subject:(Cytoskeletal proteins)

Hong Kong University of Science and Technology

1. Shen, Yuehong LIFS. Regulatory studies of the microtubule nucleator γ-tubulin ring complex.

Degree: 2017, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-102094 ; https://doi.org/10.14711/thesis-b1781166 ; http://repository.ust.hk/ir/bitstream/1783.1-102094/1/th_redirect.html

► The spatial and temporal organization of the microtubule cytoskeleton requires γ-tubulin ring complexes (γTuRCs), which initiate microtubule growth and mediate microtubule attachment at microtubule-organizing centers,… (more)

▼ The spatial and temporal organization of the microtubule cytoskeleton requires γ-tubulin ring complexes (γTuRCs), which initiate microtubule growth and mediate microtubule attachment at microtubule-organizing centers, such as centrosomes and the Golgi complex. In a search for γTuRC-interacting proteins, I identified the catalytic subunit of DNA polymerase δ (PolD1). Polδ is a major DNA polymerase which is responsible for DNA replication. It is also involved in DNA repair and recombination. PolD1 binds directly to γTuRCs and potently inhibits γTuRC-mediated microtubule nucleation. Whereas PolD1 depletion through RNA interference augments microtubule nucleation at the Golgi, PolD1 overexpression interferes with Golgi-based nucleation. By contrast, the depletion of PolD1 does not influence centrosome-based microtubule growth. Suppression of PolD1 expression impairs Golgi reassembly after nocodazole-induced disassembly and causes defects of Golgi reorientation during cell polarization. These results reveal a mechanism for the control of non-centrosomal γTuRC activity and a mechanism that regulates Golgi-mediated microtubule organization and functions. A body of evidence has shown that CDK5RAP2 and Nedd1 play key roles in γTuRC attachment to centrosomes, microtubule nucleation, and mitotic spindle organization. I investigated the γTuRC association with CDK5RAP2 and Nedd1, and found that most of the CDK5RAP2- and Nedd1-associated γTuRCs contain either CDK5RAP2 or Nedd1 and that their binding with γTuRCs is controlled by unknown protein factors. I found that CDK5RAP2 and Nedd1-bound γTuRCs undergo dynamic changes of the complex composition during the cell cycle. Moreover, the interphase and mitotic γTuRCs showed different microtubule-nucleating activities in an in vitro assay. Therefore, γTuRCs are regulated in a cell cycle-dependent manner. My results also suggest that CDK5RAP2 and Nedd1 may be under distinct controls for interacting with γTuRCs. In summary, I identified PolD1 to be a γTuRC inhibitor and revealed a new control mechanism of γTuRC-mediated microtubule nucleation in the Golgi complex. In addition, I showed that γTuRCs undergo cell cycle-dependent changes of subunit stoichiometry and associated proteins. My findings expand our knowledge on γTuRC regulation studies and provide insights into the organization mechanism on microtubule networks during the cell cycle.

Subjects/Keywords: Tubulins ; Microtubules ; Cytoskeletal proteins

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APA (6^th Edition):

Shen, Y. L. (2017). Regulatory studies of the microtubule nucleator γ-tubulin ring complex. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-102094 ; https://doi.org/10.14711/thesis-b1781166 ; http://repository.ust.hk/ir/bitstream/1783.1-102094/1/th_redirect.html

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):

Shen, Yuehong LIFS. “Regulatory studies of the microtubule nucleator γ-tubulin ring complex.” 2017. Thesis, Hong Kong University of Science and Technology. Accessed January 18, 2021. http://repository.ust.hk/ir/Record/1783.1-102094 ; https://doi.org/10.14711/thesis-b1781166 ; http://repository.ust.hk/ir/bitstream/1783.1-102094/1/th_redirect.html.

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

MLA Handbook (7^th Edition):

Shen, Yuehong LIFS. “Regulatory studies of the microtubule nucleator γ-tubulin ring complex.” 2017. Web. 18 Jan 2021.

Vancouver:

Shen YL. Regulatory studies of the microtubule nucleator γ-tubulin ring complex. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2017. [cited 2021 Jan 18]. Available from: http://repository.ust.hk/ir/Record/1783.1-102094 ; https://doi.org/10.14711/thesis-b1781166 ; http://repository.ust.hk/ir/bitstream/1783.1-102094/1/th_redirect.html.

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

Council of Science Editors:

Shen YL. Regulatory studies of the microtubule nucleator γ-tubulin ring complex. [Thesis]. Hong Kong University of Science and Technology; 2017. Available from: http://repository.ust.hk/ir/Record/1783.1-102094 ; https://doi.org/10.14711/thesis-b1781166 ; http://repository.ust.hk/ir/bitstream/1783.1-102094/1/th_redirect.html

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

University of Texas Southwestern Medical Center

2. Byers, Christopher Eugene. Analysis of the Interaction and Functional Determinants of Arc and Its Regulation of Dynamin.

Degree: 2011, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/845

► Recent evidence indicates that the activity-regulated cytoskeleton-associated protein, Arc, facilitates endocytosis of glutamate receptors and regulates cytoskeletal organization in neuronal dendrites. Both of these functions… (more)

Subjects/Keywords: Dynamin II; Cytoskeletal Proteins; GTP Phosphohydrolase Activators

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APA (6^th Edition):

Byers, C. E. (2011). Analysis of the Interaction and Functional Determinants of Arc and Its Regulation of Dynamin. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/845

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):

Byers, Christopher Eugene. “Analysis of the Interaction and Functional Determinants of Arc and Its Regulation of Dynamin.” 2011. Thesis, University of Texas Southwestern Medical Center. Accessed January 18, 2021. http://hdl.handle.net/2152.5/845.

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

MLA Handbook (7^th Edition):

Byers, Christopher Eugene. “Analysis of the Interaction and Functional Determinants of Arc and Its Regulation of Dynamin.” 2011. Web. 18 Jan 2021.

Vancouver:

Byers CE. Analysis of the Interaction and Functional Determinants of Arc and Its Regulation of Dynamin. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2011. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/2152.5/845.

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

Council of Science Editors:

Byers CE. Analysis of the Interaction and Functional Determinants of Arc and Its Regulation of Dynamin. [Thesis]. University of Texas Southwestern Medical Center; 2011. Available from: http://hdl.handle.net/2152.5/845

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

Montana State University

3. Kary, Marcia Rebecca. Involvement of the neck coiled-coil in the velocity of UNC104, a kinesin-related motor protein.

Degree: MS, College of Letters & Science, 2001, Montana State University

URL: https://scholarworks.montana.edu/xmlui/handle/1/8102

Subjects/Keywords: Kinesin.; Cytoskeletal proteins.

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APA (6^th Edition):

Kary, M. R. (2001). Involvement of the neck coiled-coil in the velocity of UNC104, a kinesin-related motor protein. (Masters Thesis). Montana State University. Retrieved from https://scholarworks.montana.edu/xmlui/handle/1/8102

Chicago Manual of Style (16^th Edition):

Kary, Marcia Rebecca. “Involvement of the neck coiled-coil in the velocity of UNC104, a kinesin-related motor protein.” 2001. Masters Thesis, Montana State University. Accessed January 18, 2021. https://scholarworks.montana.edu/xmlui/handle/1/8102.

MLA Handbook (7^th Edition):

Kary, Marcia Rebecca. “Involvement of the neck coiled-coil in the velocity of UNC104, a kinesin-related motor protein.” 2001. Web. 18 Jan 2021.

Vancouver:

Kary MR. Involvement of the neck coiled-coil in the velocity of UNC104, a kinesin-related motor protein. [Internet] [Masters thesis]. Montana State University; 2001. [cited 2021 Jan 18]. Available from: https://scholarworks.montana.edu/xmlui/handle/1/8102.

Council of Science Editors:

Kary MR. Involvement of the neck coiled-coil in the velocity of UNC104, a kinesin-related motor protein. [Masters Thesis]. Montana State University; 2001. Available from: https://scholarworks.montana.edu/xmlui/handle/1/8102

University of Alberta

4. Crawford, Ellen. Tubulin structure and implications for the self regulation of microtubules and their interaction with kinesin.

Degree: MS, Department of Physics, 2002, University of Alberta

URL: https://era.library.ualberta.ca/files/nz806213x

Subjects/Keywords: Tubulins.; Cytoskeletal proteins.; Kinesin.

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

APA (6^th Edition):

Crawford, E. (2002). Tubulin structure and implications for the self regulation of microtubules and their interaction with kinesin. (Masters Thesis). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/nz806213x

Chicago Manual of Style (16^th Edition):

Crawford, Ellen. “Tubulin structure and implications for the self regulation of microtubules and their interaction with kinesin.” 2002. Masters Thesis, University of Alberta. Accessed January 18, 2021. https://era.library.ualberta.ca/files/nz806213x.

MLA Handbook (7^th Edition):

Crawford, Ellen. “Tubulin structure and implications for the self regulation of microtubules and their interaction with kinesin.” 2002. Web. 18 Jan 2021.

Vancouver:

Crawford E. Tubulin structure and implications for the self regulation of microtubules and their interaction with kinesin. [Internet] [Masters thesis]. University of Alberta; 2002. [cited 2021 Jan 18]. Available from: https://era.library.ualberta.ca/files/nz806213x.

Council of Science Editors:

Crawford E. Tubulin structure and implications for the self regulation of microtubules and their interaction with kinesin. [Masters Thesis]. University of Alberta; 2002. Available from: https://era.library.ualberta.ca/files/nz806213x

University of Texas Southwestern Medical Center

5. Niere, Farr. A Study on an FMRP-Mediated Translational Switch in the MGluR-Triggered Translation of Arc and Synaptic Plasticity.

Degree: 2012, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/1002

► The group 1 metabotropic glutamate receptor (mGluR)-stimulated protein synthesis and long-term synaptic depression (mGluR-LTD) are altered in a mouse model of Fragile X Syndrome, Fmr1… (more)

Subjects/Keywords: Fragile X Mental Retardation Protein; Receptors, Metabotropic Glutamate; Cytoskeletal Proteins

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APA (6^th Edition):

Niere, F. (2012). A Study on an FMRP-Mediated Translational Switch in the MGluR-Triggered Translation of Arc and Synaptic Plasticity. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/1002

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):

Niere, Farr. “A Study on an FMRP-Mediated Translational Switch in the MGluR-Triggered Translation of Arc and Synaptic Plasticity.” 2012. Thesis, University of Texas Southwestern Medical Center. Accessed January 18, 2021. http://hdl.handle.net/2152.5/1002.

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

MLA Handbook (7^th Edition):

Niere, Farr. “A Study on an FMRP-Mediated Translational Switch in the MGluR-Triggered Translation of Arc and Synaptic Plasticity.” 2012. Web. 18 Jan 2021.

Vancouver:

Niere F. A Study on an FMRP-Mediated Translational Switch in the MGluR-Triggered Translation of Arc and Synaptic Plasticity. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2012. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/2152.5/1002.

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

Council of Science Editors:

Niere F. A Study on an FMRP-Mediated Translational Switch in the MGluR-Triggered Translation of Arc and Synaptic Plasticity. [Thesis]. University of Texas Southwestern Medical Center; 2012. Available from: http://hdl.handle.net/2152.5/1002

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

Columbia University

6. Schrank, Benjamin Robin. Nuclear Arp2/3 drives DNA double-strand break clustering for homology-directed repair.

Degree: 2019, Columbia University

URL: https://doi.org/10.7916/D8B86S2K

► Severing the DNA double helix is a requisite step in the exchange of genetic material between homologous chromosomes in meiosis and between immunoglobulin domains during… (more)

▼ Severing the DNA double helix is a requisite step in the exchange of genetic material between homologous chromosomes in meiosis and between immunoglobulin domains during the generation of immune-receptor diversity. While these DNA transactions are essential for human fertility and the development of the immune system, misrepaired or unrepaired DNA double-strand breaks (DSBs) can lead to chromosome rearrangements or cell death. Indeed, ionizing radiation which generates DSBs in tumors is a cornerstone of cancer therapy. However, tumor cells can tolerate otherwise lethal levels of DNA damage by exploiting DNA repair pathways. Thus, discovering new strategies to selectively inhibit the repair of DSBs remains a major goal in the development of more effective cancer therapies. DSB repair may occur by multiple pathways, and the decision to use one pathway over another is influenced by cell cycle stage, the chromatin state, and the complexity of the inciting lesion. Mammalian cells primarily resolve DSBs by ligating the free ends together during a process termed “non-homologous end joining” (NHEJ). However, chemically modified or damaged DSB ends cannot be directly ligated by the NHEJ machinery. If NHEJ fails, DSBs may be nucleolytically cleaved to generate 3’ single-stranded DNA overhangs via a process called end resection. The resected DNA strands are poor substrates for NHEJ and instead search for homology in the genome to resynthesize the sequence surrounding the break site. This process is termed “homology-directed repair” (HDR). HDR is tightly coupled to cell cycle phase to ensure that resection occurs during late S and G2 when the ideal template, the sister chromatid, may be utilized. Following DNA damage, repair factors accumulate at DSB sites and form microscopically-detectable DNA repair foci. The dynamics of these foci may be observed by time-lapse microscopy making it possible to observe the behavior of breaks undergoing HDR and NHEJ. Interestingly, in yeast and mammalian cells, DNA motion is increased following DSB generation. DNA movements can lead to the clustering of DSBs into a common repair focus. DSB movements are intricately related to repair by HDR and require factors critical for resection initiation and downstream recombination. In contrast, DSBs undergoing NHEJ are relatively immobile. These observations suggest that the commitment of DSB repair to HDR regulates DSB movement and clustering; however, how DSB clustering might promote repair and whether active mechanisms drive this process remain relatively obscure. Recent studies have proposed roles for cytoskeletal proteins in genome organization and chromosomal dynamics. The Arp2/3 complex generates propulsive forces by nucleating a highly branched network of actin filaments. Genotoxic agents trigger actin polymerization in the nucleus. However, how DSB repair pathways might harness nuclear Arp2/3 machinery is unknown. Chapter 1 provides an overview of these pathways including the key steps of DSB repair, the regulation of actin…

Subjects/Keywords: Genetics; Oncology; Biology; DNA damage; DNA repair; Cytoskeletal proteins

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

APA (6^th Edition):

Schrank, B. R. (2019). Nuclear Arp2/3 drives DNA double-strand break clustering for homology-directed repair. (Doctoral Dissertation). Columbia University. Retrieved from https://doi.org/10.7916/D8B86S2K

Chicago Manual of Style (16^th Edition):

Schrank, Benjamin Robin. “Nuclear Arp2/3 drives DNA double-strand break clustering for homology-directed repair.” 2019. Doctoral Dissertation, Columbia University. Accessed January 18, 2021. https://doi.org/10.7916/D8B86S2K.

MLA Handbook (7^th Edition):

Schrank, Benjamin Robin. “Nuclear Arp2/3 drives DNA double-strand break clustering for homology-directed repair.” 2019. Web. 18 Jan 2021.

Vancouver:

Schrank BR. Nuclear Arp2/3 drives DNA double-strand break clustering for homology-directed repair. [Internet] [Doctoral dissertation]. Columbia University; 2019. [cited 2021 Jan 18]. Available from: https://doi.org/10.7916/D8B86S2K.

Council of Science Editors:

Schrank BR. Nuclear Arp2/3 drives DNA double-strand break clustering for homology-directed repair. [Doctoral Dissertation]. Columbia University; 2019. Available from: https://doi.org/10.7916/D8B86S2K

Columbia University

7. Tinaztepe, Sedef. Biochemical and Genetic Investigation of Immature Murine Leukemia Virus Assembly.

Degree: 2017, Columbia University

URL: https://doi.org/10.7916/D82V2TNG

► Production of infectious retrovirus particles is a complex and poorly-understood process with multiple steps that are often linked to one another. Our aim in this… (more)

Subjects/Keywords: Virology; Biochemistry; Cytology; Mouse leukemia viruses; Cytoskeletal proteins; Retroviruses

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APA (6^th Edition):

Tinaztepe, S. (2017). Biochemical and Genetic Investigation of Immature Murine Leukemia Virus Assembly. (Doctoral Dissertation). Columbia University. Retrieved from https://doi.org/10.7916/D82V2TNG

Chicago Manual of Style (16^th Edition):

Tinaztepe, Sedef. “Biochemical and Genetic Investigation of Immature Murine Leukemia Virus Assembly.” 2017. Doctoral Dissertation, Columbia University. Accessed January 18, 2021. https://doi.org/10.7916/D82V2TNG.

MLA Handbook (7^th Edition):

Tinaztepe, Sedef. “Biochemical and Genetic Investigation of Immature Murine Leukemia Virus Assembly.” 2017. Web. 18 Jan 2021.

Vancouver:

Tinaztepe S. Biochemical and Genetic Investigation of Immature Murine Leukemia Virus Assembly. [Internet] [Doctoral dissertation]. Columbia University; 2017. [cited 2021 Jan 18]. Available from: https://doi.org/10.7916/D82V2TNG.

Council of Science Editors:

Tinaztepe S. Biochemical and Genetic Investigation of Immature Murine Leukemia Virus Assembly. [Doctoral Dissertation]. Columbia University; 2017. Available from: https://doi.org/10.7916/D82V2TNG

University of Missouri – Columbia

8. Barry, Devin. Molecular mechanisms of radial axonal growth : insights from analysis of neurofilament gene-targeted mice.

Degree: 2012, University of Missouri – Columbia

URL: https://doi.org/10.32469/10355/14977

► For the nervous system to send signals rapidly, axons must undergo growth that expands their diameter. This process is known as radial growth and is… (more)

Subjects/Keywords: neurofilament; conduction velocity; radial growth; myelin; cytoskeletal proteins

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APA (6^th Edition):

Barry, D. (2012). Molecular mechanisms of radial axonal growth : insights from analysis of neurofilament gene-targeted mice. (Thesis). University of Missouri – Columbia. Retrieved from https://doi.org/10.32469/10355/14977

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):

Barry, Devin. “Molecular mechanisms of radial axonal growth : insights from analysis of neurofilament gene-targeted mice.” 2012. Thesis, University of Missouri – Columbia. Accessed January 18, 2021. https://doi.org/10.32469/10355/14977.

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

MLA Handbook (7^th Edition):

Barry, Devin. “Molecular mechanisms of radial axonal growth : insights from analysis of neurofilament gene-targeted mice.” 2012. Web. 18 Jan 2021.

Vancouver:

Barry D. Molecular mechanisms of radial axonal growth : insights from analysis of neurofilament gene-targeted mice. [Internet] [Thesis]. University of Missouri – Columbia; 2012. [cited 2021 Jan 18]. Available from: https://doi.org/10.32469/10355/14977.

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

Council of Science Editors:

Barry D. Molecular mechanisms of radial axonal growth : insights from analysis of neurofilament gene-targeted mice. [Thesis]. University of Missouri – Columbia; 2012. Available from: https://doi.org/10.32469/10355/14977

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

University of Missouri – Columbia

9. Roberts-Pilgrim, Anna M., 1977-. Glomerulosclerosis in the Col1a2-deficient mouse model : homotrimer pathogenesis and MMP expression.

Degree: 2009, University of Missouri – Columbia

URL: https://doi.org/10.32469/10355/6155

► The Col1a2-deficient (oim) mouse model exclusively synthesizes homotrimeric type I collagen due to the lack of functional pro [alpha] 2(I) collagen chains. The mouse develops… (more)

Subjects/Keywords: Kidney glomerulus – Diseases; Cytoskeletal proteins

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APA (6^th Edition):

Roberts-Pilgrim, Anna M., 1. (2009). Glomerulosclerosis in the Col1a2-deficient mouse model : homotrimer pathogenesis and MMP expression. (Thesis). University of Missouri – Columbia. Retrieved from https://doi.org/10.32469/10355/6155

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):

Roberts-Pilgrim, Anna M., 1977-. “Glomerulosclerosis in the Col1a2-deficient mouse model : homotrimer pathogenesis and MMP expression.” 2009. Thesis, University of Missouri – Columbia. Accessed January 18, 2021. https://doi.org/10.32469/10355/6155.

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

MLA Handbook (7^th Edition):

Roberts-Pilgrim, Anna M., 1977-. “Glomerulosclerosis in the Col1a2-deficient mouse model : homotrimer pathogenesis and MMP expression.” 2009. Web. 18 Jan 2021.

Vancouver:

Roberts-Pilgrim, Anna M. 1. Glomerulosclerosis in the Col1a2-deficient mouse model : homotrimer pathogenesis and MMP expression. [Internet] [Thesis]. University of Missouri – Columbia; 2009. [cited 2021 Jan 18]. Available from: https://doi.org/10.32469/10355/6155.

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

Council of Science Editors:

Roberts-Pilgrim, Anna M. 1. Glomerulosclerosis in the Col1a2-deficient mouse model : homotrimer pathogenesis and MMP expression. [Thesis]. University of Missouri – Columbia; 2009. Available from: https://doi.org/10.32469/10355/6155

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

University of Missouri – Columbia

10. Roberts-Pilgrim, Anna M., 1977-. Glomerulosclerosis in the Col1a2-deficient mouse model : homotrimer pathogenesis and MMP expression.

Degree: 2009, University of Missouri – Columbia

URL: http://hdl.handle.net/10355/6155

► The Col1a2-deficient (oim) mouse model exclusively synthesizes homotrimeric type I collagen due to the lack of functional pro [alpha] 2(I) collagen chains. The mouse develops… (more)

Subjects/Keywords: Kidney glomerulus – Diseases; Cytoskeletal proteins

Record Details Similar Records Cite « Share

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

APA (6^th Edition):

Roberts-Pilgrim, Anna M., 1. (2009). Glomerulosclerosis in the Col1a2-deficient mouse model : homotrimer pathogenesis and MMP expression. (Thesis). University of Missouri – Columbia. Retrieved from http://hdl.handle.net/10355/6155

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):

Roberts-Pilgrim, Anna M., 1977-. “Glomerulosclerosis in the Col1a2-deficient mouse model : homotrimer pathogenesis and MMP expression.” 2009. Thesis, University of Missouri – Columbia. Accessed January 18, 2021. http://hdl.handle.net/10355/6155.

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

MLA Handbook (7^th Edition):

Roberts-Pilgrim, Anna M., 1977-. “Glomerulosclerosis in the Col1a2-deficient mouse model : homotrimer pathogenesis and MMP expression.” 2009. Web. 18 Jan 2021.

Vancouver:

Roberts-Pilgrim, Anna M. 1. Glomerulosclerosis in the Col1a2-deficient mouse model : homotrimer pathogenesis and MMP expression. [Internet] [Thesis]. University of Missouri – Columbia; 2009. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/10355/6155.

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

Council of Science Editors:

Roberts-Pilgrim, Anna M. 1. Glomerulosclerosis in the Col1a2-deficient mouse model : homotrimer pathogenesis and MMP expression. [Thesis]. University of Missouri – Columbia; 2009. Available from: http://hdl.handle.net/10355/6155

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

University of Missouri – Columbia

11. Barry, Devin. Molecular mechanisms of radial axonal growth : insights from analysis of neurofilament gene-targeted mice.

Degree: 2012, University of Missouri – Columbia

URL: http://hdl.handle.net/10355/14977

► For the nervous system to send signals rapidly, axons must undergo growth that expands their diameter. This process is known as radial growth and is… (more)

Subjects/Keywords: neurofilament; conduction velocity; radial growth; myelin; cytoskeletal proteins

Record Details Similar Records Cite « Share

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

APA (6^th Edition):

Barry, D. (2012). Molecular mechanisms of radial axonal growth : insights from analysis of neurofilament gene-targeted mice. (Thesis). University of Missouri – Columbia. Retrieved from http://hdl.handle.net/10355/14977

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):

Barry, Devin. “Molecular mechanisms of radial axonal growth : insights from analysis of neurofilament gene-targeted mice.” 2012. Thesis, University of Missouri – Columbia. Accessed January 18, 2021. http://hdl.handle.net/10355/14977.

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

MLA Handbook (7^th Edition):

Barry, Devin. “Molecular mechanisms of radial axonal growth : insights from analysis of neurofilament gene-targeted mice.” 2012. Web. 18 Jan 2021.

Vancouver:

Barry D. Molecular mechanisms of radial axonal growth : insights from analysis of neurofilament gene-targeted mice. [Internet] [Thesis]. University of Missouri – Columbia; 2012. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/10355/14977.

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

Council of Science Editors:

Barry D. Molecular mechanisms of radial axonal growth : insights from analysis of neurofilament gene-targeted mice. [Thesis]. University of Missouri – Columbia; 2012. Available from: http://hdl.handle.net/10355/14977

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

University of Texas Southwestern Medical Center

12. Kumar, Jaswinder Singh. Novel Roles for the Activity-Regulated Genes Arc and Npas4 in Stress- and Cocaine-Induced Plasticity.

Degree: 2016, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/5293

► Mood, anxiety, and substance abuse disorders are chronic medical illnesses that contribute significantly to morbidity and mortality worldwide. Currently, these conditions are treated symptomatically using… (more)

▼ Mood, anxiety, and substance abuse disorders are chronic medical illnesses that contribute significantly to morbidity and mortality worldwide. Currently, these conditions are treated symptomatically using pharmacological and psychotherapeutic approaches; however, the efficacy of these modalities is limited by the dearth of understanding of neurobiological mechanisms underlying mental illness. The high rate of mortality associated with mood, anxiety, and substance abuse disorders is compounded by their shared comorbidity, warranting an investigation into potential shared pathophysiological mechanisms. Studies from human patients and rodent models suggest that these mechanisms may be attributed to disrupted structural and functional plasticity in brain regions involved in mood, reward, and motivation, including the nucleus accumbens (NAc) and medial prefrontal cortex (mPFC). However, the molecules and signaling pathways within these structures that regulate these behaviors, and how they are dysregulated in pathological psychiatric conditions, have yet to be fully identified and characterized. Here, we focus on two key proteins that participate in activity-dependent synaptic plasticity, the neuronal Per Arnt Sim Domain protein 4 (NPAS4) and the activity-regulated cytoskeleton-associated protein (Arc). We utilize a series of ethologically relevant behavioral paradigms to identify Arc and NPAS4 as two important mediators of stress, anxiety, and addiction-related behaviors. Npas4 and Arc, two activity-regulated genes, are robustly induced by stressful, anxiogenic stimuli. Loss of either gene confers an antidepressant and anxiolytic response in mice, and these behavioral phenotypes are mediated by local function of these two proteins in limbic forebrain regions. In a related study, we ask whether loss of Arc influences behavioral responses to cocaine administration. We find that Arc knockout (KO) animals exhibit increased sensitivity to the locomotor activating and rewarding effects of cocaine, and these two phenotypes are associated with a selective increase in synaptic strength in the NAc. Taken together, our results highlight a heretofore-unidentified role for Arc and NPAS4 in stress- and anxiety-like behaviors, as well as Arc in cocaine-related behavioral adaptations. We propose that these two molecules play a vital role in regulating synaptic and behavioral plasticity evoked by exposure to stress and drugs of abuse, likely via experience-dependent synaptic remodeling. Advisors/Committee Members: Huber, Kimberly M., Cowan, Christopher W., Olson, Eric N., Zinn, Andrew R..

Subjects/Keywords: Cocaine-Related Disorders; Cytoskeletal Proteins; Nerve Tissue Proteins; Neuronal Plasticity; Nucleus Accumbens

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APA (6^th Edition):

Kumar, J. S. (2016). Novel Roles for the Activity-Regulated Genes Arc and Npas4 in Stress- and Cocaine-Induced Plasticity. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/5293

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):

Kumar, Jaswinder Singh. “Novel Roles for the Activity-Regulated Genes Arc and Npas4 in Stress- and Cocaine-Induced Plasticity.” 2016. Thesis, University of Texas Southwestern Medical Center. Accessed January 18, 2021. http://hdl.handle.net/2152.5/5293.

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

MLA Handbook (7^th Edition):

Kumar, Jaswinder Singh. “Novel Roles for the Activity-Regulated Genes Arc and Npas4 in Stress- and Cocaine-Induced Plasticity.” 2016. Web. 18 Jan 2021.

Vancouver:

Kumar JS. Novel Roles for the Activity-Regulated Genes Arc and Npas4 in Stress- and Cocaine-Induced Plasticity. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2016. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/2152.5/5293.

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

Council of Science Editors:

Kumar JS. Novel Roles for the Activity-Regulated Genes Arc and Npas4 in Stress- and Cocaine-Induced Plasticity. [Thesis]. University of Texas Southwestern Medical Center; 2016. Available from: http://hdl.handle.net/2152.5/5293

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

University of Texas Southwestern Medical Center

13. Rich, Shannon Kay Good. Regulatory Mechanisms of Semaphorin/Plexin/Mical-Mediated F-actin Disassembly and Cellular Remodeling.

Degree: 2017, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/6613

► Dynamic changes to the actin cytoskeleton modify the shape of cells and their membranous extensions, and underlie diverse developmental and functional events in multiple tissues… (more)

▼ Dynamic changes to the actin cytoskeleton modify the shape of cells and their membranous extensions, and underlie diverse developmental and functional events in multiple tissues including migration, navigation, and connectivity. Semaphorins, together with their Plexin receptors, are a large family of extracellular cues that trigger complex cytoskeletal rearrangements to direct these cellular phenomena, but the mechanisms regulating their effects are poorly understood. Emerging evidence identifies Mical, a conserved oxidoreductase (Redox) enzyme, as a critical component in Semaphorin/Plexin signaling through its post-translational oxidation of F-actin, which promotes actin instability and disassembly. How this Mical-mediated redox regulation of actin dynamics is locally positioned and coordinated with the activity of other actin regulatory proteins to achieve specific, targeted effects on the cytoskeleton remains unknown. Therefore, as a part of my dissertation research, I used a genetic assay to begin to address these questions and search for proteins that could alter Semaphorin/Plexin/Mical signaling effects on the cytoskeleton. In this dissertation, I present my discovery of a functional interplay between Mical and two critical new interactors - cofilin, a well-known ubiquitous F-actin regulatory protein, and Sisyphus, an unconventional class XV myosin. With regards to cofilin, my in vivo genetic/functional assays reveal that cofilin activity is required for and enhances Semaphorin/Plexin/Mical-dependent cytoskeletal rearrangements and morphological changes. Additionally, in vitro biochemical assays demonstrate that cofilin preferentially binds Mical-oxidized actin and accelerates its disassembly. Together, these findings indicate that cofilin and Mical act as a functional pair in both neuronal and non-neuronal cells to rapidly and efficiently disassemble actin filaments. Similarly, my results reveal that Sisyphus is necessary and sufficient for triggering Semaphorin/Plexin/Mical-dependent F-actin disassembly/cellular remodeling. Moreover, using in vivo functional assays, I find that Sisyphus uses its myosin motor activity and the first MyTH4 domain of its C-terminal tail region to modify the subcellular localization of Mical. In this way, Sisyphus spatially controls Mical-dependent F-actin disassembly/cellular remodeling. Therefore, both cofilin and Sisyphus function to promote Mical-mediated F-actin disassembly; thereby, they act as critical regulators of Semaphorin/Plexin/Mical-mediated effects on cytoskeletal and morphological dynamics. Thus, my findings unveil novel molecular and biochemical mechanisms that orchestrate cellular, developmental, and neural biology. Advisors/Committee Members: Johnson, Jane E., Terman, Jonathan R., Krämer, Helmut, Alto, Neal.

Subjects/Keywords: Adaptor Proteins, Signal Transducing; Cell Adhesion Molecules; Cytoskeletal Proteins; LIM Domain Proteins; Nerve Tissue Proteins; Semaphorins

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APA (6^th Edition):

Rich, S. K. G. (2017). Regulatory Mechanisms of Semaphorin/Plexin/Mical-Mediated F-actin Disassembly and Cellular Remodeling. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/6613

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):

Rich, Shannon Kay Good. “Regulatory Mechanisms of Semaphorin/Plexin/Mical-Mediated F-actin Disassembly and Cellular Remodeling.” 2017. Thesis, University of Texas Southwestern Medical Center. Accessed January 18, 2021. http://hdl.handle.net/2152.5/6613.

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

MLA Handbook (7^th Edition):

Rich, Shannon Kay Good. “Regulatory Mechanisms of Semaphorin/Plexin/Mical-Mediated F-actin Disassembly and Cellular Remodeling.” 2017. Web. 18 Jan 2021.

Vancouver:

Rich SKG. Regulatory Mechanisms of Semaphorin/Plexin/Mical-Mediated F-actin Disassembly and Cellular Remodeling. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2017. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/2152.5/6613.

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

Council of Science Editors:

Rich SKG. Regulatory Mechanisms of Semaphorin/Plexin/Mical-Mediated F-actin Disassembly and Cellular Remodeling. [Thesis]. University of Texas Southwestern Medical Center; 2017. Available from: http://hdl.handle.net/2152.5/6613

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

14. Gupta, Sneha. Understanding Regulation of the Cytoskeleton during Cell Cycle Transitions through Examination of Crosstalk between Homologous Fission Yeast Pathways, Septation Initiation Network and Morphogenesis ORB6 Network: A Dissertation.

Degree: Interdisciplinary Graduate Program, Biochemistry and Molecular Pharmacology, 2013, U of Massachusetts : Med

URL: http://escholarship.umassmed.edu/gsbs_diss/693

► The fission yeast Schizosaccharomyces pombe has become a powerful model system for studying cytokinesis, a process of cytoplasmic division by which one cell divides… (more)

▼ The fission yeast Schizosaccharomyces pombe has become a powerful model system for studying cytokinesis, a process of cytoplasmic division by which one cell divides into two identical daughter cells. Like mammalian cells, S. pombe divides through the use of an actomyosin contractile ring, which is composed of a set of highly conserved cytoskeletal proteins. Cytokinesis in S. pombe is primarily regulated by the SIN pathway, which is activated in late mitosis and is required for actomyosin contractile ring and septum assembly, and also plays a role in spindle checkpoint inactivation, and telophase nuclear positioning. The various functions of the SIN are carried out by the terminal kinase in the pathway called Sid2. The lack of information in the downstream targets of Sid2 has limited our understanding of the different functions of the SIN. We recently showed that, in addition to its other functions, the SIN promotes cytokinesis through inhibition the MOR signaling pathway, which normally drives cell separation and initiation of polarized growth following completion of cytokinesis (Ray et al, 2010). The molecular details of this inhibition and the physiological significance of inhibiting MOR during cytokinesis was unclear. The results presented in Chapter II describe our approach to identify Sid2 substrates, particularly focusing on Nak1 and Sog2 that function in the MOR signaling cascade. We identified and characterized Sid2 phosphorylation sites on the Nak1 and Sog2 proteins. Chapter III explores how post translational modification of MOR proteins by Sid2 regulates polarized growth during cytokinesis. This includes delineating the effect of Sid2 mediated phosphorylation of Nak1 and Sog2 on protein-protein interactions in the MOR pathway as well as on the regulation of their localization during late mitosis. Finally, results in Chapter IV demonstrate that failure to inhibit MOR signaling is lethal because cells initiate septum degradation/cell separation before completing cytokinesis thereby emphasizing the importance of cross-regulation between the two pathways to prevent initiation of the interphase polarity program during cytokinesis. Advisors/Committee Members: Dannel McCollum, PhD.

Subjects/Keywords: Cytokinesis; Cell Cycle; Cell Cycle Proteins; Cytoskeleton; Cytoskeletal Proteins; Schizosaccharomyces; Schizosaccharomyces pombe Proteins; Cellular and Molecular Physiology

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

APA (6^th Edition):

Gupta, S. (2013). Understanding Regulation of the Cytoskeleton during Cell Cycle Transitions through Examination of Crosstalk between Homologous Fission Yeast Pathways, Septation Initiation Network and Morphogenesis ORB6 Network: A Dissertation. (Doctoral Dissertation). U of Massachusetts : Med. Retrieved from http://escholarship.umassmed.edu/gsbs_diss/693

Chicago Manual of Style (16^th Edition):

Gupta, Sneha. “Understanding Regulation of the Cytoskeleton during Cell Cycle Transitions through Examination of Crosstalk between Homologous Fission Yeast Pathways, Septation Initiation Network and Morphogenesis ORB6 Network: A Dissertation.” 2013. Doctoral Dissertation, U of Massachusetts : Med. Accessed January 18, 2021. http://escholarship.umassmed.edu/gsbs_diss/693.

MLA Handbook (7^th Edition):

Gupta, Sneha. “Understanding Regulation of the Cytoskeleton during Cell Cycle Transitions through Examination of Crosstalk between Homologous Fission Yeast Pathways, Septation Initiation Network and Morphogenesis ORB6 Network: A Dissertation.” 2013. Web. 18 Jan 2021.

Vancouver:

Gupta S. Understanding Regulation of the Cytoskeleton during Cell Cycle Transitions through Examination of Crosstalk between Homologous Fission Yeast Pathways, Septation Initiation Network and Morphogenesis ORB6 Network: A Dissertation. [Internet] [Doctoral dissertation]. U of Massachusetts : Med; 2013. [cited 2021 Jan 18]. Available from: http://escholarship.umassmed.edu/gsbs_diss/693.

Council of Science Editors:

Gupta S. Understanding Regulation of the Cytoskeleton during Cell Cycle Transitions through Examination of Crosstalk between Homologous Fission Yeast Pathways, Septation Initiation Network and Morphogenesis ORB6 Network: A Dissertation. [Doctoral Dissertation]. U of Massachusetts : Med; 2013. Available from: http://escholarship.umassmed.edu/gsbs_diss/693

15. Osterloh, Jeannette M. dSarm/Sarm1 Governs a Conserved Axon Death Program: A Dissertation.

Degree: Neuroscience, Department of Neurobiology; Freeman Lab, 2013, U of Massachusetts : Med

URL: http://escholarship.umassmed.edu/gsbs_diss/668

► Axonal and synaptic degeneration is a hallmark of peripheral neuropathy, brain injury, and neurodegenerative disease. Axonal degeneration has been proposed to be mediated by… (more)

Subjects/Keywords: Axons; Nerve Degeneration; Neurodegenerative Diseases; Drosophila Proteins; Cytoskeletal Proteins; Armadillo Domain Proteins; Molecular and Cellular Neuroscience

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APA (6^th Edition):

Osterloh, J. M. (2013). dSarm/Sarm1 Governs a Conserved Axon Death Program: A Dissertation. (Doctoral Dissertation). U of Massachusetts : Med. Retrieved from http://escholarship.umassmed.edu/gsbs_diss/668

Chicago Manual of Style (16^th Edition):

Osterloh, Jeannette M. “dSarm/Sarm1 Governs a Conserved Axon Death Program: A Dissertation.” 2013. Doctoral Dissertation, U of Massachusetts : Med. Accessed January 18, 2021. http://escholarship.umassmed.edu/gsbs_diss/668.

MLA Handbook (7^th Edition):

Osterloh, Jeannette M. “dSarm/Sarm1 Governs a Conserved Axon Death Program: A Dissertation.” 2013. Web. 18 Jan 2021.

Vancouver:

Osterloh JM. dSarm/Sarm1 Governs a Conserved Axon Death Program: A Dissertation. [Internet] [Doctoral dissertation]. U of Massachusetts : Med; 2013. [cited 2021 Jan 18]. Available from: http://escholarship.umassmed.edu/gsbs_diss/668.

Council of Science Editors:

Osterloh JM. dSarm/Sarm1 Governs a Conserved Axon Death Program: A Dissertation. [Doctoral Dissertation]. U of Massachusetts : Med; 2013. Available from: http://escholarship.umassmed.edu/gsbs_diss/668

University of Texas Southwestern Medical Center

16. Loerwald, Kristofer William. Development of Neocortical Circuits: a Cell Autonomous Examination of mGluR5 and MEF2C.

Degree: 2015, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/4124

► Development of neocortical circuits requires both genetic programs and sensory experience-dependent modification of synaptic function. The rules that dictate how synapses develop and respond to… (more)

▼ Development of neocortical circuits requires both genetic programs and sensory experience-dependent modification of synaptic function. The rules that dictate how synapses develop and respond to changing patterns of input influence both the emergence of receptive fields and the capacity for learning. In turn, the factors that determine the rules for synaptic plasticity are defined by the proteins functioning at the synapse. This project investigates two proteins situated to have wide-reaching impacts on synaptic function. One of the challenges in detailing the roles a protein plays in regulating synapses is discerning not only its acute role on synaptic function, but also its long-term impact on circuit development. Therefore, studying how a protein is engaged by physiological patterns of input in vivo over an extended period of time will provide a broader picture of how it influences synaptic function and circuit development. mGluR5 has previously been implicated in several forms of plasticity that act to directly weaken synaptic function. In this document, I provide evidence that the net-effect of mGluR5 on synaptic function throughout the first few weeks of postnatal development is to promote synaptic input pathway strength, as demonstrated in 2 prominent and well-characterized input pathways to L2/3 pyramidal cells of barrel cortex. Furthermore, I demonstrate a possible role for mGluR5 in a homeostatic mechanism, offsetting the enhanced evoked synaptic input by suppressing both spontaneous transmission and intrinsic excitability. The transcription factor MEF2 also has established roles in regulating synaptic function. However, much less is known about the synaptic mechanisms through which MEF2 mediates its effects. Here, I implicate MEF2C as the critical MEF2 family member involved in regulating synaptic function in L2/3 pyramidal cells in barrel cortex, and provide potential synaptic and molecular mechanisms by which MEF2C regulates pathway input. Advisors/Committee Members: Johnson, Jane E., Meeks, Julian P., Powell, Craig M., Huber, Kimberly M., Gibson, Jay R..

Subjects/Keywords: Cytoskeletal Proteins; MEF2 Transcription Factors; Neocortex; Neuronal Plasticity; Receptor, Metabotropic Glutamate 5; Synapses

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APA (6^th Edition):

Loerwald, K. W. (2015). Development of Neocortical Circuits: a Cell Autonomous Examination of mGluR5 and MEF2C. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/4124

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):

Loerwald, Kristofer William. “Development of Neocortical Circuits: a Cell Autonomous Examination of mGluR5 and MEF2C.” 2015. Thesis, University of Texas Southwestern Medical Center. Accessed January 18, 2021. http://hdl.handle.net/2152.5/4124.

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

MLA Handbook (7^th Edition):

Loerwald, Kristofer William. “Development of Neocortical Circuits: a Cell Autonomous Examination of mGluR5 and MEF2C.” 2015. Web. 18 Jan 2021.

Vancouver:

Loerwald KW. Development of Neocortical Circuits: a Cell Autonomous Examination of mGluR5 and MEF2C. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2015. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/2152.5/4124.

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

Council of Science Editors:

Loerwald KW. Development of Neocortical Circuits: a Cell Autonomous Examination of mGluR5 and MEF2C. [Thesis]. University of Texas Southwestern Medical Center; 2015. Available from: http://hdl.handle.net/2152.5/4124

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

University of St Andrews

17. Angus, Liselotte. Willin as a novel 4.1 ezrin radixin moesin (FERM) domain protein in the mammalian Hippo signalling pathway.

Degree: PhD, 2011, University of St Andrews

URL: http://hdl.handle.net/10023/2489

► The Salvador/Warts/Hippo (Hippo) pathway defines a novel signalling cascade regulating cell contact inhibition, organ size control, cell growth, proliferation, apoptosis and cancer development in mammals.… (more)

Subjects/Keywords: 612; Willin; Hippo pathway; QP552.C96A6; Cytoskeletal proteins; Gene expression; Cellular signal transduction

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APA (6^th Edition):

Angus, L. (2011). Willin as a novel 4.1 ezrin radixin moesin (FERM) domain protein in the mammalian Hippo signalling pathway. (Doctoral Dissertation). University of St Andrews. Retrieved from http://hdl.handle.net/10023/2489

Chicago Manual of Style (16^th Edition):

Angus, Liselotte. “Willin as a novel 4.1 ezrin radixin moesin (FERM) domain protein in the mammalian Hippo signalling pathway.” 2011. Doctoral Dissertation, University of St Andrews. Accessed January 18, 2021. http://hdl.handle.net/10023/2489.

MLA Handbook (7^th Edition):

Angus, Liselotte. “Willin as a novel 4.1 ezrin radixin moesin (FERM) domain protein in the mammalian Hippo signalling pathway.” 2011. Web. 18 Jan 2021.

Vancouver:

Angus L. Willin as a novel 4.1 ezrin radixin moesin (FERM) domain protein in the mammalian Hippo signalling pathway. [Internet] [Doctoral dissertation]. University of St Andrews; 2011. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/10023/2489.

Council of Science Editors:

Angus L. Willin as a novel 4.1 ezrin radixin moesin (FERM) domain protein in the mammalian Hippo signalling pathway. [Doctoral Dissertation]. University of St Andrews; 2011. Available from: http://hdl.handle.net/10023/2489

Columbia University

18. Tsitkov, Stanislav. Emergent Properties of Biomolecular Organization.

Degree: 2021, Columbia University

URL: https://doi.org/10.7916/d8-dmje-n287

► The organization of molecules within a cell is central to cellular processes ranging from metabolism and damage repair to migration and replication. Uncovering the emergent… (more)

▼ The organization of molecules within a cell is central to cellular processes ranging from metabolism and damage repair to migration and replication. Uncovering the emergent properties of this biomolecular organization can improve our understanding of how organisms function and reveal ways to repurpose their components outside of the cell. This dissertation focuses on the role of organization in two widely studied systems: enzyme cascades and active cytoskeletal filaments.Part I of this dissertation studies the emergent properties of the spatial organization of enzyme cascades. Enzyme cascades consist of a series of enzymes that catalyze sequential reactions: the product of one enzyme is the substrate of a subsequent enzyme. Enzyme cascades are a fundamental component of cellular reaction pathways, and spatial organization of the cascading enzymes is often essential to their function. For example, cascading enzymes assembled into multi-enzyme complexes can protect unstable cascade intermediates from the environment by forming tunnels between active sites. We use mathematical modeling to investigate the role of spatial organization in three specific systems. First, we examine enzyme cascade reactions occurring in multi-enzyme complexes where active sites are connected by tunnels. Using stochastic simulations and theoretical results from queueing theory, we demonstrate that the fluctuations arising from the small number of molecules involved can cause non-negligible disruptions to cascade throughput. Second, we develop a set of design principles for a compartmentalized cascade reaction with an unstable intermediate and show that there exists a critical kinetics-dependent threshold at which compartments become useful. Third, we investigate enzyme cascades immobilized on a synthetic DNA origami scaffold and show that the scaffold can create a favorable microenvironment for catalysis. Part II of this dissertation focuses on the organization of active cytoskeletal filaments. Many mechanical processes of a cell, such as cell division, cell migration, and intracellular transport, are driven by the ATP-fueled motion of motor proteins (kinesin, dynein, or myosin) along cytoskeletal filaments (microtubules or actin filaments). Over the past two decades, researchers have been repurposing motor protein-driven propulsion outside of the cell to create systems where cytoskeletal filaments glide on surfaces coated with motor proteins. The study of these systems not only elucidates the mechanisms of force production within the cell, but also opens new avenues for applications ranging from molecular detection to computation. We examine how microtubules gliding on surfaces coated with kinesin motor proteins can generate collective behavior in response to mutualistic interactions between the filaments and motors, thereby maximizing the utilization of system components and production. To this end, we used a microtubule-kinesin system where motors reversibly bind to the surface. In experiments, microtubules gliding on these reversibly…

Subjects/Keywords: Biomedical engineering; Biocatalysis; Catalysis; Microtubules; Cytoskeletal proteins; Kinesin; Molecular biology – Mathematical models; Stochastic analysis

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APA (6^th Edition):

Tsitkov, S. (2021). Emergent Properties of Biomolecular Organization. (Doctoral Dissertation). Columbia University. Retrieved from https://doi.org/10.7916/d8-dmje-n287

Chicago Manual of Style (16^th Edition):

Tsitkov, Stanislav. “Emergent Properties of Biomolecular Organization.” 2021. Doctoral Dissertation, Columbia University. Accessed January 18, 2021. https://doi.org/10.7916/d8-dmje-n287.

MLA Handbook (7^th Edition):

Tsitkov, Stanislav. “Emergent Properties of Biomolecular Organization.” 2021. Web. 18 Jan 2021.

Vancouver:

Tsitkov S. Emergent Properties of Biomolecular Organization. [Internet] [Doctoral dissertation]. Columbia University; 2021. [cited 2021 Jan 18]. Available from: https://doi.org/10.7916/d8-dmje-n287.

Council of Science Editors:

Tsitkov S. Emergent Properties of Biomolecular Organization. [Doctoral Dissertation]. Columbia University; 2021. Available from: https://doi.org/10.7916/d8-dmje-n287

Michigan State University

19. Smith, Harley M. S. Functional analysis and intracellular targeting of the nuclear localization signal receptor, importin [alpha], [in Arabidopsis thaliana].

Degree: PhD, Genetics Program, 1998, Michigan State University

URL: http://etd.lib.msu.edu/islandora/object/etd:26959

Subjects/Keywords: Arabidopsis thaliana – Genetics; Biological transport; Cytoskeletal proteins; Plant proteins

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APA (6^th Edition):

Smith, H. M. S. (1998). Functional analysis and intracellular targeting of the nuclear localization signal receptor, importin [alpha], [in Arabidopsis thaliana]. (Doctoral Dissertation). Michigan State University. Retrieved from http://etd.lib.msu.edu/islandora/object/etd:26959

Chicago Manual of Style (16^th Edition):

Smith, Harley M S. “Functional analysis and intracellular targeting of the nuclear localization signal receptor, importin [alpha], [in Arabidopsis thaliana].” 1998. Doctoral Dissertation, Michigan State University. Accessed January 18, 2021. http://etd.lib.msu.edu/islandora/object/etd:26959.

MLA Handbook (7^th Edition):

Smith, Harley M S. “Functional analysis and intracellular targeting of the nuclear localization signal receptor, importin [alpha], [in Arabidopsis thaliana].” 1998. Web. 18 Jan 2021.

Vancouver:

Smith HMS. Functional analysis and intracellular targeting of the nuclear localization signal receptor, importin [alpha], [in Arabidopsis thaliana]. [Internet] [Doctoral dissertation]. Michigan State University; 1998. [cited 2021 Jan 18]. Available from: http://etd.lib.msu.edu/islandora/object/etd:26959.

Council of Science Editors:

Smith HMS. Functional analysis and intracellular targeting of the nuclear localization signal receptor, importin [alpha], [in Arabidopsis thaliana]. [Doctoral Dissertation]. Michigan State University; 1998. Available from: http://etd.lib.msu.edu/islandora/object/etd:26959

Hong Kong University of Science and Technology

20. Leung, Doreen Siu Yi. Dynamic changes of cytoskeletal proteins in primary astrocyte cultures post scratch injury.

Degree: 1994, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-3807 ; https://doi.org/10.14711/thesis-b447465 ; http://repository.ust.hk/ir/bitstream/1783.1-3807/1/th_redirect.html

► Irrespective to the types of CNS injury, astrocytes are activated and become gliotic. Glial fibrillary acidic protein (GFAP) is one of the specific markers for… (more)

▼ Irrespective to the types of CNS injury, astrocytes are activated and become gliotic. Glial fibrillary acidic protein (GFAP) is one of the specific markers for astrocytes. Increment in GFAP is well documented in astrogliosis, the scar formation process by astrocytes in response to injury. Astrogliosis is also characterised by hyperplasia, hypertrophy and rearrangement of the cytoskeletons. The response of astrocytes to injury is so vigorous and fast that astrocytic scar formed can have harmful effect in neuronal regeneration and axonal remyelination. As GFAP and other cytoskeleton (including microtubules, actin and vimentin) are important in the change of morphology of reactive astrocytes, it is important to investigate the changes of these proteins in injured astrocytes. In this study, an in vitro scratch-wound model was used to study mechanical injury. A plastic pipette tip was used to scratch a confluent primary culture of astrocytes which was prepared from rat cerebral cortex. Confocal Scanning Laser Microscopy (CSLM) and Western Blotting techniques were used as tools to examine the morphological and biochemical changes of actin, GFAP, vimentin and β-tubulin. These proteins: were visualized by immunocytochemical staining and quantified by densitometer. The changes of cytoskeletal proteins in the astrocytes along the scratched zone and the distant inner non scratch region were compared at 8 time points (0,6 and 12 hours, day 1,2,3,5 and 9). Western Blotting quantified the total pooled responses of both scratched and non scratched astrocytes of the whole culture whereas CSLM was able to detect the regional differences of astrocvtes along and distant from the scratch injury. With analysis, the detected responses of the four cytoskeletal proteins to scratch injury were different. GFAP of the scratched astrocytes had an intense initial elevation, then decreased gradually and increased at a later stage. Microtubules as reflected by Western blotting remained at a constant level throughout the whole time course with only slight fluctuations. Actin had a significant decrease of about 50% at day 1 and 20% at day 2. Vimentin had a significant decrease of about 15% at day 1 and 50% increase at day 9. For regional comparison, all astrocytes along the scratch showed higher and dramatic changes in the intensity of staining of GFAP, vimentin, actin and β-tubulin. No changes were observed in the non scratched astrocytes in the inner region except vimentin which showed changes in both scratched and non scratched region. Staining for oncogene proteins for heat shock, c-myc and n-myc demonstrated intense immunofluorescence in astrocytes localized along the scratch edge. These proteins are good markers for injured cells. These observations concluded that CSLM and Western Blotting are a good combination in studying the changes in cytoskeletal proteins in injured astrocytes. The cytoskeletal proteins, GFAP, vimentin, β-tubulin and actin, altered differently in astrocytes in response to injury suggested that GFAP may not be the only…

Subjects/Keywords: Central nervous system – Regeneration ; Cytoskeletal proteins ; Astrocytes

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APA (6^th Edition):

Leung, D. S. Y. (1994). Dynamic changes of cytoskeletal proteins in primary astrocyte cultures post scratch injury. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-3807 ; https://doi.org/10.14711/thesis-b447465 ; http://repository.ust.hk/ir/bitstream/1783.1-3807/1/th_redirect.html

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):

Leung, Doreen Siu Yi. “Dynamic changes of cytoskeletal proteins in primary astrocyte cultures post scratch injury.” 1994. Thesis, Hong Kong University of Science and Technology. Accessed January 18, 2021. http://repository.ust.hk/ir/Record/1783.1-3807 ; https://doi.org/10.14711/thesis-b447465 ; http://repository.ust.hk/ir/bitstream/1783.1-3807/1/th_redirect.html.

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

MLA Handbook (7^th Edition):

Leung, Doreen Siu Yi. “Dynamic changes of cytoskeletal proteins in primary astrocyte cultures post scratch injury.” 1994. Web. 18 Jan 2021.

Vancouver:

Leung DSY. Dynamic changes of cytoskeletal proteins in primary astrocyte cultures post scratch injury. [Internet] [Thesis]. Hong Kong University of Science and Technology; 1994. [cited 2021 Jan 18]. Available from: http://repository.ust.hk/ir/Record/1783.1-3807 ; https://doi.org/10.14711/thesis-b447465 ; http://repository.ust.hk/ir/bitstream/1783.1-3807/1/th_redirect.html.

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

Council of Science Editors:

Leung DSY. Dynamic changes of cytoskeletal proteins in primary astrocyte cultures post scratch injury. [Thesis]. Hong Kong University of Science and Technology; 1994. Available from: http://repository.ust.hk/ir/Record/1783.1-3807 ; https://doi.org/10.14711/thesis-b447465 ; http://repository.ust.hk/ir/bitstream/1783.1-3807/1/th_redirect.html

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

University of Georgia

21. King, Lori Marie. A functional genomic and genetic analysis of subclass III Actin Depolymerizing Factor (ADF) proteins in Arabidopsis thaliana.

Degree: 2014, University of Georgia

URL: http://hdl.handle.net/10724/27743

► The Actin Depolymerizing Factor (ADF)/Cofilin family of proteins are essential actin-binding proteins found in all eukaryotes. ADF proteins modulate actin filament dynamics by severing monomers… (more)

Subjects/Keywords: Actin; Actin Binding Proteins; Actin Depolymerizing Factor; ADF; Cytoskeletal Dynamics; DNA Microarray; FLC; Gene Transcription; Transcriptome Analysis

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APA (6^th Edition):

King, L. M. (2014). A functional genomic and genetic analysis of subclass III Actin Depolymerizing Factor (ADF) proteins in Arabidopsis thaliana. (Thesis). University of Georgia. Retrieved from http://hdl.handle.net/10724/27743

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):

King, Lori Marie. “A functional genomic and genetic analysis of subclass III Actin Depolymerizing Factor (ADF) proteins in Arabidopsis thaliana.” 2014. Thesis, University of Georgia. Accessed January 18, 2021. http://hdl.handle.net/10724/27743.

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

MLA Handbook (7^th Edition):

King, Lori Marie. “A functional genomic and genetic analysis of subclass III Actin Depolymerizing Factor (ADF) proteins in Arabidopsis thaliana.” 2014. Web. 18 Jan 2021.

Vancouver:

King LM. A functional genomic and genetic analysis of subclass III Actin Depolymerizing Factor (ADF) proteins in Arabidopsis thaliana. [Internet] [Thesis]. University of Georgia; 2014. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/10724/27743.

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

Council of Science Editors:

King LM. A functional genomic and genetic analysis of subclass III Actin Depolymerizing Factor (ADF) proteins in Arabidopsis thaliana. [Thesis]. University of Georgia; 2014. Available from: http://hdl.handle.net/10724/27743

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

University of Sydney

22. Singh, Anish D. Regulation and function of the non-muscle [beta]-actin and [gamma]-actin genes .

Degree: 2004, University of Sydney

URL: http://hdl.handle.net/2123/11556

Subjects/Keywords: Actin genes; Cells – Morphology; Gene expression; Cytoskeletal proteins

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APA (6^th Edition):

Singh, A. D. (2004). Regulation and function of the non-muscle [beta]-actin and [gamma]-actin genes . (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/11556

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):

Singh, Anish D. “Regulation and function of the non-muscle [beta]-actin and [gamma]-actin genes .” 2004. Thesis, University of Sydney. Accessed January 18, 2021. http://hdl.handle.net/2123/11556.

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

MLA Handbook (7^th Edition):

Singh, Anish D. “Regulation and function of the non-muscle [beta]-actin and [gamma]-actin genes .” 2004. Web. 18 Jan 2021.

Vancouver:

Singh AD. Regulation and function of the non-muscle [beta]-actin and [gamma]-actin genes . [Internet] [Thesis]. University of Sydney; 2004. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/2123/11556.

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

Council of Science Editors:

Singh AD. Regulation and function of the non-muscle [beta]-actin and [gamma]-actin genes . [Thesis]. University of Sydney; 2004. Available from: http://hdl.handle.net/2123/11556

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

23. Lai, YuShuan (Cindy). EspFU, an Enterohemorrhagic E. Coli Secreted Effector, Hijacks Mammalian Actin Assembly Proteins by Molecular Mimicry and Repetition: A Dissertation.

Degree: PhD, Molecular Genetics and Microbiology, 2014, U of Massachusetts : Med

URL: http://escholarship.umassmed.edu/gsbs_diss/715

► Enterohemorrhagic E. coli (EHEC) is a major cause of food borne diarrheal illness worldwide. While disease symptoms are usually self-resolving and limited to severe… (more)

Subjects/Keywords: Actin Cytoskeleton; Actins; Calpain; Cytoskeletal Proteins; Enterohemorrhagic Escherichia coli; Escherichia coli Infections; Escherichia coli Proteins; Microvilli; Bacterial Infections and Mycoses; Bacteriology; Cellular and Molecular Physiology; Microbial Physiology

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APA (6^th Edition):

Lai, Y. (. (2014). EspFU, an Enterohemorrhagic E. Coli Secreted Effector, Hijacks Mammalian Actin Assembly Proteins by Molecular Mimicry and Repetition: A Dissertation. (Doctoral Dissertation). U of Massachusetts : Med. Retrieved from http://escholarship.umassmed.edu/gsbs_diss/715

Chicago Manual of Style (16^th Edition):

Lai, YuShuan (Cindy). “EspFU, an Enterohemorrhagic E. Coli Secreted Effector, Hijacks Mammalian Actin Assembly Proteins by Molecular Mimicry and Repetition: A Dissertation.” 2014. Doctoral Dissertation, U of Massachusetts : Med. Accessed January 18, 2021. http://escholarship.umassmed.edu/gsbs_diss/715.

MLA Handbook (7^th Edition):

Lai, YuShuan (Cindy). “EspFU, an Enterohemorrhagic E. Coli Secreted Effector, Hijacks Mammalian Actin Assembly Proteins by Molecular Mimicry and Repetition: A Dissertation.” 2014. Web. 18 Jan 2021.

Vancouver:

Lai Y(. EspFU, an Enterohemorrhagic E. Coli Secreted Effector, Hijacks Mammalian Actin Assembly Proteins by Molecular Mimicry and Repetition: A Dissertation. [Internet] [Doctoral dissertation]. U of Massachusetts : Med; 2014. [cited 2021 Jan 18]. Available from: http://escholarship.umassmed.edu/gsbs_diss/715.

Council of Science Editors:

Lai Y(. EspFU, an Enterohemorrhagic E. Coli Secreted Effector, Hijacks Mammalian Actin Assembly Proteins by Molecular Mimicry and Repetition: A Dissertation. [Doctoral Dissertation]. U of Massachusetts : Med; 2014. Available from: http://escholarship.umassmed.edu/gsbs_diss/715

24. Vlahovich, Nicole. The role of cytoskeletal tropomyosins in skeletal muscle and muscle disease.

Degree: 2007, Western Sydney University

URL: http://handle.uws.edu.au:8081/1959.7/32176

► Cells contain an elaborate cytoskeleton which plays a major role in a variety of cellular functions including: maintenance of cell shape and dimension, providing mechanical… (more)

▼ Cells contain an elaborate cytoskeleton which plays a major role in a variety of cellular functions including: maintenance of cell shape and dimension, providing mechanical strength, cell motility, cytokinesis during mitosis and meiosis and intracellular transport. The cell cytoskeleton is made up of three types of protein filaments: the microtubules, the intermediate filaments and the actin cytoskeleton. These components interact with each other to allow the cell to function correctly. When functioning incorrectly, disruptions to many cellular pathway have been observed with mutations in various cytoskeletal proteins causing an assortment of human disease phenotypes. Characterization of these filament systems in different cell types is essential to the understanding of basic cellular processes and disease causation. The studies in this thesis are concerned with examining specific cytoskeletal tropomyosin-defined actin filament systems in skeletal muscle. The diversity of the actin filament system relies, in part, on the family of actin binding proteins, the tropomyosins (Tms). There are in excess of forty Tm isoforms found in mammals which are derived from four genes: α, β, γ and δTm. The role of the musclespecific Tms in striated muscle is well understood, with sarcomeric Tm isoforms functioning as part of the thin filament where it regulates actin-myosin interactions and hence muscle contraction. However, relatively little known about the roles of the many cytoskeletal Tm isoforms. Cytoskeletal Tms have been shown to compartmentalise to form functionally distinct filaments in a range of cell types including neurons (Bryce et al., 2003), fibroblasts (Percival et al., 2000) and epithelial cells (Dalby-Payne et al., 2003). Recently it has been shown that cytoskeletal Tm, Tm5NM1 defines a cytoskeletal structure in skeletal muscle called the Z-line associated cytoskeleton (Z-LAC) (Kee et al., 2004).The disruption of this structure by over-expression of an exogenous Tm in transgenic mice results in a muscular dystrophy phenotype, indicating that the Z-LAC plays an important role in maintenance of muscle structure (Kee et al., 2004). In this study, specific cytoskeletal Tms are further investigated in the context of skeletal muscle. Here, we examine the expression, localisation and potential function of cytoskeletal Tm isoforms, focussing on Tm4 (derived from the δ- gene) and Tm5NM1 (derived from the γ-gene). By western blotting and immuno-staining mouse skeletal muscle, we show that cytoskeletal Tms are expressed in a range of muscles and define separate populations of filaments. These filaments are found in association with a number of muscle structures including the myotendinous junction, neuromuscular junction, the sarcolemma, the t-tubules and the sarcoplasmic reticulum. Of particular interest, Tm4 and Tm5NM1 define cytoskeletal elements in association with the saroplasmic reticulum and T-tubules, respectively, with a separation of less than 90 nm between distinct filamentous populations. The segregation of Tm… Advisors/Committee Members: University of Western Sydney (Host institution), College of Health and Science (Host institution), School of Natural Sciences (Host institution).

Subjects/Keywords: Doctor of Philosophy (PhD); tropomyosins; cytoskeletal proteins; muscle proteins; muscles; diseases; actin

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APA (6^th Edition):

Vlahovich, N. (2007). The role of cytoskeletal tropomyosins in skeletal muscle and muscle disease. (Thesis). Western Sydney University. Retrieved from http://handle.uws.edu.au:8081/1959.7/32176

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):

Vlahovich, Nicole. “The role of cytoskeletal tropomyosins in skeletal muscle and muscle disease.” 2007. Thesis, Western Sydney University. Accessed January 18, 2021. http://handle.uws.edu.au:8081/1959.7/32176.

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

MLA Handbook (7^th Edition):

Vlahovich, Nicole. “The role of cytoskeletal tropomyosins in skeletal muscle and muscle disease.” 2007. Web. 18 Jan 2021.

Vancouver:

Vlahovich N. The role of cytoskeletal tropomyosins in skeletal muscle and muscle disease. [Internet] [Thesis]. Western Sydney University; 2007. [cited 2021 Jan 18]. Available from: http://handle.uws.edu.au:8081/1959.7/32176.

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

Council of Science Editors:

Vlahovich N. The role of cytoskeletal tropomyosins in skeletal muscle and muscle disease. [Thesis]. Western Sydney University; 2007. Available from: http://handle.uws.edu.au:8081/1959.7/32176

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

East Carolina University

25. Kingsbury, Nathaniel. Fesselin, an intrinsically disordered smooth muscle protein, organizes and stabilizes actin-myosin and myosin.

Degree: MS, Biomedical Sciences, 2014, East Carolina University

URL: http://hdl.handle.net/10342/4663

► Fesselin is an intrinsically disordered protein that is known to bind a large variety of cytoskeletal proteins. The proteins fesselin is known to bind include:… (more)

▼ Fesselin is an intrinsically disordered protein that is known to bind a large variety of cytoskeletal proteins. The proteins fesselin is known to bind include: actin (Leinweber et al. 1999), [alpha]-actinin (Pham et al. 2006), calmodulin (Schroeter et al. 2004), filamin (Weins et al. 2001), and smooth myosin (Schroeter et al. 2005). The binding of fessilin to smooth myosin is of particular interest because unphosphorylated smooth muscle myosin filaments are unstable in the presence of ATP (Trybus et al. 1982, Ikebe et al. 1983, Suzuki et al. 1978). However, in smooth muscle cells unphosphorylated myosin filaments are maintained (Milton et al. 2011). Several proteins have been identified that stabilize myosin filaments and actin-myosin filament interactions. Our experiments show that fesselin may be one such protein. The organization of F-actin and myosin filaments by fesselin was observed by monitoring the rate of dissociation of actin-myosin by ATP in a stopped-flow device. Actin-myosin dissociation was measured by light scattering (a measure of particle size) and by pyrene-actin or acrylodan-tropomyosin fluorescence (a measure of myosin-actin bond breaking). The stopped-flow studies were further supported with electron microscopy analysis. These experiments showed that fesselin was able to tether actin and myosin filaments together without significantly impacting the rate of the actin-myosin bond breaking. The stabilization of myosin filaments by fesselin was tested using a similar method. First, stopped-flow rapid kinetics were used to measure the rate of ATP induced myosin filament break down. Next, electron microscopy was used to support the stopped-flow data and observe the effects of fesselin on myosin filament organization. Through the stopped-flow and electron microscopy experiments it was found that fesselin stabilizes myosin filaments. The electron microscopy experiments further revealed that fesselin enhanced myosin filament size and organized them into bundles. Previously published results showed that the interaction between fesselin and actin is regulated by calmodulin (Schroeter et al. 2004). The final set of experiments presented here examined the possibility that calmodulin regulates the interactions between fessilin and myosin. The calmodulin regulation of fesselin myosin interactions would greatly expand the role that fesselin has within smooth muscle by placing it within the calcium signaling pathway. The regulation of fesselin-myosin interactions by calmodulin was tested using pyrene labeled actin as well as N,N'-Dimethyl-N-(Iodoacetyl)-N'-(7-Nitrobenz-2-Oxa-1,3-Diazol-4-yl)Ethylenediamine labeled fesselin (IANBD-fesselin). These experiments showed that the interactions between fesselin and myosin are regulated by calmodulin. Overall, our results support that fesselin plays a critical role within smooth muscle to organize contractile elements. Advisors/Committee Members: Chalovich, Joseph M. (advisor).

Subjects/Keywords: Biochemistry; Molecular biology; Actin; Fesselin; Myosin; Rapid kinetics; Synaptopodin-2; Smooth Muscle Myosins – metabolism; Cytoskeletal Proteins – metabolism; Actins – metabolism; Adenosine Triphosphatases – metabolism; Membrane Proteins – physiology; Myosins – metabolism

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

APA (6^th Edition):

Kingsbury, N. (2014). Fesselin, an intrinsically disordered smooth muscle protein, organizes and stabilizes actin-myosin and myosin. (Masters Thesis). East Carolina University. Retrieved from http://hdl.handle.net/10342/4663

Chicago Manual of Style (16^th Edition):

Kingsbury, Nathaniel. “Fesselin, an intrinsically disordered smooth muscle protein, organizes and stabilizes actin-myosin and myosin.” 2014. Masters Thesis, East Carolina University. Accessed January 18, 2021. http://hdl.handle.net/10342/4663.

MLA Handbook (7^th Edition):

Kingsbury, Nathaniel. “Fesselin, an intrinsically disordered smooth muscle protein, organizes and stabilizes actin-myosin and myosin.” 2014. Web. 18 Jan 2021.

Vancouver:

Kingsbury N. Fesselin, an intrinsically disordered smooth muscle protein, organizes and stabilizes actin-myosin and myosin. [Internet] [Masters thesis]. East Carolina University; 2014. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/10342/4663.

Council of Science Editors:

Kingsbury N. Fesselin, an intrinsically disordered smooth muscle protein, organizes and stabilizes actin-myosin and myosin. [Masters Thesis]. East Carolina University; 2014. Available from: http://hdl.handle.net/10342/4663

26. Indran, Sabarish Vellatheri. Role of the human cytomegalovirus tegument protein pp150 in the trafficking and assembly of infectious virions.

Degree: PhD, 2010, University of Alabama – Birmingham

URL: http://contentdm.mhsl.uab.edu/u?/etd,1351

►

Human cytomegalovirus, a ubiquitous human pathogen, establishes a persistent infection in the infected host. HCMV assembly takes place in the nucleus and cytoplasm of infected… (more)

▼

Human cytomegalovirus, a ubiquitous human pathogen, establishes a persistent infection in the infected host. HCMV assembly takes place in the nucleus and cytoplasm of infected cells by a complex and incompletely defined process. The viral DNA is enclosed by the capsid, which is surrounded by a proteinaceous tegument, which is covered by a cell-derived envelope studded with viral glycoproteins. The assembly pathway and protein interactions required for formation of the tegument layer and the function of most of the proteins in the tegument remain poorly understood. In this study, we investigated the functions of an essential abundant tegument protein, pp150, in the assembly of the virus. This protein is thought to bind to capsids and play an important role in the cytoplasmic maturation of HCMV. However, a major issue that remains unexplained is the mechanism by which this protein is localized to the cytoplasmic assembly compartment (AC), the putative site of virus maturation. The cellular and viral proteins that interact with pp150, and thus contribute to its function are also unknown. We conducted a series of yeast two-hybrid screens to identify potential interactors of pp150. Among the many potential interactors we found, we concentrated on a cellular protein Bicaudal-D1 and a viral tegument protein ppUL25. The interaction between pp150 and BicD1 was confirmed by co-immunoprecipitation, co-localization and proven to be direct using Fluorescence Resonance Energy Transfer. BicD1 was found to be essential for specifically trafficking pp150 to the cytoplasmic viral assembly compartment (AC). We found that pp150 interacted with the C-terminal coiled-coil domain of BicD1, which also interacts with the GTPase Rab6. Next, we found that Rab6 also form part of the pp150-BicD1 complex and plays a role in trafficking of pp150, potentially by addressing the pp150-BicD1 complex to the Rab6-associated membranes. Also, the AC depends on the microtubule network and the dynein molecular motor for its formation/maintainence. Finally, we confirmed that the pp150 directly interacted with ppUL25. This interaction, combined with the BicD1-Rab6-Dynein-dependent trafficking of pp150 may explain how ppUL25 gets trafficked to the AC, and provides evidence that tegumentation of HCMV involves nucleation of tegument subunits that utilize host cell proteins to target to the AC.

1 online resource (xiv, 164 p.) :ill., digital, PDF file.

Microbiology

Joint Health Sciences

UNRESTRICTED

Advisors/Committee Members: William J. Britt, Additional advisors: Terje Dokland, Casey D. Morrow, Elizabeth Szutul, Sunnie Thompson..

Subjects/Keywords: Adaptor Proteins, Signal Transducing – physiology.<; br>; Cytomegalovirus<; br>; Cytoskeletal Proteins – physiology<; br>; Host-Pathogen Interactions.<; br>; Phosphoproteins – metabolism<; br>; Viral Matrix Proteins – metabolism.<; br>; Virus Assembly.<; br>; rab GTP-Binding Proteins – metabolism.

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

APA (6^th Edition):

Indran, S. V. (2010). Role of the human cytomegalovirus tegument protein pp150 in the trafficking and assembly of infectious virions. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1351

Chicago Manual of Style (16^th Edition):

Indran, Sabarish Vellatheri. “Role of the human cytomegalovirus tegument protein pp150 in the trafficking and assembly of infectious virions.” 2010. Doctoral Dissertation, University of Alabama – Birmingham. Accessed January 18, 2021. http://contentdm.mhsl.uab.edu/u?/etd,1351.

MLA Handbook (7^th Edition):

Indran, Sabarish Vellatheri. “Role of the human cytomegalovirus tegument protein pp150 in the trafficking and assembly of infectious virions.” 2010. Web. 18 Jan 2021.

Vancouver:

Indran SV. Role of the human cytomegalovirus tegument protein pp150 in the trafficking and assembly of infectious virions. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2010. [cited 2021 Jan 18]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1351.

Council of Science Editors:

Indran SV. Role of the human cytomegalovirus tegument protein pp150 in the trafficking and assembly of infectious virions. [Doctoral Dissertation]. University of Alabama – Birmingham; 2010. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1351

27. Campos, Luciene Cristina Gastalho. Identificação e caracterização de proteínas modificadas em enxertos de veias safenas humanas arterializadas no modelo ex vivo.

Degree: PhD, Cardiologia, 2008, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/5/5131/tde-16122008-174047/ ;

►

A revascularização cardíaca utilizando a ponte de safena é um procedimento bastante utilizado para restabelecer o fluxo coronariano. Apesar do sucesso deste procedimento, a patência… (more)

▼

A revascularização cardíaca utilizando a ponte de safena é um procedimento bastante utilizado para restabelecer o fluxo coronariano. Apesar do sucesso deste procedimento, a patência deste enxerto pode chegar a menos de 50% em 10 anos. Atribui-se parte deste insucesso a variações no processo adaptativo à nova condição hemodinâmica, onde o shear stress e o estiramento aumentados podem estar interferindo na função endotelial e vascular. Este processo envolve a participação de diversas proteínas e o estudo de como elas participam conjuntamente é uma importante abordagem para entender as alterações fisiológicas e patológicas que ocorrem no enxerto vascular. Neste trabalho, tecnologias proteômicas, gel 2-D e ICAT, foram utilizadas para identificar as proteínas que são modificadas nas fases precoces da arterialização do enxerto venoso. Foi utilizado um sistema ex vivo de perfusão controlada, desenvolvido em nosso laboratório, onde a veia safena humana foi cultivada tanto em regime hemodinâmico venoso (5 mL/min) e arterial (50 mL/min, 80 mmHg) por 24 horas. Dentre as proteínas identificadas, a maioria apresenta funções estruturais como, por exemplo, -actina de músculo liso, CRP1, colágeno VI, tropomiosina, miosina, desmina e vimentina. Para avaliação funcional foram selecionadas a -SMA e a CRP. A -SMA mostrou-se diminuída nas fases mais precoces da arterialização venosa, com quase desaparecimento após 3 dias da cirurgia, seguido de um aumento nos períodos subseqüentes. A CRP3 mostrou-se com expressão predominantemente arterial tanto em amostra humana como de rato. A arterialização de segmentos venosos induziu a expressão da CRP3, sendo dependente do aumento do estiramento (stretch) nas células musculares lisas e não do aumento do shear stress na superfície endotelial. Coletivamente, neste trabalho caracterizamos duas proteínas que foram modificadas durante o processo de arterialização e/ou adaptação da veia à condição hemodinâmica arterial. As proteínas identificadas contribuirão para o melhor entendimento do processo de arterialização venosa e poderão ser testadas como novos alvos terapêuticos para melhorar a patência destes enxertos

Coronary artery bypass surgery by saphenous vein graft is still widely used to revascularization of ischemic heart. Despite the success of this procedure, about 50% occlude after 5-10 years. The vein graft is subjected to increased tensile stress and the adaptive vein response to the arterial hemodynamic condition may predispose to bypass occlusion. Several proteins are modulated during arterialization, the understanding of the molecular changes of this process may be useful to new therapeutics approaches development attempting to increase vein graft patency. In this work, proteomics plataform, gel 2-D and ICAT, were used to identify the proteins that are modified in the early stages of vein graft rterialization. Human saphenous vein were cultured in an ex vivo flow through system in both venous (5 ml / min) and arterial (50 ml / min, 80 mm Hg) hemodymanic conditions for 24 hours. The…

Advisors/Committee Members: Krieger, Jose Eduardo.

Subjects/Keywords: Actinas; Actins; Biologia molecular; Cytoskeletal proteins; Graft occlusion vascular; Molecular biology; Myocardial revascularization; Oclusão de enxerto vascular; Proteínas citoesqueleto; Proteoma; Proteome; Revascularização miocárdica; Saphenous vein; Veia safena

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

APA (6^th Edition):

Campos, L. C. G. (2008). Identificação e caracterização de proteínas modificadas em enxertos de veias safenas humanas arterializadas no modelo ex vivo. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5131/tde-16122008-174047/ ;

Chicago Manual of Style (16^th Edition):

Campos, Luciene Cristina Gastalho. “Identificação e caracterização de proteínas modificadas em enxertos de veias safenas humanas arterializadas no modelo ex vivo.” 2008. Doctoral Dissertation, University of São Paulo. Accessed January 18, 2021. http://www.teses.usp.br/teses/disponiveis/5/5131/tde-16122008-174047/ ;.

MLA Handbook (7^th Edition):

Campos, Luciene Cristina Gastalho. “Identificação e caracterização de proteínas modificadas em enxertos de veias safenas humanas arterializadas no modelo ex vivo.” 2008. Web. 18 Jan 2021.

Vancouver:

Campos LCG. Identificação e caracterização de proteínas modificadas em enxertos de veias safenas humanas arterializadas no modelo ex vivo. [Internet] [Doctoral dissertation]. University of São Paulo; 2008. [cited 2021 Jan 18]. Available from: http://www.teses.usp.br/teses/disponiveis/5/5131/tde-16122008-174047/ ;.

Council of Science Editors:

Campos LCG. Identificação e caracterização de proteínas modificadas em enxertos de veias safenas humanas arterializadas no modelo ex vivo. [Doctoral Dissertation]. University of São Paulo; 2008. Available from: http://www.teses.usp.br/teses/disponiveis/5/5131/tde-16122008-174047/ ;

University of Michigan

28. Lumeng, Carey Nien-Kai. Characterization of dystrophin and utrophin expression and identification of novel associated proteins.

Degree: PhD, Molecular biology, 2000, University of Michigan

URL: http://hdl.handle.net/2027.42/132415

► Dystrophin and utrophin are homologous membrane associated cytoskeletal proteins that are required for proper muscle function. These proteins bind to a protein complex at the… (more)

▼ Dystrophin and utrophin are homologous membrane associated cytoskeletal proteins that are required for proper muscle function. These proteins bind to a protein complex at the muscle sarcolemma that links with the extracellular matrix and signalling proteins. Dystrophin and utrophin are also produced in non-muscle tissues; however, less is known about their function in this context. This dissertation focuses on the characterization of dystrophin and utrophin in the mouse. Comparisons between dystrophin and utrophin expression revealed conservation of many features of the dystrophin gene in the utrophin gene. Utrophin was shown to be widely expressed in adult tissues and several putative small utrophin isoforms were identified. Also, experiments determined that the COOH-terminal domain of utrophin was sufficient for associations with neuromuscular junctions. Analysis of the major nonmuscle dystrophin isoform (Dp71) by gene replacement with a reporter gene detected cell specific expression of the Dp71 promoter in the central nervous system, retina, and kidney. In an effort to further define the properties of the dystrophin associated cytoskeleton, the yeast two-hybrid system was utilized to identify novel components of the dystrophin and utrophin complexes. Several new proteins were identified as members of the utrophin associated protein complex via their interactions with beta2-syntrophin, a neuromuscular junction-specific utrophin-associated protein. Two of these proteins, MAST205 (microtubule associated serine/threonine kinase-205 kDa) and SAST (syntrophin associated serine/threonine kinase), were found to be microtubule associated serine/threonine kinases. This study presents the first evidence for an association of a kinase with the dystrophin/utrophin network. MAST205 and SAST localize to postsynaptic regions in muscle and neuronal tissues along with dystrophin and utrophin. Furthermore, evidence was found for associations between syntrophin, dystrophin, and utrophin and microtubules. MAST205 and SAST were found to be members of a larger family of genes called the STP gene family (serine/threonine kinase and PDZ domain). The expression pattern of the STP genes was characterized. The SAST gene was mapped to gene dense regions of mouse chromosome 8 and human chromosome 19p13.2. The identification of novel dystrophin/utrophin associated proteins suggests mechanisms by which the dystrophin network can be regulated and coordinated with other cytoskeletal components. Advisors/Committee Members: Chamberlain, Jeffrey (advisor).

Subjects/Keywords: Associated; Characterization; Cytoskeletal Proteins; Dystrophin; Expression; Identification; Mast205; Novel; Sast; Utrophin

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APA (6^th Edition):

Lumeng, C. N. (2000). Characterization of dystrophin and utrophin expression and identification of novel associated proteins. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/132415

Chicago Manual of Style (16^th Edition):

Lumeng, Carey Nien-Kai. “Characterization of dystrophin and utrophin expression and identification of novel associated proteins.” 2000. Doctoral Dissertation, University of Michigan. Accessed January 18, 2021. http://hdl.handle.net/2027.42/132415.

MLA Handbook (7^th Edition):

Lumeng, Carey Nien-Kai. “Characterization of dystrophin and utrophin expression and identification of novel associated proteins.” 2000. Web. 18 Jan 2021.

Vancouver:

Lumeng CN. Characterization of dystrophin and utrophin expression and identification of novel associated proteins. [Internet] [Doctoral dissertation]. University of Michigan; 2000. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/2027.42/132415.

Council of Science Editors:

Lumeng CN. Characterization of dystrophin and utrophin expression and identification of novel associated proteins. [Doctoral Dissertation]. University of Michigan; 2000. Available from: http://hdl.handle.net/2027.42/132415

Universidade Estadual de Campinas

29. Duarte, Adriana da Silva Santos. Caracterização molecular e funcional de ANKHD1 na hematopoese normal e neoplasica: Molecular and functional characterization of ANKHD1 in normal and neoplastic hematopoiesis.

Degree: 2009, Universidade Estadual de Campinas

URL: http://repositorio.unicamp.br/jspui/handle/REPOSIP/311971

► Abstract: The identification and the structural and functional characterization of genes differentially expressed between tumors and normal tissues are fundamental steps towards the understanding of… (more)

▼ Abstract: The identification and the structural and functional characterization of genes differentially expressed between tumors and normal tissues are fundamental steps towards the understanding of the neoplastic process and the development of new anti-cancer strategies. The Ankyrin Repeat Single KH Domain containing 1 (ANKHD1) was first described in humans in a prostate carcinoma cell line LNCaP, in 2003; however, the expression pattern and function of ANKHD1 have not yet been described. ANKHD1 is an orthologous protein of the Drosophila melanogaster, MASK (Multiple Ankyrin repeat and single KH domain), where it was first identified using a genetic screen designed to discover proteins that interact with the protein tyrosine phosphatase Corkscrew (CSW), which is a homolog to the SH2-containing protein tyrosine phosphatase (SHP2) in humans. SHP2 is a cytoplasmic protein-tyrosine phosphatase, coded by the PTPN11 gene and plays an important role in the development of normal hematopoiese and leukemogenesis. The aim of the present study was to characterize the gene expression pattern of ANKHD1 in normal and leukemic hematopoietic cells and to determine their function in cellular process.This study has demonstrated that the ANKHD1 gene is located on chromosome 5, this gene has several possible variant transcripts generated by splicing alternative mechanisms and encodes proteins with domains of ankyrin repeats. The promoter region of this gene has several regulatory elements such as the transcription factor GATA-1 binding sites and rich sequences in dinucleotide CG, CpG islands.The expression of the ANKHD1 gene and some of the gene's variants in normal tissues and neoplastic cell lines was detected in different intensities. The increase in the expression of this gene was demonstrated using cellular differentiation and proliferation models. However, during the process of apoptosis, a decrease in the expression of ANKHD1 transcripts variants was observed. In the cells of patients with myelodysplastic syndrome (MDS), a low expression of ANKHD1 was observed. During erythroid differentiation of CD34+ cells obtained from the bone marrow of these patients, no increase in the expression of ANKHD1 gene and transcription factor GATA-1 was observed, as expected. The mononuclear cells of MDS patients were treated with decitabine, a demethylation agent, and showed an increase in the ANKHD1 gene expression compared to untreated cells. The same was observed in CD34+ cells treated during erythroid differentiation. However in cells of acute myeloid leukemia (AML) or Multiple Myeloma (MM) patients, characterized by proliferation and resistance mechanisms of apoptosis, the high expression of gene transcripts ANKHD1 and its variants was demonstrated. The association of SHP2 with ANKHD1 was identified by Western Blot in RPMI 8226 MM cell line. A decrease in the ANKHD1 gene expression in these cells when the process of apoptosis was induced by dexamethasone was observed. In conclusion, this study identified ANKHD1 and some of gene's transcripts… Advisors/Committee Members: UNIVERSIDADE ESTADUAL DE CAMPINAS (CRUESP), Saad, Sara Teresinha Olalla, 1956- (advisor), Universidade Estadual de Campinas. Faculdade de Ciências Médicas (institution), Programa de Pós-Graduação em Fisiopatologia Médica (nameofprogram), Chauffaille, Maria de Lourdes (committee member), Rego, Eduardo Magalhães (committee member), Luzo, Angela Cristina Malheiros (committee member), Lorand-Metze, Irene (committee member).

Subjects/Keywords: Proteinas citoesqueleto; Hematopoese; Tumores; Expressão gênica; Cytoskeletal proteins; Hematopoiesis; Neoplasms; Gene expression

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

APA (6^th Edition):

Duarte, A. d. S. S. (2009). Caracterização molecular e funcional de ANKHD1 na hematopoese normal e neoplasica: Molecular and functional characterization of ANKHD1 in normal and neoplastic hematopoiesis. (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/311971

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):

Duarte, Adriana da Silva Santos. “Caracterização molecular e funcional de ANKHD1 na hematopoese normal e neoplasica: Molecular and functional characterization of ANKHD1 in normal and neoplastic hematopoiesis.” 2009. Thesis, Universidade Estadual de Campinas. Accessed January 18, 2021. http://repositorio.unicamp.br/jspui/handle/REPOSIP/311971.

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

MLA Handbook (7^th Edition):

Duarte, Adriana da Silva Santos. “Caracterização molecular e funcional de ANKHD1 na hematopoese normal e neoplasica: Molecular and functional characterization of ANKHD1 in normal and neoplastic hematopoiesis.” 2009. Web. 18 Jan 2021.

Vancouver:

Duarte AdSS. Caracterização molecular e funcional de ANKHD1 na hematopoese normal e neoplasica: Molecular and functional characterization of ANKHD1 in normal and neoplastic hematopoiesis. [Internet] [Thesis]. Universidade Estadual de Campinas; 2009. [cited 2021 Jan 18]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/311971.

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

Council of Science Editors:

Duarte AdSS. Caracterização molecular e funcional de ANKHD1 na hematopoese normal e neoplasica: Molecular and functional characterization of ANKHD1 in normal and neoplastic hematopoiesis. [Thesis]. Universidade Estadual de Campinas; 2009. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/311971

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

University of North Carolina – Greensboro

30. Keener, Mary Elizabeth. Studies of the Actin Binding Activity of Dictyostelium discoideum Myosin II Heavy Chain Kinase A.

Degree: 2008, University of North Carolina – Greensboro

URL: http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=2519

► Dictyostelium discoideum is a primitive, eukaryotic organism that relies on myosin II and actin contraction for cytokinesis, migration, and other important cellular processes. In order… (more)

▼ Dictyostelium discoideum is a primitive, eukaryotic organism that relies on myosin II and actin contraction for cytokinesis, migration, and other important cellular processes. In order for contraction to occur, myosin II monomers must first assemble into bipolar filaments. In Dictyostelium, bipolar filament assembly is negatively regulated by myosin heavy chain (MHC) phosphorylation. Three kinases have been shown to catalyze MHC phosphorylation (MHK-A, -B, -C), driving myosin II disassembly. Of the three, MHK-A is the most extensively studied. Structurally, MHK-A is comprised of three functional domains: an N-terminal coiled coil region (CC), a catalytic domain, and a WD repeat domain. The CC domain has been shown, in vitro, to bind and bundle actin filaments and inhibit myosin II binding to F-actin. The studies described in this thesis focus on two aims: 1) to understand the role of the CC domain in reorganizing myosin II and actin within the cell and 2) to determine if intramolecular interactions between the CC and WD repeat domains within the MHK-A molecule are involved in regulating MHKA’s activity. To address the first aim, the triton cytoskeleton ghost isolation assay was conducted on Ax2, Ax2 + GFP-CC, Ax2 + GFP-C800A, MHK-A null, and MHK-A null + GFP-CC cell lines containing various truncations to determine the analyze the effects of over-expressing the CC domain on myosin II and F-actin organization within the cell. Complementary localization studies were also conducted involving Ax2 wild-type cells and GFP-tagged cells over-expressing the CC domain (GFP-CC) to visually determine myosin II and actin localization within the cell via confocal imaging. Results from the triton cytoskeleton studies indicate that over-expression of the CC domain in the Ax2 cells leads to an increase in cytoskeletal myosin II. MHK-A null and MHK-A null cells over-expressing the CC domain showed a significant increase in cytoskeletal myosin II in comparison to the Ax2 cells. However, the CC domain had no apparent effect in the absence of endogenous MHK-A as indicated by the relatively equal amounts of myosin II in both MHK-A null and MHK-null + GFP-CC pellet fractions. Ax2 + GFP-C800A cells exhibit essentially the same level of cytoskeletal myosin II compared to that of the Ax2 cells. Localization studies revealed increased amounts of cytoplasmically localized myosin II aggregates in the Ax2 + GFP-CC cells in comparison to the Ax2 cells. Also, cells over-expressing the CC domain appear to have more cytoplasmic F-actin than the Ax2 cells. Furthermore, the actin appears to be more aggregated in the over-expressed CC cells. To address the second aim, purified CC and GSTtagged WD repeat domains were subjected to a GST “pull-down” assay and Western blot to determine if an interaction between the domains exists. Results from these experiments revealed no interaction between the WD repeat and CC domains, evident by the absence of CC in the GST-WD bead-associated fraction. This study shows that the CC domain plays an integral role in… Advisors/Committee Members: Paul Steimle (advisor).

Subjects/Keywords: Dictyostelium discoideum – Physiology.; Cytokinesis – Physiology.; Cytoskeletal proteins.; Myosin.; Actin.; Protein kinases.

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

APA (6^th Edition):

Keener, M. E. (2008). Studies of the Actin Binding Activity of Dictyostelium discoideum Myosin II Heavy Chain Kinase A. (Masters Thesis). University of North Carolina – Greensboro. Retrieved from http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=2519

Chicago Manual of Style (16^th Edition):

Keener, Mary Elizabeth. “Studies of the Actin Binding Activity of Dictyostelium discoideum Myosin II Heavy Chain Kinase A.” 2008. Masters Thesis, University of North Carolina – Greensboro. Accessed January 18, 2021. http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=2519.

MLA Handbook (7^th Edition):

Keener, Mary Elizabeth. “Studies of the Actin Binding Activity of Dictyostelium discoideum Myosin II Heavy Chain Kinase A.” 2008. Web. 18 Jan 2021.

Vancouver:

Keener ME. Studies of the Actin Binding Activity of Dictyostelium discoideum Myosin II Heavy Chain Kinase A. [Internet] [Masters thesis]. University of North Carolina – Greensboro; 2008. [cited 2021 Jan 18]. Available from: http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=2519.

Council of Science Editors:

Keener ME. Studies of the Actin Binding Activity of Dictyostelium discoideum Myosin II Heavy Chain Kinase A. [Masters Thesis]. University of North Carolina – Greensboro; 2008. Available from: http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=2519

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