comprenant la synaptogenèse, la maturation et la plasticité synaptique. Les molécules d’adhésion et les récepteurs ionotropiques du glutamate ont des rôles clés dans ces processus. Lors de ma thèse, je me suis intéressée à la dynamique des interactions impliquant deux protéines membranaires, la N-cadhérine et le récepteur NMDA. La N-cadhérine joue un rôle important dans l’induction de la croissance axonale mais les mécanismes moléculaires sous-jacents sont peu connus. Par des approches de vidéo-microscopie et de pinces optiques, j’ai démontré que la transmission directe des forces générées par le flux rétrograde d’actine aux adhésions N-cadhérines, via les caténines, induit l’avancée du cône de croissance. Les récepteurs NMDA synaptiques ont un rôle crucial dans la maturation et la plasticité synaptique, néanmoins, les mécanismes moléculaires régulant la distribution des récepteurs NMDA synaptiques sont peu connus. En combinant le développement de peptides compétiteurs divalents et des approches d’imagerie haute résolution, nous avons étudié la dynamique de surface des récepteurs NMDA endogènes. Mes résultats montrent que l’interaction dynamique entre les protéines d’échafaudage à domaine PDZ et les récepteurs NMDA contenant la sous-unité NR2A régule leur rétention synaptique et leur distribution de surface. Le déplacement des récepteurs NMDA contenant la sous-unité NR2A en dehors des synapses est compensé par une insertion synaptique de récepteurs contenant la sous-unité NR2B, indiquant que l’ancrage synaptique des différents sous-types de récepteurs NMDA est différentiellement régulé. De plus, cette redistribution des récepteurs NMDA affecte la maturation et la plasticité synaptique. L’ensemble de ces résultats révèle une régulation rapide et spécifique des récepteurs NMDA synaptiques par les protéines à domaine PDZ suggérant un rôle de l’organisation de la densité postsynaptique dans la stabilisation synaptique des récepteurs et les processus adaptatifs.

The formation of synapses follows different steps including synaptogenesis, maturation and plasticity. Adhesion molecules and ionotropic receptors play key roles in these processes. During my thesis, I have been interested in the dynamics of the interactions mediated by two membrane proteins, N-cadherin and the NMDA receptor N-cadherin plays important roles in axon outgrowth, but the molecular mechanisms underlying this effect are mostly unknown. Using live imaging and optical trapping, I demonstrated that the direct transmission of actin-based traction forces to N-cadherin adhesions, through catenin partners, drives growth cone advance. Synaptic NMDA receptors (NMDARs) play key roles during synaptic refinement and plasticity, however the molecular mechanisms that govern the distribution of the synaptic surface NMDARs are largely unknown. We investigated the dynamics of endogenous NMDARs using high-resolution single particle imaging and a newly-developed biomimetic divalent competing ligand. My results show that…

Advisors/Committee Members: Groc, Laurent (thesis director).

Subjects/Keywords: N-cadhérine; Récepteur NMDA; Synapse; Développement; Trafic; N-cadherin; NMDA receptor; Synapse; Development; Trafficking

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Bard, L. (2009). Dynamique des interactions protéiques lors de la maturation synaptique : etude du trafic de surface des récepteurs NMDA : Valorization of Mexican agriculture by preservation and drying by instant autovaporization : case of green pepper. (Doctoral Dissertation). Université de Bordeaux Segalen. Retrieved from http://www.theses.fr/2009BOR21640

Chicago Manual of Style (16^th Edition):

Bard, Lucie. “Dynamique des interactions protéiques lors de la maturation synaptique : etude du trafic de surface des récepteurs NMDA : Valorization of Mexican agriculture by preservation and drying by instant autovaporization : case of green pepper.” 2009. Doctoral Dissertation, Université de Bordeaux Segalen. Accessed January 27, 2021. http://www.theses.fr/2009BOR21640.

MLA Handbook (7^th Edition):

Bard, Lucie. “Dynamique des interactions protéiques lors de la maturation synaptique : etude du trafic de surface des récepteurs NMDA : Valorization of Mexican agriculture by preservation and drying by instant autovaporization : case of green pepper.” 2009. Web. 27 Jan 2021.

Vancouver:

Bard L. Dynamique des interactions protéiques lors de la maturation synaptique : etude du trafic de surface des récepteurs NMDA : Valorization of Mexican agriculture by preservation and drying by instant autovaporization : case of green pepper. [Internet] [Doctoral dissertation]. Université de Bordeaux Segalen; 2009. [cited 2021 Jan 27]. Available from: http://www.theses.fr/2009BOR21640.

Council of Science Editors:

Bard L. Dynamique des interactions protéiques lors de la maturation synaptique : etude du trafic de surface des récepteurs NMDA : Valorization of Mexican agriculture by preservation and drying by instant autovaporization : case of green pepper. [Doctoral Dissertation]. Université de Bordeaux Segalen; 2009. Available from: http://www.theses.fr/2009BOR21640

8. Poppe, Ana Carolina Machado. Avaliação de marcadores relacionados à transição epitélio-mesênquima na endometriose pélvica.

Degree: Mestrado, Obstetrícia e Ginecologia, 2013, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/5/5139/tde-20022014-092016/ ;

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Introdução: A endometriose é uma doença ginecológica comum caracterizada pela presença de estroma e/ou glândula endometrial fora da cavidade uterina, e que não possui sua… (more)

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Introdução: A endometriose é uma doença ginecológica comum caracterizada pela presença de estroma e/ou glândula endometrial fora da cavidade uterina, e que não possui sua etiopatogenia bem estabelecida. A transição epitélio-mesênquima (TEM) é um processo que consiste em uma série de mudanças no fenótipo de células epiteliais que fazem com que estas células assumam características de células mesenquimais. Assim como observado na TEM, as células endometriais no contexto da endometriose apresentam capacidade migratória, invasibilidade e elevada resistência à apoptose. As moléculas de adesão têm adquirido crescente relevância na TEM, pois relacionam-se à perda de adesão célula-célula com o aumento da invasão e metástase. O objetivo deste estudo foi investigar a expressão de marcadores relacionados com a TEM na endometriose superficial, ovariana e profunda. Pacientes e Métodos: Foram selecionadas 103 mulheres que preenchiam os critérios de inclusão estabelecidos, constituindo 2 grupos de estudo independentes entre si: 18 mulheres com endometriose peritoneal, ovariana e profunda concomitantes; 85 mulheres com endometriose ovariana e/ou profunda, dividido em 44 mulheres com endometriose ovariana e 41 com endometriose intestinal. Através de reações de imunoistoquímica, a expressão proteica dos marcadores e-caderina, n-caderina, betacatenina, receptor de estrogênio e receptor de progesterona foram avaliados nos tecidos de interesse em cada grupo de estudo. Além dos locais de doença, as mulheres foram avaliadas quanto à relação com a fase do ciclo e à classificação histológica da doença. Resultados: As lesões de endometriose de ovário mostraram uma menor expressão de n-caderina em comparação às lesões de intestino e peritônio (p=0,032). O receptor de estrogênio e receptor de progesterona se mostraram significativamente menos expressos no componente epitelial da doença de ovário do que no epitélio da endometriose de peritônio e intestino (p=0,002; p=0,48). A expressão da n-caderina apresentou uma correlação direta com a expressão do receptor de estrogênio no estroma da endometriose de intestino (p=0,036). Conclusão: Estes resultados sugerem que a transição epitélio-mesênquima esteja envolvida na etiopatogenia da endometriose, demonstrando que a doença de ovário se comporta de maneira diferente da doença superficial e da doença infiltrativa profunda, sendo a n-caderina um importante fator envolvido neste processo possivelmente influenciada pela ação do estrogênio

Background: Endometriosis is a common gynecological disease defined as the presence of ectopic endometrial glands and stroma outside the uterine cavity, and its pathogenesis is not well established. The epithelial to mesenchymal transition (EMT) is a process consisting of a series of changes in the phenotype of epithelial cells that make these cells assume the characteristics of mesenchymal cells. As observed in the EMT, endometrial cells in the context of endometriosis have the capacity of migration, invasiveness and high resistance to apoptosis. . The adhesion…

Advisors/Committee Members: Abrão, Mauricio Simões.

Subjects/Keywords: beta-catenin; Beta-catenina; E-caderinas; E-cadherin; Endometriose; Endometriosis; Epithelial-mesenchymal transition; Estrogen receptor; N-caderinas; N-cadherin; Progesterone receptor; Receptores de progesterona; Receptores estrogênicos; Transição epitélial-mesenquimal

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Poppe, A. C. M. (2013). Avaliação de marcadores relacionados à transição epitélio-mesênquima na endometriose pélvica. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5139/tde-20022014-092016/ ;

Chicago Manual of Style (16^th Edition):

Poppe, Ana Carolina Machado. “Avaliação de marcadores relacionados à transição epitélio-mesênquima na endometriose pélvica.” 2013. Masters Thesis, University of São Paulo. Accessed January 27, 2021. http://www.teses.usp.br/teses/disponiveis/5/5139/tde-20022014-092016/ ;.

MLA Handbook (7^th Edition):

Poppe, Ana Carolina Machado. “Avaliação de marcadores relacionados à transição epitélio-mesênquima na endometriose pélvica.” 2013. Web. 27 Jan 2021.

Vancouver:

Poppe ACM. Avaliação de marcadores relacionados à transição epitélio-mesênquima na endometriose pélvica. [Internet] [Masters thesis]. University of São Paulo; 2013. [cited 2021 Jan 27]. Available from: http://www.teses.usp.br/teses/disponiveis/5/5139/tde-20022014-092016/ ;.

Council of Science Editors:

Poppe ACM. Avaliação de marcadores relacionados à transição epitélio-mesênquima na endometriose pélvica. [Masters Thesis]. University of São Paulo; 2013. Available from: http://www.teses.usp.br/teses/disponiveis/5/5139/tde-20022014-092016/ ;

Washington State University

9. [No author]. SYNERGISTIC ROLES OF CHEMICAL AND MECHANICAL STIMULI IN IMPROVING THE ELASTICITIES OF ENGINEERED ARTICULAR CARTILAGE TISSUES THROUGH MECHANOTRANSDUCTION PATHWAYS .

Degree: 2016, Washington State University

URL: http://hdl.handle.net/2376/12053

► Articular cartilage (AC) acts as a bearing surface to transmit forces within a joint. Because AC is avascular and has a low cellular density, it… (more)

▼ Articular cartilage (AC) acts as a bearing surface to transmit forces within a joint. Because AC is avascular and has a low cellular density, it has a limited ability for self-repair upon injury. Current clinical treatments are incapable of restoring the functionality of the tissue. Tissue engineering of AC offers a promising alternative to current therapies. As such, the overall objective of this dissertation is to better understand the factors that improve the mechanical function of engineered AC tissues. Toward this end, we examine the synergistic effects of oscillating hydrostatic pressure (OHP) and transforming growth factor beta 3 (TGF-β3) on the elastic moduli of engineered AC from human adipose-derived stem cells (hASCs). Tissues grown with OHP were compared with static cultures in the form of micromass and pellet. Using atomic force microscopy (AFM) to quantify the elastic modulus of the engineered tissues, we found that OHP induces a 44-fold increase in the elastic modulus compared to the micromass and pellet samples. Supplementation with TGF-β3 further increased the elastic modulus in OHP samples by 1.86-fold. Because N-cadherins are important in the initial steps of mesenchymal stem cell chondrogenic differentiation, single molecule force spectroscopy (SMFS) was used to quantify the expression of N-cadherins on the surfaces of hASCs undergoing chondrogenesis. Tissues grown in the bioreactor with or without OHP exhibited a positive correlation between SOX9 mRNA expression and N-cadherin expression and TGF-β3 supplementation increased SOX9 and N-cadherin expression. These results suggest that TGF-β3 supplementation in the CBR improves chondrogenic differentiation through a path dependent on N-cadherin expression. Since OHP significantly increased the elastic modulus of engineered tissues, we believe that the mechanical stimulation is being transduced into the cell via mechanotransduction. To investigate this mechanism, we probed for the mechanoreceptor β1-integrin because of its frequency in chondrocytes and function in cell adhesion. From this exploration, we found that tissues with a less robust extracellular matrix (ECM), lower elastic modulus, had a lower expression of β1-integrins on their cell surfaces. With OHP, TGF-β3 increased the elastic modulus by 1.9-fold and decreased the β1-integrin count by 1.1-fold. Advisors/Committee Members: Abu-Lail, Nehal I (advisor).

Subjects/Keywords: Biomedical engineering; articular cartilage; Atomic force microscopy; Integrin; N-cadherin; tissue engineering

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APA (6^th Edition):

author], [. (2016). SYNERGISTIC ROLES OF CHEMICAL AND MECHANICAL STIMULI IN IMPROVING THE ELASTICITIES OF ENGINEERED ARTICULAR CARTILAGE TISSUES THROUGH MECHANOTRANSDUCTION PATHWAYS . (Thesis). Washington State University. Retrieved from http://hdl.handle.net/2376/12053

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

author], [No. “SYNERGISTIC ROLES OF CHEMICAL AND MECHANICAL STIMULI IN IMPROVING THE ELASTICITIES OF ENGINEERED ARTICULAR CARTILAGE TISSUES THROUGH MECHANOTRANSDUCTION PATHWAYS .” 2016. Thesis, Washington State University. Accessed January 27, 2021. http://hdl.handle.net/2376/12053.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

author], [No. “SYNERGISTIC ROLES OF CHEMICAL AND MECHANICAL STIMULI IN IMPROVING THE ELASTICITIES OF ENGINEERED ARTICULAR CARTILAGE TISSUES THROUGH MECHANOTRANSDUCTION PATHWAYS .” 2016. Web. 27 Jan 2021.

Vancouver:

author] [. SYNERGISTIC ROLES OF CHEMICAL AND MECHANICAL STIMULI IN IMPROVING THE ELASTICITIES OF ENGINEERED ARTICULAR CARTILAGE TISSUES THROUGH MECHANOTRANSDUCTION PATHWAYS . [Internet] [Thesis]. Washington State University; 2016. [cited 2021 Jan 27]. Available from: http://hdl.handle.net/2376/12053.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

author] [. SYNERGISTIC ROLES OF CHEMICAL AND MECHANICAL STIMULI IN IMPROVING THE ELASTICITIES OF ENGINEERED ARTICULAR CARTILAGE TISSUES THROUGH MECHANOTRANSDUCTION PATHWAYS . [Thesis]. Washington State University; 2016. Available from: http://hdl.handle.net/2376/12053

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Toronto

10. Xu, Songyi. N-cadherin Regulation of Vascular Smooth Muscle Cells; the Role of DDR1 and Rho GTPases.

Degree: PhD, 2020, University of Toronto

URL: http://hdl.handle.net/1807/101328

► N-cadherin mediates cell-cell contacts in vascular smooth muscle cells (VSMCs) and regulates VSMC behaviours. Discoidin domain receptor 1 (DDR1) is a collagen binding receptor also… (more)

Subjects/Keywords: Cell-cell interaction; DDR1; N-cadherin; Rho GTPases; Vascular smooth muscle cells; 0307

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Xu, S. (2020). N-cadherin Regulation of Vascular Smooth Muscle Cells; the Role of DDR1 and Rho GTPases. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/101328

Chicago Manual of Style (16^th Edition):

Xu, Songyi. “N-cadherin Regulation of Vascular Smooth Muscle Cells; the Role of DDR1 and Rho GTPases.” 2020. Doctoral Dissertation, University of Toronto. Accessed January 27, 2021. http://hdl.handle.net/1807/101328.

MLA Handbook (7^th Edition):

Xu, Songyi. “N-cadherin Regulation of Vascular Smooth Muscle Cells; the Role of DDR1 and Rho GTPases.” 2020. Web. 27 Jan 2021.

Vancouver:

Xu S. N-cadherin Regulation of Vascular Smooth Muscle Cells; the Role of DDR1 and Rho GTPases. [Internet] [Doctoral dissertation]. University of Toronto; 2020. [cited 2021 Jan 27]. Available from: http://hdl.handle.net/1807/101328.

Council of Science Editors:

Xu S. N-cadherin Regulation of Vascular Smooth Muscle Cells; the Role of DDR1 and Rho GTPases. [Doctoral Dissertation]. University of Toronto; 2020. Available from: http://hdl.handle.net/1807/101328

Duke University

11. Hwang, Priscilla Y. Cadherin-Mediated Cell-Cell Interactions Regulates Phenotype And Morphology of Nucleus Pulposus Cells Of The Intervertebral Disc .

Degree: 2015, Duke University

URL: http://hdl.handle.net/10161/9870

► Juvenile nucleus pulposus (NP) cells of the intervertebral disc (IVD) are large, vacuolated cells that form cell clusters with numerous cell-cell interactions. With maturation… (more)

▼ Juvenile nucleus pulposus (NP) cells of the intervertebral disc (IVD) are large, vacuolated cells that form cell clusters with numerous cell-cell interactions. With maturation and aging, NP cells lose their ability to form these cell clusters, with associated changes in NP cell phenotype, morphology and proteoglycan synthesis that may contribute to IVD degeneration. Studies demonstrate healthy, juvenile NP cells exhibit potential for preservation of multi-cell clusters and NP cell phenotype when cultured upon soft, laminin-containing substrates; however, the mechanisms that regulate metabolism and phenotype of these NP cells are not understood. N-cadherin is a cell adhesion molecule that is present in juvenile NP cells, but disappears with age. The goal of this dissertation was to reveal the role of N-cadherin for NP cells in multi-cell clusters that contribute to the maintenance of the juvenile NP cell morphology and phenotype in vitro, and to evaluate the potential for laminin- functionalized poly(ethylene glycol) (PEG-LM) hydrogels to promote human NP cells towards a juvenile NP cell phenotype. In this dissertation, juvenile porcine IVD cells were promoted to form cell clusters in vitro, and analyzed for preservation of the juvenile NP phenotype on soft, laminin-rich hydrogels. In the first part of this dissertation, preservation of the porcine juvenile NP cell phenotype and presence of N-cadherin was analyzed by culturing porcine NP cells on soft, laminin-rich or PEG-LM hydrogels. Secondly, cadherin-blocking experiments were performed to prevent cluster formation in order to study the importance of cluster formation in NP cell signaling. Finally, human IVD cells were cultured on PEG-LM hydrogels to investigate the potential to revert degenerate, human NP cells toward a juvenile NP cell phenotype and morphology. Findings reveal soft (<500 Pa), laminin-rich substrates promote NP cell clustering, a key feature of the juvenile NP cell that is associated with N-cadherin positive expression. Additionally, N-cadherin-mediated cell-clustering regulates NP cell matrix production and gene expression of NP-specific and NP-matrix related markers. Inhibition of N-cadherin-mediated contacts resulted in decreased expression of juvenile NP cell features. Finally, juvenile human NP cells are also able to form N-cadherin positive cell clusters on soft, PEG-LM hydrogels with higher expression of juvenile NP cell features compared to culturing on stiff PEG-LM hydrogels. Some degenerate, human NP cells are also able to form N-cadherin positive cell clusters with some features of the juvenile NP cell. The studies presented in this dissertation support the proposed hypothesis and establish the importance of soft, laminin-rich substrates in promoting NP cell clustering behaviors with associated features of a juvenile cell phenotype and morphology. Additionally, these studies establish a regulatory role for N-cadherin in juvenile NP cells and suggest that preservation of N-cadherin-mediated cell-cell contacts is… Advisors/Committee Members: Setton, Lori A (advisor).

Subjects/Keywords: Biomedical engineering; Biomechanics; intervertebral disc; laminin; microenvironmental cues; N-cadherin; nucleus pulposus; polyethylene glycol (PEG)

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Hwang, P. Y. (2015). Cadherin-Mediated Cell-Cell Interactions Regulates Phenotype And Morphology of Nucleus Pulposus Cells Of The Intervertebral Disc . (Thesis). Duke University. Retrieved from http://hdl.handle.net/10161/9870

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Hwang, Priscilla Y. “Cadherin-Mediated Cell-Cell Interactions Regulates Phenotype And Morphology of Nucleus Pulposus Cells Of The Intervertebral Disc .” 2015. Thesis, Duke University. Accessed January 27, 2021. http://hdl.handle.net/10161/9870.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Hwang, Priscilla Y. “Cadherin-Mediated Cell-Cell Interactions Regulates Phenotype And Morphology of Nucleus Pulposus Cells Of The Intervertebral Disc .” 2015. Web. 27 Jan 2021.

Vancouver:

Hwang PY. Cadherin-Mediated Cell-Cell Interactions Regulates Phenotype And Morphology of Nucleus Pulposus Cells Of The Intervertebral Disc . [Internet] [Thesis]. Duke University; 2015. [cited 2021 Jan 27]. Available from: http://hdl.handle.net/10161/9870.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Hwang PY. Cadherin-Mediated Cell-Cell Interactions Regulates Phenotype And Morphology of Nucleus Pulposus Cells Of The Intervertebral Disc . [Thesis]. Duke University; 2015. Available from: http://hdl.handle.net/10161/9870

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Louisiana State University

12. Yang, Yunlong. Molecular mechanisms of Bacillus thuringiensis resistance in the sugarcane borer.

Degree: PhD, Entomology, 2011, Louisiana State University

URL: etd-04212011-153427 ; https://digitalcommons.lsu.edu/gradschool_dissertations/2501

► The sugarcane borer, Diatraea saccharalis, is a major target pest of transgenic corn expressing Bacillus thuringiensis (Bt) proteins in many areas of the U.S. mid-southern… (more)

▼ The sugarcane borer, Diatraea saccharalis, is a major target pest of transgenic corn expressing Bacillus thuringiensis (Bt) proteins in many areas of the U.S. mid-southern region. A Cry1Ab-resistant (Cry1Ab-RR) strain of D. saccharalis has been developed from a single two-parent family-line. To examine the molecular mechanisms of the Cry1Ab resistance in this insect strain, cDNAs of five types of potential candidate genes related to Bt resistance were sequenced using reverse transcriptase polymerase chain reaction (RT-PCR) and 5’ rapid amplification of cDNA end (5’ RACE). The Bt resistance candidate genes examined included three trypsins (DsTRYs), three chymotrypsins (DsCHYs), three aminopeptidases N (DsAPNs), one cadherin (DsCAD1), and three alkaline phosphatases (DsALPs). cDNA sequence of each gene and its expression levels were compared between a Cry1Ab-susceptible strain (Cry1Ab-SS) and the Cry1Ab-RR at different larval growth stages. The cDNA sequences of these genes were identical between Cry1Ab-SS and -RR strains. Gene expression levels of the trypsins, chymotrypsins, and alkaline phosphatases were similar between the two strains. There were also no significant differences in total enzymatic activity of trypsins, chymotrypsins, and alkaline phosphatases between Cry1Ab-SS and -RR. However, the gene expression levels of the three DsAPNs and the DsCAD1 in Cry1Ab-RR were significantly lower than those of the Cry1Ab-SS. RNA interference (RNAi) was employed to knock-down the three DsAPNs and the DsCAD1 in the Cry1Ab-SS strain by oral droplet feeding to neonates. Down-regulations of the expressions of these four genes by RNAi were correlated with the decrease in susceptibility to Cry1Ab toxin. Silencing each of the three DsAPNs in D. saccharalis in vivo by RNAi resulted in a decrease of total APN activity. In addition, the total specific APN activities from Cry1Ab-RR larvae were significantly lower than those of the Cry1Ab-SS strain. These results suggest that reduction in expression of the three DsAPNs and DsCAD1 is functionally associated with the Cry1Ab resistance in D. saccharalis.

Subjects/Keywords: trypsin; insecticide resistance mechanism; Bacillus thuringiensis; Diatraea saccharalis; alkaline phosphatase; cadherin; aminopeptidase N; chymotrypsin

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Yang, Y. (2011). Molecular mechanisms of Bacillus thuringiensis resistance in the sugarcane borer. (Doctoral Dissertation). Louisiana State University. Retrieved from etd-04212011-153427 ; https://digitalcommons.lsu.edu/gradschool_dissertations/2501

Chicago Manual of Style (16^th Edition):

Yang, Yunlong. “Molecular mechanisms of Bacillus thuringiensis resistance in the sugarcane borer.” 2011. Doctoral Dissertation, Louisiana State University. Accessed January 27, 2021. etd-04212011-153427 ; https://digitalcommons.lsu.edu/gradschool_dissertations/2501.

MLA Handbook (7^th Edition):

Yang, Yunlong. “Molecular mechanisms of Bacillus thuringiensis resistance in the sugarcane borer.” 2011. Web. 27 Jan 2021.

Vancouver:

Yang Y. Molecular mechanisms of Bacillus thuringiensis resistance in the sugarcane borer. [Internet] [Doctoral dissertation]. Louisiana State University; 2011. [cited 2021 Jan 27]. Available from: etd-04212011-153427 ; https://digitalcommons.lsu.edu/gradschool_dissertations/2501.

Council of Science Editors:

Yang Y. Molecular mechanisms of Bacillus thuringiensis resistance in the sugarcane borer. [Doctoral Dissertation]. Louisiana State University; 2011. Available from: etd-04212011-153427 ; https://digitalcommons.lsu.edu/gradschool_dissertations/2501

Louisiana State University

13. Yang, Yunlong. Molecular Mechanisms of Bacillus thuringiensis Resistance in the Sugarcane Borer.

Degree: PhD, Entomology, 2011, Louisiana State University

URL: etd-04212011-160643 ; https://digitalcommons.lsu.edu/gradschool_dissertations/3473

► The sugarcane borer, Diatraea saccharalis, is a major target pest of transgenic corn expressing Bacillus thuringiensis (Bt) proteins in many areas of the U.S. mid-southern… (more)

▼ The sugarcane borer, Diatraea saccharalis, is a major target pest of transgenic corn expressing Bacillus thuringiensis (Bt) proteins in many areas of the U.S. mid-southern region. A Cry1Ab-resistant (Cry1Ab-RR) strain of D. saccharalis has been developed from a single two-parent family-line. To examine the molecular mechanisms of the Cry1Ab resistance in this insect strain, cDNAs of five types of potential candidate genes related to Bt resistance were sequenced using reverse transcriptase polymerase chain reaction (RT-PCR) and 5’ rapid amplification of cDNA end (5’ RACE). The Bt resistance candidate genes examined included three trypsins (DsTRYs), three chymotrypsins (DsCHYs), three aminopeptidases N (DsAPNs), one cadherin (DsCAD1), and three alkaline phosphatases (DsALPs). cDNA sequence of each gene and its expression levels were compared between a Cry1Ab-susceptible strain (Cry1Ab-SS) and the Cry1Ab-RR at different larval growth stages. The cDNA sequences of these genes were identical between Cry1Ab-SS and -RR strains. Gene expression levels of the trypsins, chymotrypsins, and alkaline phosphatases were similar between the two strains. There were also no significant differences in total enzymatic activity of trypsins, chymotrypsins, and alkaline phosphatases between Cry1Ab-SS and -RR. However, the gene expression levels of the three DsAPNs and the DsCAD1 in Cry1Ab-RR were significantly lower than those of the Cry1Ab-SS. RNA interference (RNAi) was employed to knock-down the three DsAPNs and the DsCAD1 in the Cry1Ab-SS strain by oral droplet feeding to neonates. Down-regulations of the expressions of these four genes by RNAi were correlated with the decrease in susceptibility to Cry1Ab toxin. Silencing each of the three DsAPNs in D. saccharalis in vivo by RNAi resulted in a decrease of total APN activity. In addition, the total specific APN activities from Cry1Ab-RR larvae were significantly lower than those of the Cry1Ab-SS strain. These results suggest that reduction in expression of the three DsAPNs and DsCAD1 is functionally associated with the Cry1Ab resistance in D. saccharalis.

Subjects/Keywords: Bacillus thuringiensis; insecticide resistance mechanism; Diatraea saccharalis; alkaline phosphatase; aminopeptidase N; cadherin; chymotrypsin; trypsin

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Yang, Y. (2011). Molecular Mechanisms of Bacillus thuringiensis Resistance in the Sugarcane Borer. (Doctoral Dissertation). Louisiana State University. Retrieved from etd-04212011-160643 ; https://digitalcommons.lsu.edu/gradschool_dissertations/3473

Chicago Manual of Style (16^th Edition):

Yang, Yunlong. “Molecular Mechanisms of Bacillus thuringiensis Resistance in the Sugarcane Borer.” 2011. Doctoral Dissertation, Louisiana State University. Accessed January 27, 2021. etd-04212011-160643 ; https://digitalcommons.lsu.edu/gradschool_dissertations/3473.

MLA Handbook (7^th Edition):

Yang, Yunlong. “Molecular Mechanisms of Bacillus thuringiensis Resistance in the Sugarcane Borer.” 2011. Web. 27 Jan 2021.

Vancouver:

Yang Y. Molecular Mechanisms of Bacillus thuringiensis Resistance in the Sugarcane Borer. [Internet] [Doctoral dissertation]. Louisiana State University; 2011. [cited 2021 Jan 27]. Available from: etd-04212011-160643 ; https://digitalcommons.lsu.edu/gradschool_dissertations/3473.

Council of Science Editors:

Yang Y. Molecular Mechanisms of Bacillus thuringiensis Resistance in the Sugarcane Borer. [Doctoral Dissertation]. Louisiana State University; 2011. Available from: etd-04212011-160643 ; https://digitalcommons.lsu.edu/gradschool_dissertations/3473

14. Fievre, Sabine. Mécanismes moléculaires de la stabilisation synaptique des récepteurs du glutamate de type kaïnate dans les cellules pyramidales de CA3 : Molecular mechanisms for the synaptic stabilization of kainate receptors in CA3 pyramidal cells.

Degree: Docteur es, Neurosciences, 2015, Bordeaux

URL: http://www.theses.fr/2015BORD0226

►

Les récepteurs ionotropiques du glutamate peuvent être compartimentés de manière très spécifique au niveau des différentes afférences synaptiques d’un neurone. Dans les neurones pyramidaux de… (more)

▼

Les récepteurs ionotropiques du glutamate peuvent être compartimentés de manière très spécifique au niveau des différentes afférences synaptiques d’un neurone. Dans les neurones pyramidaux de CA3, les récepteurs de type kaïnate (rKA) post-synaptiques sont localisés à la synapse formée entre les fibres moussues et les cellules pyramidales de CA3 (synapse FM-CA3) mais ils sont totalement absents des autres afférences glutamatergiques sur ce même neurone. Nous avons cherché à comprendre les mécanismes moléculaires de cette compartimentation subcellulaire. En réalisant une cartographie fonctionnelle des récepteurs du glutamate par décageage focalisé de glutamate dans les cellules pyramidales de CA3, nous avons montré que les rKA présentent une localisation subcellulaire strictement confinée dans les excroissances épineuses, éléments post-synaptiques des synapses FM-CA3, et sont exclus des compartiments somato-dendritiques, contrairement aux récepteurs AMPA. Nous avons identifié une séquence du domaine C-terminal de GluK2a nécessaire pour la stabilisation des rKA. Cette séquence est responsable d’une interaction avec la protéine d’adhérence N-cadhérine. L’altération de la fonction de la N-cadhérine dans les cellules pyramidales de CA3 entraine une déstabilisation des rKA à la synapse FM-CA3. Ces travaux suggèrent que plusieurs mécanismes participent à la compartimentation des rKA à la synapse FMCA3 impliquant le recrutement et la stabilisation des rKA par les N-cadhérines.

Distinct subtypes of ionotropic glutamate receptors can be segregate to specific synaptic inputs in a given neuron. In CA3 pyramidal cells (PCs), kainate receptors (KARs) are present at mossy fiber (mf) synapses and absent from other glutamatergic inputs. The mechanisms for such a constrained subcellular segregation is not known. We have investigated the molecular determinants responsible for the subcellular segregation of KARs at mf-CA3 synapses. Using functional mapping of glutamate receptors by focal glutamate uncaging we show that KARs display a strictly confined expression on thorny excrescences, the postsynaptic elements of mf-CA3 synapses, being excluded from extrasynaptic somatodendritic compartments, at variance with AMPA receptors. We have identified a sequence in the GluK2a C-terminal domain necessary for restricted expression of KARs which is responsible for GluK2a interaction with N-Cadherin. Targeted deletion of N-Cadherin or overexpression of a dominant negative N-Cadherin in CA3 PCs greatly induce a destabilization of KARs at the mf-CA3 synapses. Our findings suggest that multiple mechanisms combine to control the compartmentalization of KARs at mf-CA3 synapses, including a stringent control of the amount of GluK2 subunit in CA3 PCs, a limited number of slots for KARs, and the recruitment/stabilization of KARs by N-Cadherins.

Advisors/Committee Members: Mulle, Christophe (thesis director).

Subjects/Keywords: Spécification synaptique; Ségrégation subcellulaire; Récepteur kaïnate; CA3; N-cadhérine; Synapse specification; Subcellular segregation; Kainate receptors; CA3; N-Cadherin

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Fievre, S. (2015). Mécanismes moléculaires de la stabilisation synaptique des récepteurs du glutamate de type kaïnate dans les cellules pyramidales de CA3 : Molecular mechanisms for the synaptic stabilization of kainate receptors in CA3 pyramidal cells. (Doctoral Dissertation). Bordeaux. Retrieved from http://www.theses.fr/2015BORD0226

Chicago Manual of Style (16^th Edition):

Fievre, Sabine. “Mécanismes moléculaires de la stabilisation synaptique des récepteurs du glutamate de type kaïnate dans les cellules pyramidales de CA3 : Molecular mechanisms for the synaptic stabilization of kainate receptors in CA3 pyramidal cells.” 2015. Doctoral Dissertation, Bordeaux. Accessed January 27, 2021. http://www.theses.fr/2015BORD0226.

MLA Handbook (7^th Edition):

Fievre, Sabine. “Mécanismes moléculaires de la stabilisation synaptique des récepteurs du glutamate de type kaïnate dans les cellules pyramidales de CA3 : Molecular mechanisms for the synaptic stabilization of kainate receptors in CA3 pyramidal cells.” 2015. Web. 27 Jan 2021.

Vancouver:

Fievre S. Mécanismes moléculaires de la stabilisation synaptique des récepteurs du glutamate de type kaïnate dans les cellules pyramidales de CA3 : Molecular mechanisms for the synaptic stabilization of kainate receptors in CA3 pyramidal cells. [Internet] [Doctoral dissertation]. Bordeaux; 2015. [cited 2021 Jan 27]. Available from: http://www.theses.fr/2015BORD0226.

Council of Science Editors:

Fievre S. Mécanismes moléculaires de la stabilisation synaptique des récepteurs du glutamate de type kaïnate dans les cellules pyramidales de CA3 : Molecular mechanisms for the synaptic stabilization of kainate receptors in CA3 pyramidal cells. [Doctoral Dissertation]. Bordeaux; 2015. Available from: http://www.theses.fr/2015BORD0226

University of Georgia

15. Chen, Jiang. Localization and functional studies of the cadherin BT-R1 as a Bacillus thuringiensis Cry1A-binding protein in the midgut of tobacco hornworm (Manduca sexta).

Degree: 2014, University of Georgia

URL: http://hdl.handle.net/10724/23603

► The members in Bacillus thuringiensis (Bt) Cry1A family have specific toxicity toward lepidopteran larva. A critical step in Bt-mediated insecticidal action is the binding of… (more)

▼ The members in Bacillus thuringiensis (Bt) Cry1A family have specific toxicity toward lepidopteran larva. A critical step in Bt-mediated insecticidal action is the binding of Bt toxin to its target molecules on insect midgut epithelium. Three Cry1A-binding proteins, aminopeptidase MsAPN1, the cadherin Bt-R1 and the membrane-type alkaline phosphatase (m-ALP), had been identified in the midgut of tobacco hornworm (Manduca sexta). Immunohistochemistry illustrated that these binding proteins had different localization on M. sexta larval midgut epithelia. To compare with the immunolocalization of Cry1A-binding proteins, Cry1A toxins showed co-localization on insect midgut microvilli. CR12-MPED, which is the membrane proximal part of Bt-R1, was identified as a critical region for Cry1Ab binding. This fragment was over-expressed and purified as a peptide from Escherichia coli. Unexpectedly, the Cry1Ab-induced M. sexta larval mortality was not blocked, but significantly enhanced by the addition of CR12-MPED. Further bioassays indicated that CR12-MPED could also potentiate Cry1Ac toxicity against tobacco budworm (Heliothis virescens) and corn earworm (Helicoverpa zea). When a putative Cry1A-binding epitope was removed from CR12-MPED, the derivative peptide (CR12-MPED/Del) lost binding to Cry1A 1toxins and the ability of toxicity enhancement. Far-UV circular dichroism (CD) and H-NMR spectroscopy showed that CR12-MPED was mainly composed of [beta]-strands and random coils in unfolded state. Histomicroscopy illustrated that CR12-MPED bound to midgut microvilli, but did not change Cry1A binding localization at these places. The CR12 sub-truncation was identified as the minimal region in CR12-MPED to enhance Cry1Ac toxicity against H. zea larvae. A proposed mechanism of this synergism was that the unfolded CR12-MPED accumulated onto microvilli through hydrophobic interactions, and Cry1A toxins could be attracted to these places by toxin-peptide binding, hence the Cry1A toxicity was increased. This discovery enables Cry1A toxins to effectively control lepidopteran pests even at low dosages, which can prevent insect resistance from high toxin selection pressure.

Subjects/Keywords: Bacillus thuringiensis; Cry1A; lepidopteran; Manduca sexta; Heliothis virescens; Helicoverpa zea; midgut; aminopeptidase N; cadherin; alkaline phosphatase; synergist

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Chen, J. (2014). Localization and functional studies of the cadherin BT-R1 as a Bacillus thuringiensis Cry1A-binding protein in the midgut of tobacco hornworm (Manduca sexta). (Thesis). University of Georgia. Retrieved from http://hdl.handle.net/10724/23603

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Chen, Jiang. “Localization and functional studies of the cadherin BT-R1 as a Bacillus thuringiensis Cry1A-binding protein in the midgut of tobacco hornworm (Manduca sexta).” 2014. Thesis, University of Georgia. Accessed January 27, 2021. http://hdl.handle.net/10724/23603.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Chen, Jiang. “Localization and functional studies of the cadherin BT-R1 as a Bacillus thuringiensis Cry1A-binding protein in the midgut of tobacco hornworm (Manduca sexta).” 2014. Web. 27 Jan 2021.

Vancouver:

Chen J. Localization and functional studies of the cadherin BT-R1 as a Bacillus thuringiensis Cry1A-binding protein in the midgut of tobacco hornworm (Manduca sexta). [Internet] [Thesis]. University of Georgia; 2014. [cited 2021 Jan 27]. Available from: http://hdl.handle.net/10724/23603.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Chen J. Localization and functional studies of the cadherin BT-R1 as a Bacillus thuringiensis Cry1A-binding protein in the midgut of tobacco hornworm (Manduca sexta). [Thesis]. University of Georgia; 2014. Available from: http://hdl.handle.net/10724/23603

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Freie Universität Berlin

16. Donandt, Klaus. Genetic analyses of the N-cadherin gene in patients with non-compaction cardiomyopathy and in patients with hypertrophic cardiomyopathy.

Degree: 2013, Freie Universität Berlin

URL: http://dx.doi.org/10.17169/refubium-13266

► Hypertrophic cardiomyopathy (HCM) is the second most common cardiomyopathy and the most common hereditary cardiac disease. As primary genetic cardiomyopathy the non-compaction cardiomyopathy (NC) is… (more)

▼ Hypertrophic cardiomyopathy (HCM) is the second most common cardiomyopathy and the most common hereditary cardiac disease. As primary genetic cardiomyopathy the non-compaction cardiomyopathy (NC) is becoming increasingly important. Structural changes of the coupling between N-cadherin proteins and cytoskeleton can lead to cardiomyopathy. N-cadherin is the only classic Cadherin within the connection of heart muscle cells and stabilization of the cytoskeleton. Its reduced or total loss of function showed serious aftereffects in animal studies. Detection of mutations in the N-cadherin gene, which cause a cardiomyopathy, is still pending. The demonstration of mutations in the N-cadherin gene could improve the understanding of the etiology of the disease and open up new opportunities for diagnosis and therapy. In this work, the N-cadherin genes of 58 patients with HCM and 47 Patients with NC were screened for mutations. For that the patient's DNA was extracted from leukocytes and all 16 exons of the N-cadherin gene were amplified by PCR. Afterwards is the sequencing and the comparison with the reference sequence. In the N-cadherin gene a total of 14 variants could be identified, of which six were already known. Besides eight synonymous SNPs, four non-synonymous single nucleotide polymorphisms (SNPs) and two suspected mutations were detected. Subsequently a control group of 350 healthy patients and a collective of 233 other HCM patients were screened for the mutations. In addition to the sequencing the restriction fragment length polymorphisms was applied. There were four non-synonymous SNPs and two mutations, which occured all in the group of HCM patients, identified in this study and discussed as potential genetic cause of HCM. A complete analysis of the meaning of these variants and their relationship to genetic cardiomyopathy will remain to further investigations. Advisors/Committee Members: m (gender), Priv.-Doz. Dr. med. C. Öczelik (firstReferee), Priv.-Doz. Dr. med. J. Fielitz (furtherReferee), Priv.-Doz. Dr. med. T. Neumann (furtherReferee).

Subjects/Keywords: cardiomyopathy; N-cadherin; CDH2; HCM; NC; LVNC; 600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit

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APA (6^th Edition):

Donandt, K. (2013). Genetic analyses of the N-cadherin gene in patients with non-compaction cardiomyopathy and in patients with hypertrophic cardiomyopathy. (Thesis). Freie Universität Berlin. Retrieved from http://dx.doi.org/10.17169/refubium-13266

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Donandt, Klaus. “Genetic analyses of the N-cadherin gene in patients with non-compaction cardiomyopathy and in patients with hypertrophic cardiomyopathy.” 2013. Thesis, Freie Universität Berlin. Accessed January 27, 2021. http://dx.doi.org/10.17169/refubium-13266.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Donandt, Klaus. “Genetic analyses of the N-cadherin gene in patients with non-compaction cardiomyopathy and in patients with hypertrophic cardiomyopathy.” 2013. Web. 27 Jan 2021.

Vancouver:

Donandt K. Genetic analyses of the N-cadherin gene in patients with non-compaction cardiomyopathy and in patients with hypertrophic cardiomyopathy. [Internet] [Thesis]. Freie Universität Berlin; 2013. [cited 2021 Jan 27]. Available from: http://dx.doi.org/10.17169/refubium-13266.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Donandt K. Genetic analyses of the N-cadherin gene in patients with non-compaction cardiomyopathy and in patients with hypertrophic cardiomyopathy. [Thesis]. Freie Universität Berlin; 2013. Available from: http://dx.doi.org/10.17169/refubium-13266

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Illinois – Urbana-Champaign

17. Vega Leonel, Johana Carolina. Engineering biomaterial surfaces with N-cadherin.

Degree: PhD, 0323, 2015, University of Illinois – Urbana-Champaign

URL: http://hdl.handle.net/2142/73037

► N-cadherin is a key protein that is responsible for cellular adhesion to neighboring cells in mesenchymal tissues. It plays a significant role in neural development,… (more)

Subjects/Keywords: N-Cadherin; Angiogenic; Neural Network; Microchannels; Hydrogels; Biomedical Devices; Growth Factors; Stem Cell and Cortical Neurons

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APA (6^th Edition):

Vega Leonel, J. C. (2015). Engineering biomaterial surfaces with N-cadherin. (Doctoral Dissertation). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/73037

Chicago Manual of Style (16^th Edition):

Vega Leonel, Johana Carolina. “Engineering biomaterial surfaces with N-cadherin.” 2015. Doctoral Dissertation, University of Illinois – Urbana-Champaign. Accessed January 27, 2021. http://hdl.handle.net/2142/73037.

MLA Handbook (7^th Edition):

Vega Leonel, Johana Carolina. “Engineering biomaterial surfaces with N-cadherin.” 2015. Web. 27 Jan 2021.

Vancouver:

Vega Leonel JC. Engineering biomaterial surfaces with N-cadherin. [Internet] [Doctoral dissertation]. University of Illinois – Urbana-Champaign; 2015. [cited 2021 Jan 27]. Available from: http://hdl.handle.net/2142/73037.

Council of Science Editors:

Vega Leonel JC. Engineering biomaterial surfaces with N-cadherin. [Doctoral Dissertation]. University of Illinois – Urbana-Champaign; 2015. Available from: http://hdl.handle.net/2142/73037

18. Michele Lynn Marquette. Effects of three-dimensional culture conditions on skeletal muscle myoblasts.

Degree: PhD, Cell Biology, 2007, The University of Texas Medical Branch

URL: http://hdl.handle.net/2152.3/86

► Effects of Three-dimensional Culture Conditions on Skeletal Muscle Myoblasts\r\n\r\nPublication No._____________\r\n\r\n\r\nMichele Lynn Marquette, Ph.D.\r\nThe University of Texas Medical Branch, 2007\r\n\r\nSupervisor: Marguerite A. Sognier\r\n\r\nThe objectives of this… (more)

▼ Effects of Three-dimensional Culture Conditions on Skeletal Muscle Myoblasts\r\n\r\nPublication No._____________\r\n\r\n\r\nMichele Lynn Marquette, Ph.D.\r\nThe University of Texas Medical Branch, 2007\r\n\r\nSupervisor: Marguerite A. Sognier\r\n\r\nThe objectives of this research were to: 1) develop a three-dimensional in vitro model; and 2) subsequently, utilize this model to investigate mechanisms of myoblast adhesion, fusion, and differentiation. C2C12 cells were examined as pre-aggregated single cells and multicellular aggregates in the Rotary Cell Culture System (RCCS). At the time intervals tested, RCCS cultured cells maintained viability and did not exhibit increased apoptosis markers such as Caspase 3 (activated) and phosphatydylserine. In contrast, increases in cell death and apoptotic markers were noted in suspension culture (SC) control cells. RCCS cultured cells fused to form multinucleated syncitia and expressed sarcomeric myosin heavy chain (MHC) in significantly higher levels than SC aggregates after cultivation for 3 and 6 days. This occurred in the presence of mitogens without exogenous matrix or support structures. Myoblast fusion was inhibited by exposure to soluble anti-Neural-cadherin antibody, but this treatment increased MHC levels assessed using immunohistochemistry.\r\nDuring early RCCS culture, myoblasts exhibited numerous cytoplasmic protrusions (podia). Microscopic examination of cells cultured in RCCS and SC revealed significantly more and slightly longer podia in the RCCS at 3, 6, and 9-hours. Podia were F-actin dependent as shown by exposure to an F-actin depolymerizing agent, Latrunculin A. Podia were inhibited, but recovered upon Latrunculin A removal. \r\nPodia were postulated to play a role in cell-cell adhesion in conjunction with Neural Cadherin (N-cadherin), an adhesion molecule important in myoblast differentiation. To determine if N-cadherin was critical to cell-cell adhesion, RCCS cultured cells were examined for the presence of N-cadherin at both the podia and membrane using confocal microscopy. N-cadherin levels decreased at the podia and membrane of RCCS cultured cells but not in SC cells at 3, 6, and 9-hours. \r\nIn summary, these results revealed: 1) podia formation is F-actin dependent but N-cadherin independent; 2) N-cadherin is critical for myoblast maturation; 3) synctia formation and differentiation can occur with mitogens present, without exogenous substrates in the RCCS; 4) this novel myoblast model test system is suitable for defining muscle development/regeneration processes, identification of molecular targets for development of therapies, and potential regenerative medicine applications.\r\n \r\n Advisors/Committee Members: Marguerite Sognier (advisor), Robert Leonard (committee member), Mary Moslen (committee member), Jeff Rabek (committee member), Brian Hashemi (committee member).

Subjects/Keywords: RCCS; podia; N-cadherin; fusion; F-actin; differentiation

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Marquette, M. L. (2007). Effects of three-dimensional culture conditions on skeletal muscle myoblasts. (Doctoral Dissertation). The University of Texas Medical Branch. Retrieved from http://hdl.handle.net/2152.3/86

Chicago Manual of Style (16^th Edition):

Marquette, Michele Lynn. “Effects of three-dimensional culture conditions on skeletal muscle myoblasts.” 2007. Doctoral Dissertation, The University of Texas Medical Branch. Accessed January 27, 2021. http://hdl.handle.net/2152.3/86.

MLA Handbook (7^th Edition):

Marquette, Michele Lynn. “Effects of three-dimensional culture conditions on skeletal muscle myoblasts.” 2007. Web. 27 Jan 2021.

Vancouver:

Marquette ML. Effects of three-dimensional culture conditions on skeletal muscle myoblasts. [Internet] [Doctoral dissertation]. The University of Texas Medical Branch; 2007. [cited 2021 Jan 27]. Available from: http://hdl.handle.net/2152.3/86.

Council of Science Editors:

Marquette ML. Effects of three-dimensional culture conditions on skeletal muscle myoblasts. [Doctoral Dissertation]. The University of Texas Medical Branch; 2007. Available from: http://hdl.handle.net/2152.3/86

University of Arizona

19. Alexander, Nelson Ray. The Positive and Negative Transcriptional Regulation of N-cadherin Expression During the Progression of Prostate Cancer .

Degree: 2005, University of Arizona

URL: http://hdl.handle.net/10150/195426

► For cancer cells to initiate cell migration and progress to metastasize, epithelial genes must be silenced and the expression of mesenchymal genes must be upregulated.… (more)

Subjects/Keywords: N-cadherin; integrin; twist1; FoxP1; prostate cancer; transcriptional regulation

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APA (6^th Edition):

Alexander, N. R. (2005). The Positive and Negative Transcriptional Regulation of N-cadherin Expression During the Progression of Prostate Cancer . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/195426

Chicago Manual of Style (16^th Edition):

Alexander, Nelson Ray. “The Positive and Negative Transcriptional Regulation of N-cadherin Expression During the Progression of Prostate Cancer .” 2005. Doctoral Dissertation, University of Arizona. Accessed January 27, 2021. http://hdl.handle.net/10150/195426.

MLA Handbook (7^th Edition):

Alexander, Nelson Ray. “The Positive and Negative Transcriptional Regulation of N-cadherin Expression During the Progression of Prostate Cancer .” 2005. Web. 27 Jan 2021.

Vancouver:

Alexander NR. The Positive and Negative Transcriptional Regulation of N-cadherin Expression During the Progression of Prostate Cancer . [Internet] [Doctoral dissertation]. University of Arizona; 2005. [cited 2021 Jan 27]. Available from: http://hdl.handle.net/10150/195426.

Council of Science Editors:

Alexander NR. The Positive and Negative Transcriptional Regulation of N-cadherin Expression During the Progression of Prostate Cancer . [Doctoral Dissertation]. University of Arizona; 2005. Available from: http://hdl.handle.net/10150/195426

Penn State University

20. Schenk, Rachelle Lois. Connexin Expression and Breast Cancer Metastasis to Bone.

Degree: 2010, Penn State University

URL: https://submit-etda.libraries.psu.edu/catalog/10834

► Each year, breast cancer causes over 500,000 deaths worldwide. If caught at early stages, metastasis can often be localized, confined, and treated. However, if time… (more)

▼ Each year, breast cancer causes over 500,000 deaths worldwide. If caught at early stages, metastasis can often be localized, confined, and treated. However, if time for progression of metastasis has occurred, it spreads to bone and surrounding tissues, and quickly metastasizes throughout the body. Breast cancer, in particular is among the most common to preferentially metastasize to bone, with about 73% of those affected developing bone metastasis as a result of breast cancer. However, at this point we do not fully understand why breast cancer cells preferentially metastasize to bone, and through what exact mechanism this occurs. Studies have been previously conducted utilizing human breast cancer cells extracted from metastatic mammary tumors as a model. These human studies investigated the connexin and cadherin expression profiles, as well as the metastatic characteristics of migration and adhesion. Studies have also demonstrated that it is possible to inject human cells into a mouse model if the model is in an immunocompromised state. However, the utilization of transgenic models, such as Cx43 deficient mice, presents a problem to this scenario because these models are not from an immunodeficient background. Therefore, it is important to develop an in vivo murine model of breast cancer metastasis to bone. However, in order to employ a murine model, it is critical to know the connexin and cadherin expression profiles in mice. The results of the murine studies are very different from those found in human models and, in many ways, actually present opposite results. It is important to consider this when working with mice as a model for breast cancer. At the initiation of this experiment, it was hypothesized that breast cancer cell lines express different connexin and cadherin expression profiles relative to normal breast epithelial cells. To test this hypothesis the connexin and cadherin expression profiles of murine breast cancer cells (4T1.2 cells) and normal breast epithelial cells (NMuMg cells) were characterized through Western blot and RT-PCR analyses. The results of these experiments supported the hypothesis that murine breast cancer cells (4T1.2) possess a different connexin expression profile than normal murine breast epithelial cells (NMuMG). Regarding connexin 43, though both 4T1.2 and NMuMG cells show slight expression of this gene in comparison to the positive control (MLO-Y4), the 4T1.2 cell line expressed it by almost a 50% greater amount than the NMuMG cell line. Regarding connexin 32, NMuMG cells moderately expressed Cx32 in comparison to the positive control (Mouse Liver cells), while the 4T1.2 cell line does not express this protein. Regarding, connexin 26, 4T1.2 cells display a greater expression than the NMuMG cell line, but neither cell line displays statistically significant expression of Cx26. The results of these experiments revealed that murine breast cancer cells displayed a different cadherin expression profile relative to normal breast epithelial cells. … Advisors/Committee Members: Dr Patricia Mc Laughlin, Thesis Advisor/Co-Advisor, Henry Joseph Donahue, Thesis Advisor/Co-Advisor.

Subjects/Keywords: breast cancer; metastasis; bone; 4T1.2; NMuMG; cadherins; connexins; connexin 43; connexin 32; connexin 26; E-cadherin; N-cadherin; OB-cadherin

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Schenk, R. L. (2010). Connexin Expression and Breast Cancer Metastasis to Bone. (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/10834

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Schenk, Rachelle Lois. “Connexin Expression and Breast Cancer Metastasis to Bone.” 2010. Thesis, Penn State University. Accessed January 27, 2021. https://submit-etda.libraries.psu.edu/catalog/10834.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Schenk, Rachelle Lois. “Connexin Expression and Breast Cancer Metastasis to Bone.” 2010. Web. 27 Jan 2021.

Vancouver:

Schenk RL. Connexin Expression and Breast Cancer Metastasis to Bone. [Internet] [Thesis]. Penn State University; 2010. [cited 2021 Jan 27]. Available from: https://submit-etda.libraries.psu.edu/catalog/10834.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Schenk RL. Connexin Expression and Breast Cancer Metastasis to Bone. [Thesis]. Penn State University; 2010. Available from: https://submit-etda.libraries.psu.edu/catalog/10834

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Gothenburg / Göteborgs Universitet

21. Husmark, Johanna 1970-. Cadherin mediated adhesion and barrier function in the thyroid epithelium.

Degree: 1999, University of Gothenburg / Göteborgs Universitet

URL: http://hdl.handle.net/2077/11785

► The thyroid gland is mainly composed of epithelial cells (thyrocytes) organized as follicles. The cells are connected by junction complexes that link them together into… (more)

▼ The thyroid gland is mainly composed of epithelial cells (thyrocytes) organized as follicles. The cells are connected by junction complexes that link them together into a cohesive simple epithelium. The junctions are also important for the establishment of a semipermeable barrier that restricts the paracellular flow of ions and other solutes. In the first part of this thesis, the effects of thyroid stimulating hormone (TSH) and pro-inflammatory cytokines on the epithelial barrier of primary cultured human thyrocytes were investigated. Thyroid follicle segments were prepared from surgically excised paradenomatous tissue and from resected glands with Graves´ disease. The cells formed tight, but low resistant monolayers on permeable filters in bicameral chambers. Addition of TSH further increased the transepithelial resistance to approximately 1000 * x cm2 after 3-5 days. TSH also induced an ordered organization of the tight junction protein ZO-1, promoted a polarized (apical-basolateral) ultrastructure and stimulated the secretion of thyroglobulin (Tg), preferentially in the apical direction. Treatment with IL-1a for 1-2 days induced a decreased transepithelial resistance and an increased paracellular leakage of both small ([3H]inulin) and large (125I-Tg) radiotracers irrespective of TSH and without signs of cytotoxicity. Electron microscopy showed that the main target of IL-1a action was the adherens junction where large amounts of stress fibers were formed. In contrast, other pro-inflammatory cytokines, i.e. IL-6, TNF-a, IFN-g and TGF-b, had no effect on the thyroid epithelial barrier.Changes in cell-cell adhesion have previously been correlated with tumor cell invasion and metastasis. In the second part of the thesis, cadherin-mediated adhesion and morphology in thyroid carcinoma cell lines and in cultured non-neoplastic pig and human thyrocytes were examined. E-cadherin negative cell lines established from anaplastic thyroid carcinomas (ATC) showed a variable down-regulation of catenins, known to anchor cadherins to the cytoskeleton. The reduced expression was most notable for g-catenin and p120ctn. Furthermore, the electrophoretic mobility of p120ctn was altered. A demethylating agent, 5-aza-2´-deoxycytidine, increased protein expression of E-cadherin and g-catenin although some cell lines were unresponsive. N-cadherin was detected in E-cadherin negative ATC cell lines but not in freshly isolated and primary cultured human and pig follicle segments. However, N-cadherin expression was also induced by 1-2 subcultivations of non-neoplastic thyrocytes. In this process, the upregulation of N-cadherin was paralleled by downregulation of E-cadherin and morphological alterations such as multilayering and loss of barrier function. Unexpectedly, one ATC cell line, KAT-4, expressed normal levels of E-cadherin and catenins and had a maintained epithelial morphology despite loss of barrier function and lack of contact-inhibited growth. KAT-4 cells also had a unique aberration of E-cadherin.In conclusion, human thyrocytes form…

Subjects/Keywords: Thyroid; Primary culture; TSH; IL-1; tight junction; adherens junction; E-cadherin; N-cadherin; cadherin switch; thyroid carcinoma

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APA (6^th Edition):

Husmark, J. 1. (1999). Cadherin mediated adhesion and barrier function in the thyroid epithelium. (Thesis). University of Gothenburg / Göteborgs Universitet. Retrieved from http://hdl.handle.net/2077/11785

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Husmark, Johanna 1970-. “Cadherin mediated adhesion and barrier function in the thyroid epithelium.” 1999. Thesis, University of Gothenburg / Göteborgs Universitet. Accessed January 27, 2021. http://hdl.handle.net/2077/11785.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Husmark, Johanna 1970-. “Cadherin mediated adhesion and barrier function in the thyroid epithelium.” 1999. Web. 27 Jan 2021.

Vancouver:

Husmark J1. Cadherin mediated adhesion and barrier function in the thyroid epithelium. [Internet] [Thesis]. University of Gothenburg / Göteborgs Universitet; 1999. [cited 2021 Jan 27]. Available from: http://hdl.handle.net/2077/11785.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Husmark J1. Cadherin mediated adhesion and barrier function in the thyroid epithelium. [Thesis]. University of Gothenburg / Göteborgs Universitet; 1999. Available from: http://hdl.handle.net/2077/11785

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

22. Chazeau, Anael. Rôle de l’organisation du cytosquelette d’actine branché et des adhésions N-cadhérine dans la dynamique des épines dendritiques : Role of branched actin network organization and N-cadherin in dendritic in dendritic spine dynamics.

Degree: Docteur es, Sciences, technologie, santé. Neurosciences, 2012, Université de Bordeaux Segalen

URL: http://www.theses.fr/2012BOR21967

► Les épines dendritiques sont de petites protrusions post-synaptiques présentant des changements morphologiques corrélés avec la plasticité synaptique. Elles ont pour origine les filopodes dendritiques qui… (more)

▼ Les épines dendritiques sont de petites protrusions post-synaptiques présentant des changements morphologiques corrélés avec la plasticité synaptique. Elles ont pour origine les filopodes dendritiques qui s’élargissent lors du contact avec l’axone. Ces changements morphologiques impliquent une grande variété de molécules dont des protéines associées à l’actine et des protéines d’adhésion. Cependant, comment ces différentes protéines sont coordonnées dans le temps et l’espace est encore largement méconnu. De plus, les techniques de microscopie conventionnelle ne permettent pas d’étudier l’organisation et la dynamique de ces protéines dans les épines dont la taille est proche de la limite de resolution. L’objectif de ma thèse a donc été d’explorer le rôle des protéines associées à l’actine ainsi que celui des protéines d’adhésion N-cadhérines dans l’organisation et la dynamique du cytosquelette d’actine des épines dendritiques. Dans une première étude, nous avons suivi la motilité des filopodes et épines dendritiques de neurones en visualisant l’actine-GFP. Nous avons couplé cette approche avec : 1) une technique de piégeage optique de microsphères recouvertes de N-cadhérines ou des substrats micro-imprimés également recouverts de N-cadhérines afin de contrôler temporellement et spatialement les adhésions cadhérine-cadhérine, 2) la stimulation pharmacologique de la myosine II afin d’induire la contraction F-actine/myosine et 3) l’expression de mutants de N-cadhérine non adhésifs. Nous avons ainsi démontré que la stabilisation des filopodes en épines était dépendante de l’engagement d’un embrayage moléculaire entre les adhésions trans-synaptiques N-cadhérine et le flux rétrograde d’actine généré par les myosines II. Dans une deuxième étude, nous avons utilisé la microscopie super-résolutive (PALM et dSTORM) et le suivi de protéines individuelles (sptPALM) pour étudier l’organisation et la dynamique à l’échelle nanométrique des protéines à l’origine des réseaux d’actine branchés dans les épines. Ainsi, nous avons caractérisé la localisation et la dynamique de l’actine, du complexe Arp2/3, du complexe WAVE, d’IRSp53, de VASP et de Rac-1. Nous avons montré que, contrairement aux structures motiles classiques comme lamellipode, le réseau d’actine branché dans les épines n’ést pas formé aux extrémités protrusives puis incorporé dans un flux rétrograde d’actine. Ce réseau est initié à la PSD puis croît vers l’extérieur afin de générer les protrusions membranaires responsablent des changements morphologiques de l’épine. Nos résultats montrent également qu’un contrôle strict de l’activité de Rac-1 est nécessaire au maintien de la morphologie des épines dendritiques et de l’architecture du réseau d’actine branché. L’ensemble de mon travail souligne l’importance du rôle de l’organisation à l’échelle nanométrique du réseau d’actine branché et des adhésions N-cadhérine dans la dynamique et la formation des épines dendritiques. Ces résultats pourraient avoir un rôle important dans la compréhension des changements morphologiques lors… Advisors/Committee Members: Giannone, Grégory (thesis director).

Subjects/Keywords: Épines dendritiques; Protéines régulatrices de l’actine; N-cadherine; PSD; Microscopie super-résolutive; Suivi de protéines individuelles; Dendritic spine; Actin-binding proteins; N-cadherin; PSD; Super resolution microscopy; Single protein tracking

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Chazeau, A. (2012). Rôle de l’organisation du cytosquelette d’actine branché et des adhésions N-cadhérine dans la dynamique des épines dendritiques : Role of branched actin network organization and N-cadherin in dendritic in dendritic spine dynamics. (Doctoral Dissertation). Université de Bordeaux Segalen. Retrieved from http://www.theses.fr/2012BOR21967

Chicago Manual of Style (16^th Edition):

Chazeau, Anael. “Rôle de l’organisation du cytosquelette d’actine branché et des adhésions N-cadhérine dans la dynamique des épines dendritiques : Role of branched actin network organization and N-cadherin in dendritic in dendritic spine dynamics.” 2012. Doctoral Dissertation, Université de Bordeaux Segalen. Accessed January 27, 2021. http://www.theses.fr/2012BOR21967.

MLA Handbook (7^th Edition):

Chazeau, Anael. “Rôle de l’organisation du cytosquelette d’actine branché et des adhésions N-cadhérine dans la dynamique des épines dendritiques : Role of branched actin network organization and N-cadherin in dendritic in dendritic spine dynamics.” 2012. Web. 27 Jan 2021.

Vancouver:

Chazeau A. Rôle de l’organisation du cytosquelette d’actine branché et des adhésions N-cadhérine dans la dynamique des épines dendritiques : Role of branched actin network organization and N-cadherin in dendritic in dendritic spine dynamics. [Internet] [Doctoral dissertation]. Université de Bordeaux Segalen; 2012. [cited 2021 Jan 27]. Available from: http://www.theses.fr/2012BOR21967.

Council of Science Editors:

Chazeau A. Rôle de l’organisation du cytosquelette d’actine branché et des adhésions N-cadhérine dans la dynamique des épines dendritiques : Role of branched actin network organization and N-cadherin in dendritic in dendritic spine dynamics. [Doctoral Dissertation]. Université de Bordeaux Segalen; 2012. Available from: http://www.theses.fr/2012BOR21967

23. Pechery, Adeline. Mort cellulaire et modulation du clivage de la cadhérine N par un agoniste de PPARβ/δ dans un modèle de cancer de la vessie : Cell death and modulation ofN-cadherin cleavage by a PPARβ/δ agonist in bladder cancer mode!.

Degree: Docteur es, Sciences de la vie et de la santé, 2016, Besançon

URL: http://www.theses.fr/2016BESA3003

►

Le cancer de la vessie est le deuxième cancer urologique après le cancer de la prostate. Le développement de nouveaux agents anticancéreux est nécessaire pour… (more)

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Le cancer de la vessie est le deuxième cancer urologique après le cancer de la prostate. Le développement de nouveaux agents anticancéreux est nécessaire pour le traitement de cette maladie complexe, car, en dépit d'un large éventail de traitements, aucune augmentation de la survie des patients n'a été observée. - Les effets du GW501516, un agoniste de PPARbeta/delta, n'ont jamais été explorés dans des cellules cancéreuses de la vessie. Nous montrons qu'un traitement par 25 µM de GW501516, pendant 24 h, induit la mort cellulaire par apoptose de cellules dérivées d'un carcinome urothélial invasif mais pas de cellules dérivées d'un cancer urothélial "de bon pronostic". Une stimulation de courte durée par 25 µM de GW501516 induit une augmentation du taux d'espèces réactives de l'oxygène (ROS) qui est associée à une phosphorylation de la protéine de survie Akt. L'apoptose induite par le GW501516 est concomitante à une diminution de l'expression d'une molécule d'adhérence, la cadhérine N qui est une protéine transmembranaire impliquée dans la progression tumorale. Pour la première fois dans un modèle de carcinome, nous montrons que la cadhérine N est la cible d'un clivage protéolytique, libérant des fragments solubles qui peuvent être biologiquement actifs. Le GW501516 module ce clivage à des temps qui précèdent la mort cellulaire. En effet, le GW501516 régule l'expression de protéases telles que ADAMIO à l'origine du clivage de la cadhérine N. - Les fragments de la cadhérine N pourraient intervenir dans les processus de survie ou de mort cellulaires. Par conséquent, cette étude novatrice ouvre le débat quant à la portée thérapeutique du GW501516 dans le traitement du cancer.

Bladder cancer is the most common cancer of the genitourinary tract worldwide and accounts for 5% of ail cancer deaths in human. Despite of a wide range of treatments, no substantial improvement in survival of patients with advanced-stage or metastatic disease has been achieved. The development of nove! effective chemotherapeutic agents is required for the treatment ofthis aggressive disease. Anticancer action of GW501516, an agonist of PPARbeta/delta, has never been investigated in bladder tumor cells. Our results indicated that a 24h treatment by 25 µM of GW501516 induced cell death through both extrinsic and intrinsic apoptotic pathways in T24 cells, derived from an undifferentiated high grade carcinoma but not in RT4 cells, derived from a low grade papillary tumor. GW501516 induced also an early up-regulation of ROS production which was associated with an increase ofphosphorylated Akt level, implicated in cell survival. Apoptosis induced by GW501516 is concomitant with a decrease of N-cadherin expression which is a cell adhesion molecule implicated in tumor progression. For the first time in carcinoma mode!, we showed that N-cadherin was cleaved by proteases, leading to the release of soluble fragments which could be biologically active. Our results indicated that GW501516 modulates N-cadherin cleavage before cell death through the regulation…

Advisors/Committee Members: Lascombe, Isabelle (thesis director).

Subjects/Keywords: Cancer de la vessie; PPARbeta/delta; GW501516; Apoptose; Stress oxydant; Akt; Cadhérinc N; ADAMIO; Bladder cancer; PPARbeta/dclta; GW501516; Apoptosis; Oxidative stress; Akt; N-cadherin; ADAMIO; 616.9; WJ 504

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Pechery, A. (2016). Mort cellulaire et modulation du clivage de la cadhérine N par un agoniste de PPARβ/δ dans un modèle de cancer de la vessie : Cell death and modulation ofN-cadherin cleavage by a PPARβ/δ agonist in bladder cancer mode!. (Doctoral Dissertation). Besançon. Retrieved from http://www.theses.fr/2016BESA3003

Chicago Manual of Style (16^th Edition):

Pechery, Adeline. “Mort cellulaire et modulation du clivage de la cadhérine N par un agoniste de PPARβ/δ dans un modèle de cancer de la vessie : Cell death and modulation ofN-cadherin cleavage by a PPARβ/δ agonist in bladder cancer mode!.” 2016. Doctoral Dissertation, Besançon. Accessed January 27, 2021. http://www.theses.fr/2016BESA3003.

MLA Handbook (7^th Edition):

Pechery, Adeline. “Mort cellulaire et modulation du clivage de la cadhérine N par un agoniste de PPARβ/δ dans un modèle de cancer de la vessie : Cell death and modulation ofN-cadherin cleavage by a PPARβ/δ agonist in bladder cancer mode!.” 2016. Web. 27 Jan 2021.

Vancouver:

Pechery A. Mort cellulaire et modulation du clivage de la cadhérine N par un agoniste de PPARβ/δ dans un modèle de cancer de la vessie : Cell death and modulation ofN-cadherin cleavage by a PPARβ/δ agonist in bladder cancer mode!. [Internet] [Doctoral dissertation]. Besançon; 2016. [cited 2021 Jan 27]. Available from: http://www.theses.fr/2016BESA3003.

Council of Science Editors:

Pechery A. Mort cellulaire et modulation du clivage de la cadhérine N par un agoniste de PPARβ/δ dans un modèle de cancer de la vessie : Cell death and modulation ofN-cadherin cleavage by a PPARβ/δ agonist in bladder cancer mode!. [Doctoral Dissertation]. Besançon; 2016. Available from: http://www.theses.fr/2016BESA3003

24. Ould Madi-Berthelemy, Pauline. Caractérisation des fonctions génomiques de variants du récepteur des androgènes dans le cancer de la prostate : Transcriptional activities of androgen receptor variants in prostate cancer.

Degree: Docteur es, Sciences de la vie et de la santé, 2018, Université de Strasbourg

URL: http://www.theses.fr/2018STRAJ112

►

Le récepteur des androgènes (RA) est la principale cible thérapeutique du cancer de la prostate (CaP) métastatique. Bien que cette thérapie soit initialement efficace, les… (more)

▼

Le récepteur des androgènes (RA) est la principale cible thérapeutique du cancer de la prostate (CaP) métastatique. Bien que cette thérapie soit initialement efficace, les effets sont transitoires. De nombreux mécanismes peuvent expliquer la progression du CaP vers un stade de résistance à la castration, telles les modifications du RA. Des données récentes ont montré que les variants constitutifs RA-Q641X et RA-V7, caractérisés par la perte du domaine de liaison au ligand, étaient associés à l’expression de marqueurs mésenchymateux. L’étude de la régulation de la N-cadhérine a mis en évidence que si le RA sauvage et les variants constitutifs se liaient tous deux aux éléments de réponse du gène codant, seuls les derniers étaient associés à une augmentation de l’acétylation de l’histone H4, marque positive de la transcription. Le RNA-seq a révélé que leur expression était aussi corrélée à la régulation de sets de gènes spécifiques incluant des facteurs de transcription dont certains ont déjà été caractérisés en cancérologie.En ce qui concerne le RA-T576A, porteur d’une mutation faux-sens, les données ont révélé une séquence consensus de liaison à l’ADN moins conservée pour le RA sauvage que pour ce mutant et l’importance du 11ème nucléotide des éléments de réponse. De plus, cette mutation a semblé impacter le transcriptome du RA. Ce travail met en évidence le comportement distinct des variants du RA et aide à mieux comprendre leurs modes d’action en décrivant leurs activités transcriptionnelles.

The androgen receptor (AR) is the main therapeutic target in metastatic prostate cancer (PCa). Although this therapy is initially effective, the effects are transient. Many mechanisms can explain PCa progression toward castration resistance including abnormalities in the AR. Recent data have shown that constitutive AR (e.g AR-Q641X and AR-V7), which have lost the ligand binding domain, were associated with the induction of mesenchymal marker expression. The study of N-cadherin regulation highlighted that while both constitutive AR and wild type AR bound to response elements located in the encoding gene, only the AR variants were associated with an increase of H4 acetylation, a positive transcription mark. RNA-seq revealed that their expression was also correlated to specific sets of genes regulation, including transcription factors and genes involved in migration, AR regulation, and therapeutic resistance.Concerning AR-T576A, which hold a missense mutation, data revealed a less conserved consensus sequence for the wild type AR than for this mutant and highlighted the importance of the 11th nucleotide of the response element for AR recruitment to DNA. Plus, this mutation seemed to impair AR transcriptome. This work highlights the distinct AR variants’ behavior and helps to understand their mode of action by depicting their transcriptional landscapes.

Advisors/Committee Members: Ceraline, Jocelyn (thesis director).

Subjects/Keywords: Cancer de la prostate; Variants du récepteur des androgènes; N-cadhérine; Activité transcriptionnelle; Liaison à l’ADN; Prostate cancer; Androgen receptor variants; N-cadherin; Transcriptional landscape; DNA binding; 572.8; 616.99

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ould Madi-Berthelemy, P. (2018). Caractérisation des fonctions génomiques de variants du récepteur des androgènes dans le cancer de la prostate : Transcriptional activities of androgen receptor variants in prostate cancer. (Doctoral Dissertation). Université de Strasbourg. Retrieved from http://www.theses.fr/2018STRAJ112

Chicago Manual of Style (16^th Edition):

Ould Madi-Berthelemy, Pauline. “Caractérisation des fonctions génomiques de variants du récepteur des androgènes dans le cancer de la prostate : Transcriptional activities of androgen receptor variants in prostate cancer.” 2018. Doctoral Dissertation, Université de Strasbourg. Accessed January 27, 2021. http://www.theses.fr/2018STRAJ112.

MLA Handbook (7^th Edition):

Ould Madi-Berthelemy, Pauline. “Caractérisation des fonctions génomiques de variants du récepteur des androgènes dans le cancer de la prostate : Transcriptional activities of androgen receptor variants in prostate cancer.” 2018. Web. 27 Jan 2021.

Vancouver:

Ould Madi-Berthelemy P. Caractérisation des fonctions génomiques de variants du récepteur des androgènes dans le cancer de la prostate : Transcriptional activities of androgen receptor variants in prostate cancer. [Internet] [Doctoral dissertation]. Université de Strasbourg; 2018. [cited 2021 Jan 27]. Available from: http://www.theses.fr/2018STRAJ112.

Council of Science Editors:

Ould Madi-Berthelemy P. Caractérisation des fonctions génomiques de variants du récepteur des androgènes dans le cancer de la prostate : Transcriptional activities of androgen receptor variants in prostate cancer. [Doctoral Dissertation]. Université de Strasbourg; 2018. Available from: http://www.theses.fr/2018STRAJ112

University of Pretoria

25. Ndima, Daniel, S. Investigating the potentially expanded target repertoire of murinized Internalin of Listeria monocytogenes.

Degree: MSc, Biochemistry, 2016, University of Pretoria

URL: http://hdl.handle.net/2263/56248

► The ability of intracellular pathogens to invade and spread from non-phagocytic cell to another is an imperative mechanism broadly investigated in cellular biology. Listeria monocytogenes… (more)

▼ The ability of intracellular pathogens to invade and spread from non-phagocytic cell to another is an imperative mechanism broadly investigated in cellular biology. Listeria monocytogenes (Lm) –one example of intracellular pathogens, invades specifically human epithelial cells using its surface proteins Internalin A (InlA) and InlB, respectively. InlA alone is sufficient to internalise the pathogen into the host cells by interacting with human E-cadherin –specifically the N-terminal domain 1 (hEC1). The InlA variant (InlAm) that was previously made to increase the binding affinity to hEC1 was successfully engineered in this study. This variant was found to interact with N-terminal domain 1 of murine E-cadherin (mEC1) by isothermal titration calorimetry (ITC). Previously, the InlAm was reported to allow Lm invasion into M villous cells that express murine N-cadherin –possibly via the N-terminal domain 1 (mNC1). In this study, InlAm did not have affinity for mNC1 or N-terminal domain 1 of human N-cadherin (hNC1) when analysed by ITC –possibly due to amino acid sequences variation from both mEC1 and hEC1. However, by structurally engineering the complexes (InlAm/mNC1 and InlAm/hNC1) and studying their interaction interfaces, it was revealed that mNC1 and hNC1 can be recognised by InlAm just like hEC1. This was supported by the distances between interacting amino acid residues in InlAm/hEC1 crystal structure complex, which were also conserved in the engineered complexes. These observations related to the fact that the N-terminal domains of E- and N-cadherin are structurally conserved, therefore that could have attributed to similarities observed in the engineered complexes. Therefore, future studies would aim at using alternative methods that could support or disprove one of the two findings, that is whether InlAm and any of the N-terminal domains of N-cadherin interact or not. Advisors/Committee Members: Schubert, Wolf-Dieter (advisor), Motshwene, Precious, G. (coadvisor).

Subjects/Keywords: Listeria monocytogenes; Murinized InlA; Murine N-cadherin; Human N-cadherin; Protein-protein interactions; UCTD

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ndima, Daniel, S. (2016). Investigating the potentially expanded target repertoire of murinized Internalin of Listeria monocytogenes. (Masters Thesis). University of Pretoria. Retrieved from http://hdl.handle.net/2263/56248

Chicago Manual of Style (16^th Edition):

Ndima, Daniel, S. “Investigating the potentially expanded target repertoire of murinized Internalin of Listeria monocytogenes.” 2016. Masters Thesis, University of Pretoria. Accessed January 27, 2021. http://hdl.handle.net/2263/56248.

MLA Handbook (7^th Edition):

Ndima, Daniel, S. “Investigating the potentially expanded target repertoire of murinized Internalin of Listeria monocytogenes.” 2016. Web. 27 Jan 2021.

Vancouver:

Ndima, Daniel S. Investigating the potentially expanded target repertoire of murinized Internalin of Listeria monocytogenes. [Internet] [Masters thesis]. University of Pretoria; 2016. [cited 2021 Jan 27]. Available from: http://hdl.handle.net/2263/56248.

Council of Science Editors:

Ndima, Daniel S. Investigating the potentially expanded target repertoire of murinized Internalin of Listeria monocytogenes. [Masters Thesis]. University of Pretoria; 2016. Available from: http://hdl.handle.net/2263/56248

Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ)

26. Tsekos, Antonios. Ανοσοϊστοχημική έκφραση των μεταλλοπρωτεϊνασών 2 και 9 (MMP-2, MMP-9), σε συνδυασμό με την έκφραση των μορίων καντχερίνης 2 (CADH 2) και κολλαγόνου IV (COL IV), στο βλεννοεπιδερμοειδές και αδενοκυστικό καρκίνωμα των σιελογόνων αδένων.

Degree: 2016, Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ)

URL: http://hdl.handle.net/10442/hedi/44257

► Tumor generation and progression is a complex biological procedurecharacterized by particular stage processes such as proliferation, motivation,apoptosis, detachment, migration, extra cellular matrix (ECM) degeneration,epithelial to… (more)

▼ Tumor generation and progression is a complex biological procedurecharacterized by particular stage processes such as proliferation, motivation,apoptosis, detachment, migration, extra cellular matrix (ECM) degeneration,epithelial to mesechymal transition, angiogenesis. These stages are influencedby cell-cell and cell-ECM interactions regulated by multiple signalingpathways. Ultimately, micro-molecules are the fine micro-workers of theabove interactive processes throughout tumor microenvironment, includinglocal structural proteins, proteases, adhesion molecules, growth factors,morphogenic proteins, catalysts, hormones, inhibitors, metalloproteinases,collagen IV and cadherin 2 are among the mentioned micro-molecules manifestinga crucial multifocal role in the field of certain stages with regards ofECM degeneration, cell detachment and migration, epithelial to mesechymaltransition, signaling and angiogenesis.The aim of this study was to investigate the immunohistochemical expressionof metalloproteinases 2 and 9 (MMP-2, MMP-9), in combinationwith the expression of molecules Collagen IV (Col IV) and cadherin 2 or Ncadherin(CDH 2), in Mucoepidermoid (MEC) and Adenoid Cystic Carcinoma(ACC) of the salivary glands. The expressions of these molecules and theirpossible combinations were associated with the grade of malignancy of thetwo tumors and the usefulness of the expressions as markers are appreciatedfor specific conclusions with respect to the disease. Secondary correlationswith regards of tumor size, tumor location, gland type and patient’sgender and age were sought.This is a retrospective study of 30 cases of MEC and 30 cases of ACC,treated either by Oral and Maxillofacial Surgery Clinic of Aristotle Universityof Thessaloniki or by the ENT Clinic of General Hospital "Papanikolaou" ofThessaloniki. The antibody immunostains are evaluated using an arbitraryscale of four grades correlating roughly the number of positive cells accordingto the intensity of the staining. Graduation was from 0-3, where 0 waswhen not any positive cell was obtained, grade 1 when the percentage ofpositive cells was ranged from 1-30% of specimen with mild to moderateintensity staining, grade 2 from 31-65% of the population of cells with moderate to strong staining intensity and grade 3 for percentage of 65 to 100%with a strong positive staining. Regarding statistics, beyond the dependent variables (molecules expressions), qualitative independent variables of patient’sgender and age, tumor location, gland type, T stage, tumor gradewere fixed. Correlations of dependent variables MMP-2, MMP-9 , CADH 2,COL IV and independent variables were sought using the Kendall's correlationcoefficient. Investigation of a possible cutoff value for age, which canindicate that for values greater than the cutoff expression was expected, theROC (Receiver Operating Characteristic) analysis was applied.The findings of the study can be concluded in the following results: No significant correlation between expressions of MMP-2, MMP- 9,CADH 2, COL IV or their combinations…

Subjects/Keywords: Μεταλλοπρωτεϊνάσες; Μεταλλοπρωτεϊνάση 2; Μεταλλοπρωτεϊνάση-9; Μόρια προσκόλλησης; Ν-καντχερίνη; Κολλαγόνο IV; Αδενοκυστικό καρκίνωμα; Βλεννοπιδερμοειδές καρκίνωμα; Σιελογόνοι αδένες; Καντχερίνη 2; MMP-2; MMP-9; Metalloproteinases; Adhesion molecules; N-cadherin; Cadherin 2; Collagen IV; Mucoepidermoid carcinoma; Adenoid cystic carcinoma; Salivary giands

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Tsekos, A. (2016). Ανοσοϊστοχημική έκφραση των μεταλλοπρωτεϊνασών 2 και 9 (MMP-2, MMP-9), σε συνδυασμό με την έκφραση των μορίων καντχερίνης 2 (CADH 2) και κολλαγόνου IV (COL IV), στο βλεννοεπιδερμοειδές και αδενοκυστικό καρκίνωμα των σιελογόνων αδένων. (Thesis). Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ). Retrieved from http://hdl.handle.net/10442/hedi/44257

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Tsekos, Antonios. “Ανοσοϊστοχημική έκφραση των μεταλλοπρωτεϊνασών 2 και 9 (MMP-2, MMP-9), σε συνδυασμό με την έκφραση των μορίων καντχερίνης 2 (CADH 2) και κολλαγόνου IV (COL IV), στο βλεννοεπιδερμοειδές και αδενοκυστικό καρκίνωμα των σιελογόνων αδένων.” 2016. Thesis, Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ). Accessed January 27, 2021. http://hdl.handle.net/10442/hedi/44257.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Tsekos, Antonios. “Ανοσοϊστοχημική έκφραση των μεταλλοπρωτεϊνασών 2 και 9 (MMP-2, MMP-9), σε συνδυασμό με την έκφραση των μορίων καντχερίνης 2 (CADH 2) και κολλαγόνου IV (COL IV), στο βλεννοεπιδερμοειδές και αδενοκυστικό καρκίνωμα των σιελογόνων αδένων.” 2016. Web. 27 Jan 2021.

Vancouver:

Tsekos A. Ανοσοϊστοχημική έκφραση των μεταλλοπρωτεϊνασών 2 και 9 (MMP-2, MMP-9), σε συνδυασμό με την έκφραση των μορίων καντχερίνης 2 (CADH 2) και κολλαγόνου IV (COL IV), στο βλεννοεπιδερμοειδές και αδενοκυστικό καρκίνωμα των σιελογόνων αδένων. [Internet] [Thesis]. Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ); 2016. [cited 2021 Jan 27]. Available from: http://hdl.handle.net/10442/hedi/44257.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Tsekos A. Ανοσοϊστοχημική έκφραση των μεταλλοπρωτεϊνασών 2 και 9 (MMP-2, MMP-9), σε συνδυασμό με την έκφραση των μορίων καντχερίνης 2 (CADH 2) και κολλαγόνου IV (COL IV), στο βλεννοεπιδερμοειδές και αδενοκυστικό καρκίνωμα των σιελογόνων αδένων. [Thesis]. Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ); 2016. Available from: http://hdl.handle.net/10442/hedi/44257

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Oulu

27. Railo, A. (Antti). Wnt-11 signalling, its role in cardiogenesis and identification of Wnt/β-catenin pathway target genes.

Degree: 2010, University of Oulu

URL: http://urn.fi/urn:isbn:9789514261534

► Abstract Wnt genes encode secreted signalling molecules that control embryonic development including organogenesis, while dysregulated Wnt signalling is connected to many diseases such as cancer.… (more)

Subjects/Keywords: AP-1; JNK; N-cadherin; NF-κB; TCF; Wnt signalling; Wnt-11; cardiogenesis; cell adhesion; cell viability; chromatin immunoprecipitation; target gene; β-catenin

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APA (6^th Edition):

Railo, A. (. (2010). Wnt-11 signalling, its role in cardiogenesis and identification of Wnt/β-catenin pathway target genes. (Doctoral Dissertation). University of Oulu. Retrieved from http://urn.fi/urn:isbn:9789514261534

Chicago Manual of Style (16^th Edition):

Railo, A (Antti). “Wnt-11 signalling, its role in cardiogenesis and identification of Wnt/β-catenin pathway target genes.” 2010. Doctoral Dissertation, University of Oulu. Accessed January 27, 2021. http://urn.fi/urn:isbn:9789514261534.

MLA Handbook (7^th Edition):

Railo, A (Antti). “Wnt-11 signalling, its role in cardiogenesis and identification of Wnt/β-catenin pathway target genes.” 2010. Web. 27 Jan 2021.

Vancouver:

Railo A(. Wnt-11 signalling, its role in cardiogenesis and identification of Wnt/β-catenin pathway target genes. [Internet] [Doctoral dissertation]. University of Oulu; 2010. [cited 2021 Jan 27]. Available from: http://urn.fi/urn:isbn:9789514261534.

Council of Science Editors:

Railo A(. Wnt-11 signalling, its role in cardiogenesis and identification of Wnt/β-catenin pathway target genes. [Doctoral Dissertation]. University of Oulu; 2010. Available from: http://urn.fi/urn:isbn:9789514261534

28. Jannie, Karry Marie. Activated leukocyte cell adhesion molecule (ALCAM) regulation of tumor cell behavior and neuronal targeting.

Degree: PhD, Biology, 2012, University of Iowa

URL: https://ir.uiowa.edu/etd/2901

► Numerous events during development require the tightly controlled and regulated interaction of cells - from gastrulation in the early embryo to axonal pathfinding and… (more)

Subjects/Keywords: adherens junction; ALCAM; catenin; L1; N-cadherin; uveal melanoma; Biology

…role of ALCAM in regulating N-cadherin-based adherens junctions ...107 IQGAP1 regulation… …83 Figure 3.6: Silencing of ALCAM disrupts N-cadherin and β-catenin junctions… …84 Figure 3.7: ALCAM expression in 2C-ALC cells enhances formation of N-cadherin and β… …cancer development and metastasis .....................................23 The cadherin… …the cadherin domain ......................................................25 The…

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Jannie, K. M. (2012). Activated leukocyte cell adhesion molecule (ALCAM) regulation of tumor cell behavior and neuronal targeting. (Doctoral Dissertation). University of Iowa. Retrieved from https://ir.uiowa.edu/etd/2901

Chicago Manual of Style (16^th Edition):

Jannie, Karry Marie. “Activated leukocyte cell adhesion molecule (ALCAM) regulation of tumor cell behavior and neuronal targeting.” 2012. Doctoral Dissertation, University of Iowa. Accessed January 27, 2021. https://ir.uiowa.edu/etd/2901.

MLA Handbook (7^th Edition):

Jannie, Karry Marie. “Activated leukocyte cell adhesion molecule (ALCAM) regulation of tumor cell behavior and neuronal targeting.” 2012. Web. 27 Jan 2021.

Vancouver:

Jannie KM. Activated leukocyte cell adhesion molecule (ALCAM) regulation of tumor cell behavior and neuronal targeting. [Internet] [Doctoral dissertation]. University of Iowa; 2012. [cited 2021 Jan 27]. Available from: https://ir.uiowa.edu/etd/2901.

Council of Science Editors:

Jannie KM. Activated leukocyte cell adhesion molecule (ALCAM) regulation of tumor cell behavior and neuronal targeting. [Doctoral Dissertation]. University of Iowa; 2012. Available from: https://ir.uiowa.edu/etd/2901

29. Sabatini, Peter Jarrod Bruno. Polarity Control in Migrating Vascular Smooth Muscle Cells: N-cadherin Localization and Function.

Degree: 2009, University of Toronto

URL: http://hdl.handle.net/1807/19321

►

Vascular endothelial cell loss initiates directional migration of medial smooth muscle cells into the arterial intima contributing to in-stent restenosis, atherosclerosis and coronary arterial by-pass… (more)

▼

Vascular endothelial cell loss initiates directional migration of medial smooth muscle cells into the arterial intima contributing to in-stent restenosis, atherosclerosis and coronary arterial by-pass graft failure. N-cadherin is a cell-cell adhesion molecule that mediates the interaction between vascular endothelial cells and the innermost smooth muscle cells to stabilize the arterial wall. Upon injury, I reasoned that relocalization of N-cadherin on the inner most smooth muscle cells to the posterior-lateral borders stimulates cell polarization to enable directional migration. Using an in vitro scratch-wound model to stimulate cell polarity and locally remove cell-cell contacts at one pole of smooth muscle cells, I found that N-cadherin localization provides signaling cues via a Cdc42/GSK pathway that promote polarized reorganization of the cytoskeleton and directional cell migration. I also found that N-cadherin was important to functions of lamellipodia at the anterior of migrating cells. In lamellipodia, actin polymerization drives protrusion of the leading edge and coincident, but more posterior, actin depolymerization results in retrograde flow of actin and associated plasma membrane structures. Using live cell imaging, I found that clusters of N-cadherin-GFP repeatedly accumulated at the leading edge specifically at the neck of large pinocytotic vesicles called macropinosomes that were internalized and transported away from the leading edge. This localization is consistent with a role for N-cadherin in closure and scission of vesicles during macropinocytosis. These are the first studies to examine polarity in migrating vascular smooth muscle cells, and advance our understanding concerning cell-cell adhesions in controlling directional cell migration. My results suggest that N-cadherin may serve as a viable target for the treatment of arterial stenosis that would limit smooth muscle cell migration and stabilize the arterial wall. Furthermore, I report on a novel localization and function of N-cadherin in the biogenesis of macropinosomes in the lamellipodia that contribute to cell protrusion.

PhD

Advisors/Committee Members: Bendeck, Michelle, Laboratory Medicine and Pathobiology.

Subjects/Keywords: Vascular Biology; Polarity; N-cadherin; Restenosis; Migration; 0379

…CHAPTER 4 – N-CADHERIN LOCALLY REGULATES LAMELLIPODIA DYNAMICS AND MACROPINOCYTOSIS… …98 4.2.4 Analysis of Transport of Cholesterol Rich Domains (CRD) and N-cadherin… …100 4.3.1 N-cadherin and Associated CRD Undergo Retrograde Flow at the Cell Anterior… …100 4.3.2 N-cadherin Antibody Arrests Retrograde Flow of CRD by Decoupling Membrane from the… …101 4.3.3 Local N-cadherin Ligation Decouples N-cadherin from Actin in the Lamellipodia…

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Sabatini, P. J. B. (2009). Polarity Control in Migrating Vascular Smooth Muscle Cells: N-cadherin Localization and Function. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/19321

Chicago Manual of Style (16^th Edition):

Sabatini, Peter Jarrod Bruno. “Polarity Control in Migrating Vascular Smooth Muscle Cells: N-cadherin Localization and Function.” 2009. Doctoral Dissertation, University of Toronto. Accessed January 27, 2021. http://hdl.handle.net/1807/19321.

MLA Handbook (7^th Edition):

Sabatini, Peter Jarrod Bruno. “Polarity Control in Migrating Vascular Smooth Muscle Cells: N-cadherin Localization and Function.” 2009. Web. 27 Jan 2021.

Vancouver:

Sabatini PJB. Polarity Control in Migrating Vascular Smooth Muscle Cells: N-cadherin Localization and Function. [Internet] [Doctoral dissertation]. University of Toronto; 2009. [cited 2021 Jan 27]. Available from: http://hdl.handle.net/1807/19321.

Council of Science Editors:

Sabatini PJB. Polarity Control in Migrating Vascular Smooth Muscle Cells: N-cadherin Localization and Function. [Doctoral Dissertation]. University of Toronto; 2009. Available from: http://hdl.handle.net/1807/19321

30. Revollo, Leila Denise. N-Cadherin Regulation of Bone Anabolic Responses via PTH and Wnt/Beta-Catenin Signaling.

Degree: PhD, Biology and Biomedical Sciences: Molecular Cell Biology, 2014, Washington University in St. Louis

URL: https://openscholarship.wustl.edu/etd/1339

► The main function of parathyroid hormone (PTH) is to regulate serum calcium levels, in part by stimulating osteoclast mediated bone resorption. However, PTH can… (more)

▼ The main function of parathyroid hormone (PTH) is to regulate serum calcium levels, in part by stimulating osteoclast mediated bone resorption. However, PTH can stimulate bone formation if given in intermittent doses and it is currently used as a bone anabolic agent to treat osteoporosis. The mechanisms by which PTH stimulates new bone formation are not yet completely clarified; PTH targets not only osteoblasts, where PTH receptors are abundantly expressed, but also immune cells. In this thesis, I examined the role of the calcium dependent cell-cell adhesion molecule, N-cadherin, in PTH signaling and bone anabolic responses. The findings presented in this dissertation further our understanding of PTH signaling in the context of bone anabolic responses. More to the point, this work demonstrates novel mechanisms by which N-cadherin intersects Wnt/β-catenin signaling, and how such interactions modulate osteoblast response to extracellular cues leading to bone formation. N-cadherin is abundantly expressed in cells of the osteoblast lineage, and it has been shown to modulate Wnt/β-catenin signaling by tethering low density lipoprotein receptor-related protein 5/6 (Lrp5/6) and β-catenin at the cell membrane. Lrp5/6 and β-catenin are also important components of PTH signaling and downstream effects. Indeed, formation of a complex between PTH, PTH receptor 1 (PTH1R) and Lrp6 has been linked to PTH anabolic action. Since N-cadherin regulates canonical Wnt/β-catenin pathway by interacting with Lrp5/6 and β-catenin, I hypothesized that N-cadherin may also modulate PTH signaling and bone anabolic response by interfering with Lrp6/ β-catenin signaling. To test this hypothesis, I examined signaling responses in N-cadherin-ablated primary osteoblasts from mice with a selective deletion of the N-cadherin gene (Cdh2) in osteoprogenitor cells (Cdh2^flox/flox::Osx-Cre; Cdh2-cKO). Co-immunoprecipitation experiments using control cells from Cdh2^flox/flox mice showed that PTH1R interacts with Lrp6, but not Lrp5 nor N-cadherin. This interaction was enhanced by exposure to PTH1-34 in Cdh2-cKO, but not in control cells. In primary osteoblasts, PTH1-34 promoted protein kinase A (PKA)-dependent activation of β-catenin via C-terminus phosphorylation at serine 675 (S675). This event was via non-canonical mechanisms that do not entail β-catenin's destruction complex. Interestingly, PTH-induced phosphorylation of β-catenin at S675 was accentuated in Cdh2-cKO cells relative to control. Consistent with enhanced β-catenin activation, PTH1-34 and Wnt3a stimulated expression of Tcf/Lef target genes, Lef1 and Axin2, to a larger extent in mutant cells compared to control. In addition, PTH1-34 induced rapid membrane trafficking of N-cadherin and Lrp5 from intracellular pools to the cell surface via cAMP/PKA signaling in osteoblastic cells. These changes in N-cadherin and… Advisors/Committee Members: Roberto Civitelli.

Subjects/Keywords: Beta-Catenin; Bone; N-Cadherin; Osteoblasts; Parathyroid Hormone

11 more images…

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Revollo, L. D. (2014). N-Cadherin Regulation of Bone Anabolic Responses via PTH and Wnt/Beta-Catenin Signaling. (Doctoral Dissertation). Washington University in St. Louis. Retrieved from https://openscholarship.wustl.edu/etd/1339

Chicago Manual of Style (16^th Edition):

Revollo, Leila Denise. “N-Cadherin Regulation of Bone Anabolic Responses via PTH and Wnt/Beta-Catenin Signaling.” 2014. Doctoral Dissertation, Washington University in St. Louis. Accessed January 27, 2021. https://openscholarship.wustl.edu/etd/1339.

MLA Handbook (7^th Edition):

Revollo, Leila Denise. “N-Cadherin Regulation of Bone Anabolic Responses via PTH and Wnt/Beta-Catenin Signaling.” 2014. Web. 27 Jan 2021.

Vancouver:

Revollo LD. N-Cadherin Regulation of Bone Anabolic Responses via PTH and Wnt/Beta-Catenin Signaling. [Internet] [Doctoral dissertation]. Washington University in St. Louis; 2014. [cited 2021 Jan 27]. Available from: https://openscholarship.wustl.edu/etd/1339.

Council of Science Editors:

Revollo LD. N-Cadherin Regulation of Bone Anabolic Responses via PTH and Wnt/Beta-Catenin Signaling. [Doctoral Dissertation]. Washington University in St. Louis; 2014. Available from: https://openscholarship.wustl.edu/etd/1339

Open Access Theses and Dissertations