subject:(beta catenin)

1. Marcato, Vasco. La β-caténine : un activateur de l’expression du gène codant pour l’interféron-béta et une cible du Virus de la Fièvre de la Vallée du Rift : Magnetismo cooperativo en compuestos de coordinación basados en Cu(II), Ni(II) y Co(II) con ligandos imidazol carboxílicos.

Degree: Docteur es, Génétique, 2015, Sorbonne Paris Cité

URL: http://www.theses.fr/2015USPCB103

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La réponse antivirale innée constitue la première réaction d’une cellule à une infection virale. Il s’agit d’une réponse rapide, transitoire, non-spécifique, ubiquitaire qui a été… (more)

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La réponse antivirale innée constitue la première réaction d’une cellule à une infection virale. Il s’agit d’une réponse rapide, transitoire, non-spécifique, ubiquitaire qui a été conservée sous différentes formes au cours de l’évolution. La synthèse d’interféron β (IFNβ) joue un rôle essentiel dans l’établissement de la réponse antivirale innée chez les vertébrés. L’expression du gène Ifnb1 codant pour l’IFNβ est finement régulée au niveau transcriptionnel, ce qui permet de passer de la répression de son expression en absence d’infection à son activation après infection par un virus. Bien qu’une forte et rapide expression d’IFNβ soit bénéfique lors d’une infection virale, une expression anormale d’IFNβ peut entrainer des troubles physiologiques importants (réactions auto-immunes, dérégulations inflammatoires). En s’intéressant plus particulièrement à la séquence promotrice du gène Ifnb1, codant pour l’IFNβ, nous avons identifié deux sites de liaison potentiels pour les facteurs de la famille des TCFs (T-Cell Factor). En présence de β-caténine nucléaire, les complexes TCF/β-caténine se forment au niveau des sites de liaison aux TCFs et recrutent des complexes co-activateurs de la transcription. Dans une première partie de ce travail, nous avons étudié le rôle des complexes TCF/β-caténine dans la régulation de l’expression d’Ifnb1 aussi bien en absence que suite à une infection virale. Nous avons ensuite montré que ce mécanisme était fonctionnel car il permettait aux cellules traitées par un inhibiteur de GSK3 (qui induit une accumulation de β-caténine) de mieux se protéger contre l’effet cytopathique induit par le VSV. Lors de l’étude des fonctions biologiques ciblées par le Virus de la Fièvre de la Vallée du Rift (VFVR) auquel j’ai participé, il est apparu que cet arbovirus hautement pathogène ciblait via sa protéine non-structurale NSs, les promoteurs de gènes codant pour des nombreux acteurs de la voie Wnt/β-caténine et de l’adhésion cellulaire. Dans une deuxième partie de ce travail, j’ai analysé l’effet d’une infection par la souche pathogène (+NSs) ou non-pathogène (-NSs) du VFVR sur le taux de β-caténine et la présence de celle-ci au niveau des jonctions adhérentes. Les résultats obtenus montrent que l’infection par la souche pathogène de VFVR entraine une diminution du taux global de β-caténine ex et in vivo ainsi que la redistribution de celle-ci en dehors des jonctions adhérentes, couplée à une très forte désorganisation du cytosquelette d’actine de la cellule infectée. Cette perturbation du réseau d’actine est corrélée à la dérégulation de l’expression de certains gènes codant pour des protéines affectant la morphologie cellulaire.

No abstract available

Advisors/Committee Members: Bonnefoy, Eliette (thesis director).

Subjects/Keywords: Β-caténine; Β-catenin; 616.042

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

APA (6^th Edition):

Marcato, V. (2015). La β-caténine : un activateur de l’expression du gène codant pour l’interféron-béta et une cible du Virus de la Fièvre de la Vallée du Rift : Magnetismo cooperativo en compuestos de coordinación basados en Cu(II), Ni(II) y Co(II) con ligandos imidazol carboxílicos. (Doctoral Dissertation). Sorbonne Paris Cité. Retrieved from http://www.theses.fr/2015USPCB103

Chicago Manual of Style (16^th Edition):

Marcato, Vasco. “La β-caténine : un activateur de l’expression du gène codant pour l’interféron-béta et une cible du Virus de la Fièvre de la Vallée du Rift : Magnetismo cooperativo en compuestos de coordinación basados en Cu(II), Ni(II) y Co(II) con ligandos imidazol carboxílicos.” 2015. Doctoral Dissertation, Sorbonne Paris Cité. Accessed February 28, 2021. http://www.theses.fr/2015USPCB103.

MLA Handbook (7^th Edition):

Marcato, Vasco. “La β-caténine : un activateur de l’expression du gène codant pour l’interféron-béta et une cible du Virus de la Fièvre de la Vallée du Rift : Magnetismo cooperativo en compuestos de coordinación basados en Cu(II), Ni(II) y Co(II) con ligandos imidazol carboxílicos.” 2015. Web. 28 Feb 2021.

Vancouver:

Marcato V. La β-caténine : un activateur de l’expression du gène codant pour l’interféron-béta et une cible du Virus de la Fièvre de la Vallée du Rift : Magnetismo cooperativo en compuestos de coordinación basados en Cu(II), Ni(II) y Co(II) con ligandos imidazol carboxílicos. [Internet] [Doctoral dissertation]. Sorbonne Paris Cité; 2015. [cited 2021 Feb 28]. Available from: http://www.theses.fr/2015USPCB103.

Council of Science Editors:

Marcato V. La β-caténine : un activateur de l’expression du gène codant pour l’interféron-béta et une cible du Virus de la Fièvre de la Vallée du Rift : Magnetismo cooperativo en compuestos de coordinación basados en Cu(II), Ni(II) y Co(II) con ligandos imidazol carboxílicos. [Doctoral Dissertation]. Sorbonne Paris Cité; 2015. Available from: http://www.theses.fr/2015USPCB103

2. 神宮司, 健太郎. DIF-1 inhibits the Wnt/β-catenin signaling pathway by inhibiting TCF7L2 expression in colon cancer cell lines : DIF-1は大腸がん細胞株においてTCF7L2の発現を抑制することにより、Wnt/β-cateninシグナル伝達経路を阻害する.

Degree: 博士（医学）, 2013, Kyushu University / 九州大学

URL: http://hdl.handle.net/2324/21727 ; http://dx.doi.org/10.15017/21727

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我々はこれまでに細胞性粘菌Dictyostelium discoideumが分泌する分化誘導因子Differentiation-inducing factor-1（DIF-1）がβ-cateninタンパク質の分解を誘導することでWnt/β-cateninシグナル伝達経路を阻害し、ヒトがん細胞株の増殖を抑制することを報告してきた。β-cateninタンパク質の分解がDIF-1の効果に不可欠であるか否かを明らかにするために、我々はWnt/β-cateninシグナル伝達経路が恒常的に活性化されているヒト由来大腸がん細胞株（HCT-116、SW-620、DLD-1）に対するDIF-1の効果を検討した。DIF-1はβ-cateninタンパク質の分解非依存性にcyclin D1の発現をmRNA、タンパク質レベル共に減少させ、G_0/G_1期における細胞周期拘束を起こすことにより、強力に細胞増殖を抑制した。DIF-1によるtranscription factor 7-like 2（TCF7L2）発現量の抑制によって、TCF依存性転写活性及びcyclin D1プロモーター活性が抑制されることが明らかとなった。ルシフェラーゼレポーター活性測定及びTCF7L2プロモーター断片を用いたEMSAにより、翻訳開始点を起点として-609から-601塩基上流に位置する転写因子early growth response-1（Egr-1）結合部位が、DIF-1の効果に関与していることが示された。さらに、RNAi法による内在性TCF7L2の欠失はcyclin D1プロモーター活性及びタンパク質量の減少につながり、そして、TCF7L2の強制発現はDIF-1によるTCF依存性転写活性及びcyclin D1プロモーター活性の低下効果を減弱させた。したがって、DIF-1は大腸がん細胞株において、Egr-1依存性のTCF7L2転写活性を減少させることによりTCF7L2発現を抑制し、Wnt/β-cateninシグナル伝達経路を阻害していることが示唆された。我々の結果は、DIF-1によるWnt/β-cateninシグナル伝達経路の阻害機構に新たな知見をもたらすものである。

We previously reported that differentiation-inducing factor-1 (DIF-1), a morphogen in Dictyostelium discoideum, inhibits… (more)

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我々はこれまでに細胞性粘菌Dictyostelium discoideumが分泌する分化誘導因子Differentiation-inducing factor-1（DIF-1）がβ-cateninタンパク質の分解を誘導することでWnt/β-cateninシグナル伝達経路を阻害し、ヒトがん細胞株の増殖を抑制することを報告してきた。β-cateninタンパク質の分解がDIF-1の効果に不可欠であるか否かを明らかにするために、我々はWnt/β-cateninシグナル伝達経路が恒常的に活性化されているヒト由来大腸がん細胞株（HCT-116、SW-620、DLD-1）に対するDIF-1の効果を検討した。DIF-1はβ-cateninタンパク質の分解非依存性にcyclin D1の発現をmRNA、タンパク質レベル共に減少させ、G_0/G_1期における細胞周期拘束を起こすことにより、強力に細胞増殖を抑制した。DIF-1によるtranscription factor 7-like 2（TCF7L2）発現量の抑制によって、TCF依存性転写活性及びcyclin D1プロモーター活性が抑制されることが明らかとなった。ルシフェラーゼレポーター活性測定及びTCF7L2プロモーター断片を用いたEMSAにより、翻訳開始点を起点として-609から-601塩基上流に位置する転写因子early growth response-1（Egr-1）結合部位が、DIF-1の効果に関与していることが示された。さらに、RNAi法による内在性TCF7L2の欠失はcyclin D1プロモーター活性及びタンパク質量の減少につながり、そして、TCF7L2の強制発現はDIF-1によるTCF依存性転写活性及びcyclin D1プロモーター活性の低下効果を減弱させた。したがって、DIF-1は大腸がん細胞株において、Egr-1依存性のTCF7L2転写活性を減少させることによりTCF7L2発現を抑制し、Wnt/β-cateninシグナル伝達経路を阻害していることが示唆された。我々の結果は、DIF-1によるWnt/β-cateninシグナル伝達経路の阻害機構に新たな知見をもたらすものである。

We previously reported that differentiation-inducing factor-1 (DIF-1), a morphogen in Dictyostelium discoideum, inhibits the proliferation of human cancer cell lines by inducing β-catenin degradation and suppressing the Wnt/β-catenin signaling pathway. To determine whether β-catenin degradation is essential for the effect of DIF-1, we examined the effect of DIF-1 on human colon cancer cell lines (HCT-116, SW-620 and DLD-1), in which the Wnt/β-catenin signaling pathway is constitutively active. DIF-1 strongly inhibited cell proliferation and arrested the cell cycle in the G0/G1 phase via the suppression of cyclin D1 expression at mRNA and protein levels without reducing β-catenin protein. TCF-dependent transcriptional activity and cyclin D1 promoter activity were revealed to be inhibited via suppression of transcription factor 7-like 2 (TCF7L2) expression. Luciferase reporter assays and EMSAs using the TCF7L2 promoter fragments indicated that the binding site for the transcription factor early growth response-1 (Egr-1), which is located in the –609 to –601 bp region relative to the start codon in the TCF7L2 promoter, was involved in DIF-1 activity. Moreover, RNAi-mediated depletion of endogenous TCF7L2 resulted in reduced cyclin D1 promoter activity and protein expression, and the overexpression of TCF7L2 overrode the inhibition of the TCF-dependent transcriptional activity and cyclin D1 promoter activity induced by DIF-1. Therefore, DIF-1 seemed to inhibit the Wnt/β-catenin signaling pathway by suppressing TCF7L2 expression via reduced Egr-1-dependent transcriptional activity in these colon cancer cell lines. Our results provide a novel insight into the mechanisms by which DIF-1 inhibits the Wnt/β-catenin signaling pathway.

Advisors/Committee Members: 住本, 英樹, 笹栗, 俊之.

Subjects/Keywords: DIF-1; Wnt/β-catenin

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

APA (6^th Edition):

神宮司, �. (2013). DIF-1 inhibits the Wnt/β-catenin signaling pathway by inhibiting TCF7L2 expression in colon cancer cell lines : DIF-1は大腸がん細胞株においてTCF7L2の発現を抑制することにより、Wnt/β-cateninシグナル伝達経路を阻害する. (Thesis). Kyushu University / 九州大学. Retrieved from http://hdl.handle.net/2324/21727 ; http://dx.doi.org/10.15017/21727

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):

神宮司, 健太郎. “DIF-1 inhibits the Wnt/β-catenin signaling pathway by inhibiting TCF7L2 expression in colon cancer cell lines : DIF-1は大腸がん細胞株においてTCF7L2の発現を抑制することにより、Wnt/β-cateninシグナル伝達経路を阻害する.” 2013. Thesis, Kyushu University / 九州大学. Accessed February 28, 2021. http://hdl.handle.net/2324/21727 ; http://dx.doi.org/10.15017/21727.

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

MLA Handbook (7^th Edition):

神宮司, 健太郎. “DIF-1 inhibits the Wnt/β-catenin signaling pathway by inhibiting TCF7L2 expression in colon cancer cell lines : DIF-1は大腸がん細胞株においてTCF7L2の発現を抑制することにより、Wnt/β-cateninシグナル伝達経路を阻害する.” 2013. Web. 28 Feb 2021.

Vancouver:

神宮司 �. DIF-1 inhibits the Wnt/β-catenin signaling pathway by inhibiting TCF7L2 expression in colon cancer cell lines : DIF-1は大腸がん細胞株においてTCF7L2の発現を抑制することにより、Wnt/β-cateninシグナル伝達経路を阻害する. [Internet] [Thesis]. Kyushu University / 九州大学; 2013. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/2324/21727 ; http://dx.doi.org/10.15017/21727.

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

Council of Science Editors:

神宮司 �. DIF-1 inhibits the Wnt/β-catenin signaling pathway by inhibiting TCF7L2 expression in colon cancer cell lines : DIF-1は大腸がん細胞株においてTCF7L2の発現を抑制することにより、Wnt/β-cateninシグナル伝達経路を阻害する. [Thesis]. Kyushu University / 九州大学; 2013. Available from: http://hdl.handle.net/2324/21727 ; http://dx.doi.org/10.15017/21727

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

McMaster University

3. Abdulla, Solen. INVESTIGATING NOVEL β-CATENIN SIGNALLING MECHANISMS IN AN EMBRYONIC STEM CELL MODEL.

Degree: MSc, 2017, McMaster University

URL: http://hdl.handle.net/11375/23461

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The Wnt/β-catenin pathway is a fundamental regulator of embryonic development and adult tissue homeostasis. The key effector, β-catenin, is a multifunctional protein that occupies dual… (more)

Subjects/Keywords: β-catenin; Stem Cells

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

APA (6^th Edition):

Abdulla, S. (2017). INVESTIGATING NOVEL β-CATENIN SIGNALLING MECHANISMS IN AN EMBRYONIC STEM CELL MODEL. (Masters Thesis). McMaster University. Retrieved from http://hdl.handle.net/11375/23461

Chicago Manual of Style (16^th Edition):

Abdulla, Solen. “INVESTIGATING NOVEL β-CATENIN SIGNALLING MECHANISMS IN AN EMBRYONIC STEM CELL MODEL.” 2017. Masters Thesis, McMaster University. Accessed February 28, 2021. http://hdl.handle.net/11375/23461.

MLA Handbook (7^th Edition):

Abdulla, Solen. “INVESTIGATING NOVEL β-CATENIN SIGNALLING MECHANISMS IN AN EMBRYONIC STEM CELL MODEL.” 2017. Web. 28 Feb 2021.

Vancouver:

Abdulla S. INVESTIGATING NOVEL β-CATENIN SIGNALLING MECHANISMS IN AN EMBRYONIC STEM CELL MODEL. [Internet] [Masters thesis]. McMaster University; 2017. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/11375/23461.

Council of Science Editors:

Abdulla S. INVESTIGATING NOVEL β-CATENIN SIGNALLING MECHANISMS IN AN EMBRYONIC STEM CELL MODEL. [Masters Thesis]. McMaster University; 2017. Available from: http://hdl.handle.net/11375/23461

University of Melbourne

4. Liu, He. Interaction between p21-activated kinase 1 and beta-catenin.

Degree: 2012, University of Melbourne

URL: http://hdl.handle.net/11343/38242

► Colorectal cancer (CRC) was the second most frequently occurring cancer and the second leading cause of cancer death in Australia in 2007 (AIHW2010). Hyper-activation of… (more)

▼ Colorectal cancer (CRC) was the second most frequently occurring cancer and the second leading cause of cancer death in Australia in 2007 (AIHW2010). Hyper-activation of the Wnt/β-catenin signaling pathway is a hallmark of colorectal cancer. The Wnt signaling pathway plays a critical role in embryonic development and homeostasitic maintenance in mature tissues, particularly in regeneration of intestinal epithelium (Lynch and Lynch 2005). In studies of human colon cancer over the last two decades, mutations have been identified in genes coding for Wnt/β-catenin pathway components, such as axin, adenomatous polyposis coli (APC) and β-catenin, which are known to contribute to tumor progression. Tumor genetic studies have revealed that mutations in these members of the Wnt/β-catenin pathway occur in approximately 90% of colorectal cancers (Bienz and Clevers, 2000; Cottrell et al., 1992; Morin et al., 1997; Polakis, 2000; Powell et al., 1992; Vogelstein and Kinzler, 2004). Under normoxic conditions (having a normal atmospheric oxygen concentration of 20~21%), the transcription factor 4 (TCF4) stably binds to β-catenin in the nuclei of colon carcinoma cells and is constitutively activated. This activation stimulates cell migration and proliferation, and contributes to the development of colorectal tumors (Munemitsu et al., 1995). Under hypoxic conditions β-catenin interacts with the heterodimeric transcription factor hypoxia inducible factor-1α (HIF-1α), enhances HIF-1-mediated transcription, and further promotes cell survival and adaptation to hypoxia (Kaidi et al., 2007). In a mouse model carrying a mutation in the APC gene, the gastrin gene has been identified as a downstream target of the β-catenin/TCF4 signaling pathway (Koh et al., 2000). Similarly the expression of a constitutively active β-catenin causes a threefold increase in gastrin promoter activity (Koh et al., 2000). In previous studies from this laboratory, p21-activated kinase 1 (PAK1) was found to interact with β-catenin and to be required for the regulation of the β-catenin signaling pathway by gastrins (He et al., 2008). PAK1 kinase activity has been implicated in various cellular processes such as gene regulation, cytoskeletal reorganization, cell growth, motility, and morphogenesis (Kumar et al., 2006). PAK1 also functions as a key node in various signaling pathways leading to cell growth, migration and survival. PAK1 has oncogenic functions in a broad range of cancers including CRC and its hyper-activation has been well documented in breast cancer (Dummler et al., 2009; Kumar et al., 2006). PAK1 expression has also been reported to increase in the progression of colorectal carcinomas to metastasis (Carter et al., 2004). However, the specific role of PAK1 in β-catenin signaling and the mechanism by which PAK1 interacts with β-catenin in CRC have not been investigated in detail. The studies in Chapter 3 demonstrate that PAK1 is required for maximal expression of…

Subjects/Keywords: PAK1; beta-catenin; coloractal cancer

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

APA (6^th Edition):

Liu, H. (2012). Interaction between p21-activated kinase 1 and beta-catenin. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/38242

Chicago Manual of Style (16^th Edition):

Liu, He. “Interaction between p21-activated kinase 1 and beta-catenin.” 2012. Doctoral Dissertation, University of Melbourne. Accessed February 28, 2021. http://hdl.handle.net/11343/38242.

MLA Handbook (7^th Edition):

Liu, He. “Interaction between p21-activated kinase 1 and beta-catenin.” 2012. Web. 28 Feb 2021.

Vancouver:

Liu H. Interaction between p21-activated kinase 1 and beta-catenin. [Internet] [Doctoral dissertation]. University of Melbourne; 2012. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/11343/38242.

Council of Science Editors:

Liu H. Interaction between p21-activated kinase 1 and beta-catenin. [Doctoral Dissertation]. University of Melbourne; 2012. Available from: http://hdl.handle.net/11343/38242

University of Toronto

5. Shipstone, Arun. Analysis of Alpha-catenin Mediated Intercellular Adhesion in Drosophila.

Degree: 2015, University of Toronto

URL: http://hdl.handle.net/1807/88582

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Dynamic linkage between the cadherin-catenin complex (CCC) and the actin cytoskeleton at Adherens Junctions is essential for cell-cell adhesion in epithelial cells. Alpha-catenin is a… (more)

Subjects/Keywords: alpha-catenin; Beta-catenin; catenin; cell adhesion; Drosophila; E-Cadherin; 0379

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

APA (6^th Edition):

Shipstone, A. (2015). Analysis of Alpha-catenin Mediated Intercellular Adhesion in Drosophila. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/88582

Chicago Manual of Style (16^th Edition):

Shipstone, Arun. “Analysis of Alpha-catenin Mediated Intercellular Adhesion in Drosophila.” 2015. Masters Thesis, University of Toronto. Accessed February 28, 2021. http://hdl.handle.net/1807/88582.

MLA Handbook (7^th Edition):

Shipstone, Arun. “Analysis of Alpha-catenin Mediated Intercellular Adhesion in Drosophila.” 2015. Web. 28 Feb 2021.

Vancouver:

Shipstone A. Analysis of Alpha-catenin Mediated Intercellular Adhesion in Drosophila. [Internet] [Masters thesis]. University of Toronto; 2015. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/1807/88582.

Council of Science Editors:

Shipstone A. Analysis of Alpha-catenin Mediated Intercellular Adhesion in Drosophila. [Masters Thesis]. University of Toronto; 2015. Available from: http://hdl.handle.net/1807/88582

University of Alberta

6. Ha, Jacqueline R. β-catenin is O-GlcNAc modified at Serine 23: Implications for β-catenin’s Subcellular Distribution and Transcriptional Activity.

Degree: MS, Medical Sciences-Paediatrics, 2012, University of Alberta

URL: https://era.library.ualberta.ca/files/jd472x88t

► β-catenin is a potent oncoprotein that serves as a structural anchor at the adherens junctions and as a transcriptional co-activator of the Wnt Signaling pathway.… (more)

Subjects/Keywords: β-catenin; β-catenin is O-GlcNAc modified at Serine 23; O-GlcNAcylation

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

APA (6^th Edition):

Ha, J. R. (2012). β-catenin is O-GlcNAc modified at Serine 23: Implications for β-catenin’s Subcellular Distribution and Transcriptional Activity. (Masters Thesis). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/jd472x88t

Chicago Manual of Style (16^th Edition):

Ha, Jacqueline R. “β-catenin is O-GlcNAc modified at Serine 23: Implications for β-catenin’s Subcellular Distribution and Transcriptional Activity.” 2012. Masters Thesis, University of Alberta. Accessed February 28, 2021. https://era.library.ualberta.ca/files/jd472x88t.

MLA Handbook (7^th Edition):

Ha, Jacqueline R. “β-catenin is O-GlcNAc modified at Serine 23: Implications for β-catenin’s Subcellular Distribution and Transcriptional Activity.” 2012. Web. 28 Feb 2021.

Vancouver:

Ha JR. β-catenin is O-GlcNAc modified at Serine 23: Implications for β-catenin’s Subcellular Distribution and Transcriptional Activity. [Internet] [Masters thesis]. University of Alberta; 2012. [cited 2021 Feb 28]. Available from: https://era.library.ualberta.ca/files/jd472x88t.

Council of Science Editors:

Ha JR. β-catenin is O-GlcNAc modified at Serine 23: Implications for β-catenin’s Subcellular Distribution and Transcriptional Activity. [Masters Thesis]. University of Alberta; 2012. Available from: https://era.library.ualberta.ca/files/jd472x88t

7. Sacco, Sonia. Rôle de la signalisation Rspondin dans le développement et l’homéostasie de la glande surrénale : Rspondin signaling in adrenal gland development and homeostasis.

Degree: Docteur es, Sciences de la vie et de la santé, 2016, Université Côte d'Azur (ComUE)

URL: http://www.theses.fr/2016AZUR4125

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La glande surrénale est un organe endocrinien d’une importance vitale de par son rôle dans le maintien de l’homéostasie corporelle. Pour assurer cette fonction, le… (more)

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La glande surrénale est un organe endocrinien d’une importance vitale de par son rôle dans le maintien de l’homéostasie corporelle. Pour assurer cette fonction, le cortex surrénalien est divisé en différentes zones qui produisent des hormones spécifiques. Les mécanismes de la mise en place de cette zonation au niveau embryonnaire ainsi que de son maintien tout au long de vie sont encore inconnus de nos jours. Les gènes Rspo1 et 3 sont exprimés de manière très spécifique au niveau de la capsule mais ils codent pour des protéines secrétées qui agissent sur les cellules adjacentes de la zone glomérulée afin d’induire l’activation de la voie canonique Wnt/β-caténine. La délétion du gène Rspo3 pendant le développement embryonnaire entraine un défaut d’activation des voies Shh et Wnt/β-caténine et donc en conséquence un défaut de la mise en place de la zonation. Sa fonction reste également essentielle au cours de la vie adulte puisqu’elle assure à la fois le maintien de l’homéostasie tissulaire et de la zone glomérulée. L’absence du gène Rspo1, n’affecte pas le développement ni la zonation ou l’homéostasie de la glande surrénale. Par contre, si on l’exprime de façon ectopique dans tous le cortex surrénalien, entrainant une activation anormale de la voie Wnt/β-caténine dans cette zone, on peut observer une hyperplasie des glandes surrénales. A partir de 1 an d’âge, cette hyperplasie surrénalienne entraine une formation de tumeurs. Ce travail démontre donc que la capsule par le biais du gène Rspondin 3 agit comme un centre de signalisation capable de contrôler à la fois l’homéostasie par le remplacement des cellules endommagés et le maintien de la zonation de la glande surrénale

The adrenal gland is an endocrine organ of vital importance because of its role in the maintenance of body homeostasis. To ensure this function, the adrenal cortex is divided into different areas that produce specific hormones. The mechanisms of the establishment of this zonation at the embryonic level as well as its maintenance throughout life are still unknown today. The Rspo1 and 3 genes are expressed very specifically at the capsule level but they encode secreted proteins that act on the adjacent cells of the zona glomerulosa in order to induce the activation of the Wnt / β-catenin canonical pathway. The deletion of the Rspo3 gene during embryonic development leads to a lack of activation of the Shh and Wnt / β-catenin pathways and hence a lack of zonation. Its function is also essential during adult life since it ensures both the maintenance of tissue homeostasis and the glomerular zone. The absence of the Rspo1 gene does not affect development, zonation or homeostasis of the adrenal gland. On the other hand, its ectopical expression in all the adrenal cortex leads to an abnormal activation of the Wnt / β-catenin pathway in this area and thus to an hyperplasia of the adrenal glands. From 1 year of age, this adrenal hyperplasia leads to the formation of tumors. This work demonstrates that the capsule through the Rspondin 3 gene acts as a…

Advisors/Committee Members: Schedl, Andreas (thesis director).

Subjects/Keywords: Glande surrénale; Rspondin; Β-catenin; Zonation; Homéostasie; Adrenal gland; Rspondin; Β-catenin; Zonation; Homeostasis

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APA (6^th Edition):

Sacco, S. (2016). Rôle de la signalisation Rspondin dans le développement et l’homéostasie de la glande surrénale : Rspondin signaling in adrenal gland development and homeostasis. (Doctoral Dissertation). Université Côte d'Azur (ComUE). Retrieved from http://www.theses.fr/2016AZUR4125

Chicago Manual of Style (16^th Edition):

Sacco, Sonia. “Rôle de la signalisation Rspondin dans le développement et l’homéostasie de la glande surrénale : Rspondin signaling in adrenal gland development and homeostasis.” 2016. Doctoral Dissertation, Université Côte d'Azur (ComUE). Accessed February 28, 2021. http://www.theses.fr/2016AZUR4125.

MLA Handbook (7^th Edition):

Sacco, Sonia. “Rôle de la signalisation Rspondin dans le développement et l’homéostasie de la glande surrénale : Rspondin signaling in adrenal gland development and homeostasis.” 2016. Web. 28 Feb 2021.

Vancouver:

Sacco S. Rôle de la signalisation Rspondin dans le développement et l’homéostasie de la glande surrénale : Rspondin signaling in adrenal gland development and homeostasis. [Internet] [Doctoral dissertation]. Université Côte d'Azur (ComUE); 2016. [cited 2021 Feb 28]. Available from: http://www.theses.fr/2016AZUR4125.

Council of Science Editors:

Sacco S. Rôle de la signalisation Rspondin dans le développement et l’homéostasie de la glande surrénale : Rspondin signaling in adrenal gland development and homeostasis. [Doctoral Dissertation]. Université Côte d'Azur (ComUE); 2016. Available from: http://www.theses.fr/2016AZUR4125

York University

8. Chimenti, Michael Alfredo. The Role of a -Catenin - FMRP Complex In Skeletal Muscle.

Degree: MSc -MS, Biology, 2019, York University

URL: http://hdl.handle.net/10315/36313

► Skeletal muscle consists of multinucleated myofibers which generate contractile force and regulate glucose levels in the human body. Over time, skeletal muscle can become damaged… (more)

Subjects/Keywords: Skeletal muscle; Biology; Fragile X Mental Retardation Protein; FMRP; β-catenin; Beta-catenin; translation; post-transcriptional; myofiber; C2C12 myoblast

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APA (6^th Edition):

Chimenti, M. A. (2019). The Role of a -Catenin - FMRP Complex In Skeletal Muscle. (Masters Thesis). York University. Retrieved from http://hdl.handle.net/10315/36313

Chicago Manual of Style (16^th Edition):

Chimenti, Michael Alfredo. “The Role of a -Catenin - FMRP Complex In Skeletal Muscle.” 2019. Masters Thesis, York University. Accessed February 28, 2021. http://hdl.handle.net/10315/36313.

MLA Handbook (7^th Edition):

Chimenti, Michael Alfredo. “The Role of a -Catenin - FMRP Complex In Skeletal Muscle.” 2019. Web. 28 Feb 2021.

Vancouver:

Chimenti MA. The Role of a -Catenin - FMRP Complex In Skeletal Muscle. [Internet] [Masters thesis]. York University; 2019. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/10315/36313.

Council of Science Editors:

Chimenti MA. The Role of a -Catenin - FMRP Complex In Skeletal Muscle. [Masters Thesis]. York University; 2019. Available from: http://hdl.handle.net/10315/36313

University of Rochester

9. Zhang, Yongchun. B-CATENIN Signaling Integrates with BMP and CCN1 Signaling to Regulate Chondrocyte Differentiation and Cartilage Development ate.

Degree: PhD, 2015, University of Rochester

URL: http://hdl.handle.net/1802/30113

► This work addresses the central question of how B-CATENIN signaling regulates chondrocyte differentiation during endochondral bone formation and cartilage development through integration with BMP and… (more)

▼ This work addresses the central question of how B-CATENIN signaling regulates chondrocyte differentiation during endochondral bone formation and cartilage development through integration with BMP and CCN1 signaling. Even though the functions of B-CATENIN signaling in chondrocytes have been extensively investigated through gain-of-function (GOF) and loss-of-function (LOF) mouse models, the role of B-CATENIN signaling in the committed chondrocyte and its downstream effectors are still unclear. Here we have discovered that cartilage-derived B-CATENIN signaling promotes chondrocyte maturation, angiogenesis, secondary ossification center (SOC) formation and bone ossification. B-CATENIN signaling also induces activation of BMP signaling and mediates primary ossification center (POC) formation through BMP and TAK1 signaling. Next, we identified a matricellular protein, CCN1, induced by B- CATENIN signaling in chondrocytes. In vitro assays demonstrate that CCN1 is required and sufficient to drive chondrocyte maturation. In vivo overexpression of CCN1 in chondrocytes leads to chondrodysplasia with reduced cell number but increased cell size, and results in cartilage degeneration in adult mice. The increase in the expression of CCN1 in injured mouse and human cartilage suggests a correlation between the CCN1 and osteoarthritis progression. Finally, we explored the role of CCN1 in chondrogenesis by overexpressing CCN1 in limb mesenchyme. CCN1 overexpression causes severe chondrodysplasia and reduction in the expression of chondrogenic genes indicating a repressive role of CCN1 in chondrogenesis. Mice with CCN1 overexpression in mesenchyme develop multiple joint defects, which eventually results in cartilage degradation and bone destruction in the knee joints. Taken together, these data have revealed that cartilage-derived B-CATENIN signaling regulates chondrocyte maturation and endochondral bone formation through modulating BMP signaling. Another novel finding is that CCN1 signaling induced by B-CATENIN signaling to promote chondrocyte maturation but inhibit chondrogenesis.

Subjects/Keywords: beta-CATENIN; CCN1; BMP2; Chondrocyte; Cartilage

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APA (6^th Edition):

Zhang, Y. (2015). B-CATENIN Signaling Integrates with BMP and CCN1 Signaling to Regulate Chondrocyte Differentiation and Cartilage Development ate. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/30113

Chicago Manual of Style (16^th Edition):

Zhang, Yongchun. “B-CATENIN Signaling Integrates with BMP and CCN1 Signaling to Regulate Chondrocyte Differentiation and Cartilage Development ate.” 2015. Doctoral Dissertation, University of Rochester. Accessed February 28, 2021. http://hdl.handle.net/1802/30113.

MLA Handbook (7^th Edition):

Zhang, Yongchun. “B-CATENIN Signaling Integrates with BMP and CCN1 Signaling to Regulate Chondrocyte Differentiation and Cartilage Development ate.” 2015. Web. 28 Feb 2021.

Vancouver:

Zhang Y. B-CATENIN Signaling Integrates with BMP and CCN1 Signaling to Regulate Chondrocyte Differentiation and Cartilage Development ate. [Internet] [Doctoral dissertation]. University of Rochester; 2015. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/1802/30113.

Council of Science Editors:

Zhang Y. B-CATENIN Signaling Integrates with BMP and CCN1 Signaling to Regulate Chondrocyte Differentiation and Cartilage Development ate. [Doctoral Dissertation]. University of Rochester; 2015. Available from: http://hdl.handle.net/1802/30113

University of Manchester

10. Giles, Adam Alexander. Wnt signalling in oestrogen-induced lactotroph proliferation.

Degree: 2011, University of Manchester

URL: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:121389

► The University of ManchesterAdam GilesDoctor of Philosophy – PhDWnt signalling in oestrogen-induced lactotroph hyperplasia2011The anterior pituitary gland is the major hormonal regulator in the body.… (more)

▼ The University of ManchesterAdam GilesDoctor of Philosophy – PhDWnt signalling in oestrogen-induced lactotroph hyperplasia2011The anterior pituitary gland is the major hormonal regulator in the body. The gland contains five secretory cell types whose emergence during development is defined by a tightly regulated array of transcription factors. In adult life, the gland is plastic with the relative proportions of cells varying depending on physiological context. Tumours of the pituitary gland account for 15% of all intracranial tumours in man and are caused by the selective proliferation of one of the secretory cell types. The majority of these (60%) are prolactinomas which consist of very slowly proliferating lactotroph cells, which produce the hormone prolactin. Pituitary tumours are almost never malignant and do not express common genetic markers for cancer, suggesting endogenous proliferative stimuli in the pituitary are the cause of tumour development.Oestrogen causes lactotroph hyperplasia during pregnancy and increases prolactin secretion. Our group previously showed that Wnt-4 mRNA was upregulated during oestrogen-induced lactotroph hyperplasia in Fischer 344 rats. Wnt molecules are key regulatory proteins controlling differentiation, proliferation and migration in development and adult life. Wnt-4 is involved in the emergence of lactotrophs during development, and has been implicated in pituitary tumour formation. Wnt molecules signal through three pathways. The well studied canonical pathway has been implicated in numerous cancers and centres around gene transcription initiated by translocation of β-Catenin into the nucleus. There are two non-canonical pathways: the Wnt-planar cell polarity (PCP) pathway and the Wnt-calcium pathway which are both poorly understood.In this thesis, the expression of Wnt-4 was studied in the pituitary, and effects of downstream signalling pathways in response to oestrogen were assessed. Wnt-4 was expressed in all secretory cell types of the pituitary, as well as the marginal zone (MZ), a region of the pituitary that may harbour stem cells. Oestrogen upregulated Wnt-4 protein in the somatolactotroph GH3 cell line, though this could not be replicated in primary tissue. A number of approaches (western blotting, immunofluorescence, reporter gene assays and mutant β-Catenin overexpression) were utilised to show that the canonical pathway was not activated in the pituitary. Wnt-4 had a clear inhibitory effect on calcium oscillations in GH3 cells, showing for the first time a non-canonical effect in the pituitary, though the downstream effects are currently unknown. Attempts made to study the activation of the PCP pathway were inconclusive. Efforts focused on the distribution of key structural and regulatory proteins in the anterior pituitary and the MZ. The MZ was characterised by a single layer of cells at the border of the anterior and intermediate lobes of the pituitary, with high expression of E-Cadherin and Sox 9, though no change in distribution was observed with oestrogen… Advisors/Committee Members: Davis, Julian.

Subjects/Keywords: Wnt; Pituitary; Lactotroph; Beta-Catenin; Prolactin

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APA (6^th Edition):

Giles, A. A. (2011). Wnt signalling in oestrogen-induced lactotroph proliferation. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:121389

Chicago Manual of Style (16^th Edition):

Giles, Adam Alexander. “Wnt signalling in oestrogen-induced lactotroph proliferation.” 2011. Doctoral Dissertation, University of Manchester. Accessed February 28, 2021. http://www.manchester.ac.uk/escholar/uk-ac-man-scw:121389.

MLA Handbook (7^th Edition):

Giles, Adam Alexander. “Wnt signalling in oestrogen-induced lactotroph proliferation.” 2011. Web. 28 Feb 2021.

Vancouver:

Giles AA. Wnt signalling in oestrogen-induced lactotroph proliferation. [Internet] [Doctoral dissertation]. University of Manchester; 2011. [cited 2021 Feb 28]. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:121389.

Council of Science Editors:

Giles AA. Wnt signalling in oestrogen-induced lactotroph proliferation. [Doctoral Dissertation]. University of Manchester; 2011. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:121389

Penn State University

11. Rennoll, Sherri Ann. Transcriptional regulation of the c-MYC (MYC) proto-oncogene by oncogenic Wnt/β-catenin signaling in colorectal carcinomas.

Degree: 2015, Penn State University

URL: https://submit-etda.libraries.psu.edu/catalog/26902

► Over 90% of sporadic colorectal cancers (CRCs) are associated with initiating mutations in components of the Wnt/β-catenin signaling pathway. These mutations result in elevated nuclear… (more)

▼ Over 90% of sporadic colorectal cancers (CRCs) are associated with initiating mutations in components of the Wnt/β-catenin signaling pathway. These mutations result in elevated nuclear levels of the β-catenin transcriptional co-activator. In the nucleus, β-catenin associates with the T-cell factor/Lymphoid enhancer factor (TCF/Lef) family of sequence-specific transcription factors at Wnt-responsive DNA elements (WREs) to increase target gene expression. Aberrant expression of these genes by oncogenic Wnt/β-catenin signaling leads to the formation of small, benign adenomas. The c-MYC (MYC) proto-oncogene is a direct β-catenin target gene that is required for Wnt/β-catenin-mediated intestinal tumorigenesis. However, the molecular mechanisms underlying β-catenin regulation of MYC expression are not fully defined. The work described within this thesis aimed to further define these molecular mechanisms by addressing the involvement of nuclear AXIN2 and the MYC 3’ WRE in controlling oncogenic MYC gene expression. AXIN2, a scaffolding protein and component of the Wnt/β-catenin signaling pathway, was recently demonstrated to localize to the nucleus. The function of AXIN2 within this subcellular compartment, however, was unknown. By constitutively localizing AXIN2 to the nucleus, we demonstrate that nuclear AXIN2 forms a complex with β-catenin/TCF and represses MYC gene expression by binding the MYC gene locus. These results indicate that nuclear AXIN2 functions as a molecular rheostat to maintain a “just right” level of MYC necessary for tumorigenesis in CRC. Similar to nuclear AXIN2, we find that the MYC 3’ WRE, which maps 1.4-kb downstream from the MYC transcription stop site, drives oncogenic MYC gene expression in CRC cells. Using CRISPR/Cas9 genome editing technology, we generated a knockout CRC cell line in which a single TCF binding element within the MYC 3’ WRE was deleted. Deletion of this element decreased β-catenin/TCF occupancy at the MYC 3’ WRE and MYC gene expression. The observed decrease in MYC gene expression corresponded to diminished cellular proliferation and growth of the knockout cells. Together, our studies have uncovered new mechanisms for regulation of MYC gene expression by oncogenic Wnt/β-catenin signaling, and suggest that approaches to target nuclear AXIN2 or the MYC 3’ WRE would be effective strategies for the treatment of individuals suffering from CRC. Advisors/Committee Members: Gregory Yochum, Dissertation Advisor/Co-Advisor, Gregory Yochum, Committee Chair/Co-Chair, Laura Carrel, Committee Member, Sergei A Grigoryev, Committee Member, Lisa M Shantz, Committee Member.

Subjects/Keywords: MYC; beta-catenin; AXIN2; colorectal cancer

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APA (6^th Edition):

Rennoll, S. A. (2015). Transcriptional regulation of the c-MYC (MYC) proto-oncogene by oncogenic Wnt/β-catenin signaling in colorectal carcinomas. (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/26902

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):

Rennoll, Sherri Ann. “Transcriptional regulation of the c-MYC (MYC) proto-oncogene by oncogenic Wnt/β-catenin signaling in colorectal carcinomas.” 2015. Thesis, Penn State University. Accessed February 28, 2021. https://submit-etda.libraries.psu.edu/catalog/26902.

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

MLA Handbook (7^th Edition):

Rennoll, Sherri Ann. “Transcriptional regulation of the c-MYC (MYC) proto-oncogene by oncogenic Wnt/β-catenin signaling in colorectal carcinomas.” 2015. Web. 28 Feb 2021.

Vancouver:

Rennoll SA. Transcriptional regulation of the c-MYC (MYC) proto-oncogene by oncogenic Wnt/β-catenin signaling in colorectal carcinomas. [Internet] [Thesis]. Penn State University; 2015. [cited 2021 Feb 28]. Available from: https://submit-etda.libraries.psu.edu/catalog/26902.

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

Council of Science Editors:

Rennoll SA. Transcriptional regulation of the c-MYC (MYC) proto-oncogene by oncogenic Wnt/β-catenin signaling in colorectal carcinomas. [Thesis]. Penn State University; 2015. Available from: https://submit-etda.libraries.psu.edu/catalog/26902

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

McMaster University

12. Cunanan, Joanna. Quercetin Inhibits β-catenin Transcriptional Activity During Kidney Development and Reduces the Severity of Renal Dysplasia.

Degree: MSMS, 2019, McMaster University

URL: http://hdl.handle.net/11375/24793

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M.Sc. Thesis Dissertation, August 2019, McMaster University

Renal dysplasia, defined as the abnormal development of kidney tissue, is the leading cause of kidney disease in… (more)

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M.Sc. Thesis Dissertation, August 2019, McMaster University

Renal dysplasia, defined as the abnormal development of kidney tissue, is the leading cause of kidney disease in children. While there are numerous causes of renal dysplasia (i.e. genetic, environmental and epigenetic factors), there is no cure to this abnormal defect. Kidney development occurs by two main processes: branching morphogenesis, which forms the collecting duct system, and nephrogenesis, which generates the nephrons, the functional units of the kidney. Our previous studies have demonstrated that β-catenin, a dual-function protein involved in cell adhesion and gene transcription, regulates branching morphogenesis and nephrogenesis. Furthermore, we discovered that nuclear β-catenin levels are increased in kidneys from patients with renal dysplasia, suggesting β-catenin can be a potential therapeutic target to modulate kidney development and renal dysplasia. Quercetin is a flavonoid that reduces β-catenin levels and inhibits its transcriptional activity, leading to improved outcomes in cancer and in kidney fibrosis. The role of quercetin in kidney development and in abnormal defects that arise during kidney development is yet to be examined. Using embryonic mouse kidney organ culture, I found that quercetin treatment resulted in a dose-dependent disruption in branching morphogenesis and nephrogenesis. In addition, quantitative reverse-transcriptase PCR revealed a decreased expression of β-catenin target genes essential for kidney development (i.e. Pax2, Six2 and GDNF). Immunohistochemistry for β-catenin demonstrated that quercetin reduced nuclear β-catenin expression and increased cytoplasmic and membrane-bound expression in a dose-dependent manner. These results were confirmed by Western blot analysis. These novel findings demonstrate that quercetin treatment resulted in decreased levels of nuclear β-catenin, resulting in a decrease in its transcriptional activity which manifested in alterations in kidney developmental processes, suggesting quercetin is effective at reducing nuclear β-catenin in wild-type embryonic kidneys. Next, to determine whether quercetin has any effects on renal dysplasia, I utilized transgenic mice models that overexpress β-catenin in select cells of the embryonic kidney. These models recapitulate the defects observed in human renal dysplasia, including disorganized branching morphogenesis and disrupted nephrogenesis. Quercetin treatment of embryonic dysplastic kidneys resulted in a partial rescue of renal dysplasia which was evident in marked improvements in branching morphogenesis and nephrogenesis, as well as an increase in the number of properly-developing nephrons in the kidney tissue. Analysis of β-catenin expression in quercetin-treated dysplastic kidneys revealed a decrease in nuclear levels and an increase in cytoplasmic and membrane-bound levels, resulting in a reduced expression of target genes (Pax2, Six2, and GDNF). Finally, this partial rescue of renal dysplasia was associated with an improved and organized…

Advisors/Committee Members: Bridgewater, Darren, Medical Sciences (Growth and Development).

Subjects/Keywords: kidney development; beta-catenin; renal dysplasia; quercetin

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APA (6^th Edition):

Cunanan, J. (2019). Quercetin Inhibits β-catenin Transcriptional Activity During Kidney Development and Reduces the Severity of Renal Dysplasia. (Masters Thesis). McMaster University. Retrieved from http://hdl.handle.net/11375/24793

Chicago Manual of Style (16^th Edition):

Cunanan, Joanna. “Quercetin Inhibits β-catenin Transcriptional Activity During Kidney Development and Reduces the Severity of Renal Dysplasia.” 2019. Masters Thesis, McMaster University. Accessed February 28, 2021. http://hdl.handle.net/11375/24793.

MLA Handbook (7^th Edition):

Cunanan, Joanna. “Quercetin Inhibits β-catenin Transcriptional Activity During Kidney Development and Reduces the Severity of Renal Dysplasia.” 2019. Web. 28 Feb 2021.

Vancouver:

Cunanan J. Quercetin Inhibits β-catenin Transcriptional Activity During Kidney Development and Reduces the Severity of Renal Dysplasia. [Internet] [Masters thesis]. McMaster University; 2019. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/11375/24793.

Council of Science Editors:

Cunanan J. Quercetin Inhibits β-catenin Transcriptional Activity During Kidney Development and Reduces the Severity of Renal Dysplasia. [Masters Thesis]. McMaster University; 2019. Available from: http://hdl.handle.net/11375/24793

13. Manring, Heather Renee. COMPARATIVE CELL BASED FUNCTIONAL ANALYSIS OF KEY WNT/BETA-CATENIN PATHWAY GENES AND GENE MUTATIONS.

Degree: 2012, Wake Forest University

URL: http://hdl.handle.net/10339/37663

► The Wnt/Beta-catenin signaling pathway has many roles including regulation of developmental pathways, cell proliferation, and homeostasis of adult tissues. Wnt/Beta-catenin signaling activity depends on the… (more)

Subjects/Keywords: Beta-catenin

…contribution of Wnt/β-catenin signaling to key pancreatic functions including beta-cell proliferation… …Wnt/β-catenin pathway genes on beta-cell function will be discussed in greater detail in… …blot WRE Wnt response element β-trcp Beta-transducin repeat containing protein x LIST… …OF FIGURES Page Figure 1.1. Schematic of the Wnt/β-catenin pathway in the inactive (A… …3 Figure 1.2. β-catenin function is partially mediated by its location within the cell…

10 more images…

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APA (6^th Edition):

Manring, H. R. (2012). COMPARATIVE CELL BASED FUNCTIONAL ANALYSIS OF KEY WNT/BETA-CATENIN PATHWAY GENES AND GENE MUTATIONS. (Thesis). Wake Forest University. Retrieved from http://hdl.handle.net/10339/37663

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):

Manring, Heather Renee. “COMPARATIVE CELL BASED FUNCTIONAL ANALYSIS OF KEY WNT/BETA-CATENIN PATHWAY GENES AND GENE MUTATIONS.” 2012. Thesis, Wake Forest University. Accessed February 28, 2021. http://hdl.handle.net/10339/37663.

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

MLA Handbook (7^th Edition):

Manring, Heather Renee. “COMPARATIVE CELL BASED FUNCTIONAL ANALYSIS OF KEY WNT/BETA-CATENIN PATHWAY GENES AND GENE MUTATIONS.” 2012. Web. 28 Feb 2021.

Vancouver:

Manring HR. COMPARATIVE CELL BASED FUNCTIONAL ANALYSIS OF KEY WNT/BETA-CATENIN PATHWAY GENES AND GENE MUTATIONS. [Internet] [Thesis]. Wake Forest University; 2012. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/10339/37663.

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

Council of Science Editors:

Manring HR. COMPARATIVE CELL BASED FUNCTIONAL ANALYSIS OF KEY WNT/BETA-CATENIN PATHWAY GENES AND GENE MUTATIONS. [Thesis]. Wake Forest University; 2012. Available from: http://hdl.handle.net/10339/37663

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

Boston University

14. Gowda, Asha. The effect of protein kinase C and Beta-catenin inhibitors on uveal melanoma cells.

Degree: MS, Medical Sciences, 2014, Boston University

URL: http://hdl.handle.net/2144/15046

► PURPOSE: Uveal melanoma (UM) is the most common intraocular malignancy in adults with an incidence of six per one million individuals each year. Globe conserving… (more)

▼ PURPOSE: Uveal melanoma (UM) is the most common intraocular malignancy in adults with an incidence of six per one million individuals each year. Globe conserving treatments are currently the standard of care, but unfortunately, despite successful local control, a substantial mortality risk exists due to eventual emergence of distant metastasis, which is invariably lethal. There is therefore an unmet need for novel, effective, targeted therapies for metastatic UM. Somatic mutations in the G-protein α subunits, Gαq and Gα, are present in a mutually exclusive pattern in approximately 80% of UMs, and they abolish the GTPase activity, resulting in a constitutively active protein. We have previously demonstrated that GNAQ-mutant (GNAQ^mt) UMs are addicted to the oncogenic effect of the mutant GNAQ protein and dissected the GNAQ pathway in an attempt to identify druggable targets. Our findings that the mutant GNAQ protein activates the PKC/PKD axis, which activates beta-catenin (β-Catenin), prompted us to investigate the role of PKC and β-Catenin in GNAQ^mt UM. EXPERIMENTAL DESIGN: The GNAQ^mt UM cell lines Mel202 and OMM1.3 were treated with either the PKC inhibitor bisindolylmaleimide I (BIM) alone, the Wnt/β-Catenin inhibitors FH535 or cardamonin alone, the Wnt/β-Catenin activator Wnt-3a alone, or siRNAs for β-Catenin in combination with BIM, and their viability was assessed with the MTT assay. Levels of β-Catenin, phosphorylated AKT, ERK1/2, caspase 3 and LC3BII were assessed with western blotting. β-Catenin mRNA levels were assessed with microarray analysis and RT-PCR. RESULTS: GNAQ^mt UM cells are very sensitive to PKC inhibition and respond with a decrease in cell viability that involves autophagy and cleavage and translocation of LC3BII in autophagosomes, but not caspase activation. PKC inhibition results in the upregulation of β-Catenin protein, but not mRNA levels, through a post-translational mechanism that involved the phosphorylation and activation of AKT, but not ERK1/2. β-Catenin inhibition by either small molecule inhibitors or siRNA resulted in a dose-dependent increase of cell proliferation, whereas β-Catenin activation by Wnt-3a had the opposite effects, resulting in a decrease in cell viability. CONCLUTIONS: Our study demonstrates that PKC is a mediator of the oncogenic effect of mutant Gα protein in UM through the Wnt-3/β-Catenin signaling pathway. These results open exciting opportunities for the development of personalized targeted therapies for UM in a genotype-dependent fashion.

Subjects/Keywords: Ophthalmology; Beta-catenin; Melanoma; Protein kinase C

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APA (6^th Edition):

Gowda, A. (2014). The effect of protein kinase C and Beta-catenin inhibitors on uveal melanoma cells. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/15046

Chicago Manual of Style (16^th Edition):

Gowda, Asha. “The effect of protein kinase C and Beta-catenin inhibitors on uveal melanoma cells.” 2014. Masters Thesis, Boston University. Accessed February 28, 2021. http://hdl.handle.net/2144/15046.

MLA Handbook (7^th Edition):

Gowda, Asha. “The effect of protein kinase C and Beta-catenin inhibitors on uveal melanoma cells.” 2014. Web. 28 Feb 2021.

Vancouver:

Gowda A. The effect of protein kinase C and Beta-catenin inhibitors on uveal melanoma cells. [Internet] [Masters thesis]. Boston University; 2014. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/2144/15046.

Council of Science Editors:

Gowda A. The effect of protein kinase C and Beta-catenin inhibitors on uveal melanoma cells. [Masters Thesis]. Boston University; 2014. Available from: http://hdl.handle.net/2144/15046

University of Manchester

15. Giles, Adam Alexander. Wnt signalling in oestrogen-induced lactotroph proliferation.

Degree: PhD, 2011, University of Manchester

URL: https://www.research.manchester.ac.uk/portal/en/theses/wnt-signalling-in-oestrogeninduced-lactotroph-proliferation(35c1ba30-0755-4583-bdce-69dce1382721).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.538396

► The anterior pituitary gland is the major hormonal regulator in the body. The gland contains five secretory cell types whose emergence during development is defined… (more)

▼ The anterior pituitary gland is the major hormonal regulator in the body. The gland contains five secretory cell types whose emergence during development is defined by a tightly regulated array of transcription factors. In adult life, the gland is plastic with the relative proportions of cells varying depending on physiological context. Tumours of the pituitary gland account for 15% of all intracranial tumours in man and are caused by the selective proliferation of one of the secretory cell types. The majority of these (60%) are prolactinomas which consist of very slowly proliferating lactotroph cells, which produce the hormone prolactin. Pituitary tumours are almost never malignant and do not express common genetic markers for cancer, suggesting endogenous proliferative stimuli in the pituitary are the cause of tumour development. Oestrogen causes lactotroph hyperplasia during pregnancy and increases prolactin secretion. Our group previously showed that Wnt-4 mRNA was upregulated during oestrogen-induced lactotroph hyperplasia in Fischer 344 rats. Wnt molecules are key regulatory proteins controlling differentiation, proliferation and migration in development and adult life. Wnt-4 is involved in the emergence of lactotrophs during development, and has been implicated in pituitary tumour formation. Wnt molecules signal through three pathways. The well studied canonical pathway has been implicated in numerous cancers and centres around gene transcription initiated by translocation of β-Catenin into the nucleus. There are two non-canonical pathways: the Wnt-planar cell polarity (PCP) pathway and the Wnt-calcium pathway which are both poorly understood. In this thesis, the expression of Wnt-4 was studied in the pituitary, and effects of downstream signalling pathways in response to oestrogen were assessed. Wnt-4 was expressed in all secretory cell types of the pituitary, as well as the marginal zone (MZ), a region of the pituitary that may harbour stem cells. Oestrogen upregulated Wnt-4 protein in the somatolactotroph GH3 cell line, though this could not be replicated in primary tissue. A number of approaches (western blotting, immunofluorescence, reporter gene assays and mutant β-Catenin overexpression) were utilised to show that the canonical pathway was not activated in the pituitary. Wnt-4 had a clear inhibitory effect on calcium oscillations in GH3 cells, showing for the first time a non-canonical effect in the pituitary, though the downstream effects are currently unknown. Attempts made to study the activation of the PCP pathway were inconclusive. Efforts focused on the distribution of key structural and regulatory proteins in the anterior pituitary and the MZ. The MZ was characterised by a single layer of cells at the border of the anterior and intermediate lobes of the pituitary, with high expression of E-Cadherin and Sox 9, though no change in distribution was observed with oestrogen treatment. In the anterior lobe, oestrogen treatment decreased N and E-Cadherin expression, which could be an indicator of PCP…

Subjects/Keywords: 616.4; Wnt; Pituitary; Lactotroph; Beta-Catenin; Prolactin

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

APA (6^th Edition):

Giles, A. A. (2011). Wnt signalling in oestrogen-induced lactotroph proliferation. (Doctoral Dissertation). University of Manchester. Retrieved from https://www.research.manchester.ac.uk/portal/en/theses/wnt-signalling-in-oestrogeninduced-lactotroph-proliferation(35c1ba30-0755-4583-bdce-69dce1382721).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.538396

Chicago Manual of Style (16^th Edition):

Giles, Adam Alexander. “Wnt signalling in oestrogen-induced lactotroph proliferation.” 2011. Doctoral Dissertation, University of Manchester. Accessed February 28, 2021. https://www.research.manchester.ac.uk/portal/en/theses/wnt-signalling-in-oestrogeninduced-lactotroph-proliferation(35c1ba30-0755-4583-bdce-69dce1382721).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.538396.

MLA Handbook (7^th Edition):

Giles, Adam Alexander. “Wnt signalling in oestrogen-induced lactotroph proliferation.” 2011. Web. 28 Feb 2021.

Vancouver:

Giles AA. Wnt signalling in oestrogen-induced lactotroph proliferation. [Internet] [Doctoral dissertation]. University of Manchester; 2011. [cited 2021 Feb 28]. Available from: https://www.research.manchester.ac.uk/portal/en/theses/wnt-signalling-in-oestrogeninduced-lactotroph-proliferation(35c1ba30-0755-4583-bdce-69dce1382721).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.538396.

Council of Science Editors:

Giles AA. Wnt signalling in oestrogen-induced lactotroph proliferation. [Doctoral Dissertation]. University of Manchester; 2011. Available from: https://www.research.manchester.ac.uk/portal/en/theses/wnt-signalling-in-oestrogeninduced-lactotroph-proliferation(35c1ba30-0755-4583-bdce-69dce1382721).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.538396

University of Toronto

16. Al-Jazrawe, Mushriq. Investigating the Maintenance of Desmoid Tumors beyond Beta-catenin.

Degree: PhD, 2019, University of Toronto

URL: http://hdl.handle.net/1807/97316

► Despite substantial advances in the genomic characterization of neoplasia, effective therapy of many diseases remains elusive. Beyond genomic alterations, several signalling processes maintain the neoplastic… (more)

▼ Despite substantial advances in the genomic characterization of neoplasia, effective therapy of many diseases remains elusive. Beyond genomic alterations, several signalling processes maintain the neoplastic phenotype including active protein kinases that increase proliferation, gene expression programs that maintain a neoplastic identity, and stroma-derived factors that influence tumor cell behavior. Determination of the signalling pathways involved in disease maintenance have allowed for the identification of effective therapeutic strategies in some common diseases. However, the treatment of rare diseases has seen little development because of lack of patient material and poor characterization of such material. Desmoid tumors are rare soft-tissue neoplasms with unpredictable clinical behavior that consist of mesenchymal fibroblast-like cells initiated by mutations stabilizing beta-catenin. Here we hypothesized that additional pathways are dysregulated in desmoid tumors and identifying these, and their regulators, will identify putative therapeutic targets. We integrated information from compound library screens of protein kinase inhibitors, gene expression datasets to establish a predictive molecular signature, as well as clonal approaches to identify factors contributing to the neoplastic phenotype. We found that PDGFRB signalling, microRNA-29 and glucocorticoids, and stroma-derived factors and STAT6 signalling, are all factors regulating cellular proliferation in desmoid tumors. We also describe clonal expansion techniques and identify surface markers of mutant and non-mutant cells to address intratumor heterogeneity. These findings improve our current understanding of the signalling processes that maintain desmoid tumor growth and identify several promising targets for therapy. Moreover, the methods we describe here will improve the characterization of existing and future samples and help explain the unpredictability that has been a feature of this disease. Advisors/Committee Members: Alman, Benjamin, Laboratory Medicine and Pathobiology.

Subjects/Keywords: beta-catenin; desmoid; fibromatosis; stroma; tumour; 0992

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

APA (6^th Edition):

Al-Jazrawe, M. (2019). Investigating the Maintenance of Desmoid Tumors beyond Beta-catenin. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/97316

Chicago Manual of Style (16^th Edition):

Al-Jazrawe, Mushriq. “Investigating the Maintenance of Desmoid Tumors beyond Beta-catenin.” 2019. Doctoral Dissertation, University of Toronto. Accessed February 28, 2021. http://hdl.handle.net/1807/97316.

MLA Handbook (7^th Edition):

Al-Jazrawe, Mushriq. “Investigating the Maintenance of Desmoid Tumors beyond Beta-catenin.” 2019. Web. 28 Feb 2021.

Vancouver:

Al-Jazrawe M. Investigating the Maintenance of Desmoid Tumors beyond Beta-catenin. [Internet] [Doctoral dissertation]. University of Toronto; 2019. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/1807/97316.

Council of Science Editors:

Al-Jazrawe M. Investigating the Maintenance of Desmoid Tumors beyond Beta-catenin. [Doctoral Dissertation]. University of Toronto; 2019. Available from: http://hdl.handle.net/1807/97316

University of Southern California

17. Wu, Jia. Wnt/β-catenin/p300 induced transcription is critical for the differentiation and maintenance of Paneth cells.

Degree: MS, Biochemistry and Molecular Biology, 2014, University of Southern California

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/405481/rec/7958

► Our lab's previous studies have demonstrated that Wnt/β‐catenin/p300 transcription initiates cell differentiation, whereas Wnt/β‐catenin/cyclic AMP‐responsive element binding protein‐binding protein (CBP) transcription mediates cell proliferation/maintenance of… (more)

Subjects/Keywords: Wnt; β ‐Catenin/p300; Paneth cell

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APA (6^th Edition):

Wu, J. (2014). Wnt/β-catenin/p300 induced transcription is critical for the differentiation and maintenance of Paneth cells. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/405481/rec/7958

Chicago Manual of Style (16^th Edition):

Wu, Jia. “Wnt/β-catenin/p300 induced transcription is critical for the differentiation and maintenance of Paneth cells.” 2014. Masters Thesis, University of Southern California. Accessed February 28, 2021. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/405481/rec/7958.

MLA Handbook (7^th Edition):

Wu, Jia. “Wnt/β-catenin/p300 induced transcription is critical for the differentiation and maintenance of Paneth cells.” 2014. Web. 28 Feb 2021.

Vancouver:

Wu J. Wnt/β-catenin/p300 induced transcription is critical for the differentiation and maintenance of Paneth cells. [Internet] [Masters thesis]. University of Southern California; 2014. [cited 2021 Feb 28]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/405481/rec/7958.

Council of Science Editors:

Wu J. Wnt/β-catenin/p300 induced transcription is critical for the differentiation and maintenance of Paneth cells. [Masters Thesis]. University of Southern California; 2014. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/405481/rec/7958

University of Illinois – Urbana-Champaign

18. Xu, Guanying. Diet-induced-obesity suppresses beta-catenin and promotes cell proliferation during colon development.

Degree: MS, Food Science & Human Nutrition, 2018, University of Illinois – Urbana-Champaign

URL: http://hdl.handle.net/2142/101719

► Diet induced obesity (DIO), resulting from long-term consumption of a high fat diet, modifies multiple signaling pathways. These response pathways are closely associated with cell… (more)

Subjects/Keywords: diet-induced-obesity; wnt; beta-catenin; proliferation

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APA (6^th Edition):

Xu, G. (2018). Diet-induced-obesity suppresses beta-catenin and promotes cell proliferation during colon development. (Thesis). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/101719

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):

Xu, Guanying. “Diet-induced-obesity suppresses beta-catenin and promotes cell proliferation during colon development.” 2018. Thesis, University of Illinois – Urbana-Champaign. Accessed February 28, 2021. http://hdl.handle.net/2142/101719.

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

MLA Handbook (7^th Edition):

Xu, Guanying. “Diet-induced-obesity suppresses beta-catenin and promotes cell proliferation during colon development.” 2018. Web. 28 Feb 2021.

Vancouver:

Xu G. Diet-induced-obesity suppresses beta-catenin and promotes cell proliferation during colon development. [Internet] [Thesis]. University of Illinois – Urbana-Champaign; 2018. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/2142/101719.

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

Council of Science Editors:

Xu G. Diet-induced-obesity suppresses beta-catenin and promotes cell proliferation during colon development. [Thesis]. University of Illinois – Urbana-Champaign; 2018. Available from: http://hdl.handle.net/2142/101719

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

Georgia State University

19. Hobson, Katherine. METHIONINE RESTRICTION INHIBITS NON-SMALL CELL LUNG CANCER GROWTH BY TARGETING THE BETA-CATENIN PATHWAY.

Degree: MS, Nutrition, 2018, Georgia State University

URL: https://scholarworks.gsu.edu/nutrition_theses/99

► Background: Lung cancer is the leading cause of cancer related death for both men and women. Non-small cell lung cancer (NSCLC) accounts for 80%… (more)

▼ Background: Lung cancer is the leading cause of cancer related death for both men and women. Non-small cell lung cancer (NSCLC) accounts for 80% of lung cancer with a 15% five-year survival rate. Current treatment options have serious side effects creating the need for alternative treatments. Methionine restriction (MR) has shown anti-tumor effects on various cancer cells, but the mechanisms involved in NSLCLC is unclear. The purpose of this study is to determine the anti-tumor effects of MR on NSCLC cells through the beta-catenin pathway. Objective: The purpose of this study is to determine the anti-tumor effects of MR on NSCLC cells through the beta-catenin pathway. Methods: Human NSCLC cell lines, A549 and H520 were obtained from ATCC and treated in the presence of normal or MR media (95% methionine restriction). After 48 hours of incubation, cell viability was determined by the alamar blue assay and a clonogenic assay was performed separately. A549 and H520 were treated for 24, 48, and 72 hours and cultured for harvest. Cell cycle was analyzed by measuring the DNA content of each cells determined using flow cytometry and western blot was performed using the antibodies β-actin, β-catenin, phospho β-catenin, and PARP. In order to investigate the potential molecular mechanism of MR on NSCLC cell, a human phospho-kinase array was performed. Results: MR significantly inhibits the cell proliferation in A549 and H520 cells after 48 hours. MR induces cell cycle arrest in G1 compared with the control after 24 hours of treatment. Protein expressions of PARP and phospho β-catenin are reduced in response to MR. The protein kinase array indicates MR exerts its anti-cancer effects by reducing phosphorylation of beta-catenin. Conclusion: Our results show MR has an inhibitory effect on the cell proliferation and colony formation of A549 and H520 cancer cell lines. Cell cycle arrest and reduced phosphorylated β-catenin provides insight into how methionine metabolism inhibits lung cancer development and progression. Further in vivo studies are needed in order to testify the efficacy of MR as a cancer prevention approach for NSCLC. Advisors/Committee Members: Xiangming Ji, Huanbiao Mo, Desiree Wanders.

Subjects/Keywords: Lung Cancer; Methionine Restriction; Beta-catenin

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

APA (6^th Edition):

Hobson, K. (2018). METHIONINE RESTRICTION INHIBITS NON-SMALL CELL LUNG CANCER GROWTH BY TARGETING THE BETA-CATENIN PATHWAY. (Thesis). Georgia State University. Retrieved from https://scholarworks.gsu.edu/nutrition_theses/99

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):

Hobson, Katherine. “METHIONINE RESTRICTION INHIBITS NON-SMALL CELL LUNG CANCER GROWTH BY TARGETING THE BETA-CATENIN PATHWAY.” 2018. Thesis, Georgia State University. Accessed February 28, 2021. https://scholarworks.gsu.edu/nutrition_theses/99.

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

MLA Handbook (7^th Edition):

Hobson, Katherine. “METHIONINE RESTRICTION INHIBITS NON-SMALL CELL LUNG CANCER GROWTH BY TARGETING THE BETA-CATENIN PATHWAY.” 2018. Web. 28 Feb 2021.

Vancouver:

Hobson K. METHIONINE RESTRICTION INHIBITS NON-SMALL CELL LUNG CANCER GROWTH BY TARGETING THE BETA-CATENIN PATHWAY. [Internet] [Thesis]. Georgia State University; 2018. [cited 2021 Feb 28]. Available from: https://scholarworks.gsu.edu/nutrition_theses/99.

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

Council of Science Editors:

Hobson K. METHIONINE RESTRICTION INHIBITS NON-SMALL CELL LUNG CANCER GROWTH BY TARGETING THE BETA-CATENIN PATHWAY. [Thesis]. Georgia State University; 2018. Available from: https://scholarworks.gsu.edu/nutrition_theses/99

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

University of New South Wales

20. Dietrich, Philipp. Identification of targetable components of beta-catenin signalling in Acute Myeloid Leukaemic Stem Cells.

Degree: Women's & Children's Health, 2015, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/55087 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:36505/SOURCE02?view=true

► Acute myeloid leukaemia (AML) remains the leading cause of leukaemia-related death with a relative five-year survival rate of only 24% in Australia. This poor prognosis… (more)

▼ Acute myeloid leukaemia (AML) remains the leading cause of leukaemia-related death with a relative five-year survival rate of only 24% in Australia. This poor prognosis is mainly due to disease relapse, which is thought to be attributable to the persistence of leukaemic stem cells (LSC) after chemotherapy. Previous studies have shown that β-catenin is required for the establishment of LSC in mixed lineage leukaemia (MLL)-rearranged AML. Targeted inhibition of β-catenin signalling has been hampered by the lack of pathway components amenable to pharmacoinhibition. In this study we have identified a novel β-catenin regulator, GPR84, a member of the G protein-coupled receptor family that represents a highly tractable class of drug targets. High GPR84 expression levels were confirmed in AML LSC compared to normal HSC (P=0.0114). ShRNA-mediated inhibition of GPR84 impaired cell proliferation (P=0.0009) and AML reconstitution in vivo (P<0.0001). The GPR84- deficient phenotype could be rescued by expression of constitutively active β-catenin in vivo (P=0.0039). Furthermore, GPR84 overexpression accelerated leukaemogenesis in vivo (P=0.0039). These data suggest that inhibiting GPR84/β-catenin signalling may provide a promising novel therapeutic strategy in AML. However, since a GPR84-specific inhibitor has not yet been developed, we aimed to further delineate the GPR84/β- catenin axis in order to pharmacologically inhibit other components of this pathway. Preliminary data from our lab has implicated the G protein GNA13 as a potential downstream target of GPR84. GNA13 overexpression rescued GPR84 deficiency (P=0.0012) through augmentation of cell proliferation in vivo (P<0.0001). In contrast, shRNA-mediated ablation of GNA13 impeded cell proliferation (P=0.0066) and delayed disease onset in vivo (P<0.0001). However, GNA13 may not integrate into a therapeutic regimen since GNA13-deficiency did not sensitize LSC to bortezomib as implicated by previous reports. Hence we conducted microarray studies to identify novel downstream target genes of GPR84 potentially amenable to therapeutic intervention. Bcl11a, a proto-oncogene previously shown to be involved in leukaemogenesis, was highly upregulated in cells overexpressing GPR84 compared to control (P=0.0032). Interestingly, GPR84-deficiency substantially increased the efficacy of the Bcl11a inhibitor simvastatin. Hence simvastatin may be a candidate inhibitor in combination with GPR84-directed chemotherapy in AML.

Subjects/Keywords: Acute Myeloid Leukaemia; GPR84; MLLAF9; beta-catenin

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APA (6^th Edition):

Dietrich, P. (2015). Identification of targetable components of beta-catenin signalling in Acute Myeloid Leukaemic Stem Cells. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/55087 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:36505/SOURCE02?view=true

Chicago Manual of Style (16^th Edition):

Dietrich, Philipp. “Identification of targetable components of beta-catenin signalling in Acute Myeloid Leukaemic Stem Cells.” 2015. Doctoral Dissertation, University of New South Wales. Accessed February 28, 2021. http://handle.unsw.edu.au/1959.4/55087 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:36505/SOURCE02?view=true.

MLA Handbook (7^th Edition):

Dietrich, Philipp. “Identification of targetable components of beta-catenin signalling in Acute Myeloid Leukaemic Stem Cells.” 2015. Web. 28 Feb 2021.

Vancouver:

Dietrich P. Identification of targetable components of beta-catenin signalling in Acute Myeloid Leukaemic Stem Cells. [Internet] [Doctoral dissertation]. University of New South Wales; 2015. [cited 2021 Feb 28]. Available from: http://handle.unsw.edu.au/1959.4/55087 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:36505/SOURCE02?view=true.

Council of Science Editors:

Dietrich P. Identification of targetable components of beta-catenin signalling in Acute Myeloid Leukaemic Stem Cells. [Doctoral Dissertation]. University of New South Wales; 2015. Available from: http://handle.unsw.edu.au/1959.4/55087 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:36505/SOURCE02?view=true

Université Montpellier II

21. Flacelière, Maud. La β-arrestine2, un acteur majeur de la tumorigenèse intestinale dépendante de la voie Wnt/β-caténine. : β-arrestine2, a major actor of the Wnt/β-catenin-dependent intestinal tumorigenesis.

Degree: Docteur es, Biologie Santé, 2012, Université Montpellier II

URL: http://www.theses.fr/2012MON20012

►

Les β-arrestines (Arrbs) régulent diverses voies de signalisation dont la voie Wnt/β-caténine (Wnt), un acteur clé dans le cancer colorectal. Le but de mon projet… (more)

▼

Les β-arrestines (Arrbs) régulent diverses voies de signalisation dont la voie Wnt/β-caténine (Wnt), un acteur clé dans le cancer colorectal. Le but de mon projet était d'étudier l'implication et les mécanismes régulés par les Arrbs dans la tumorigenèse intestinale dépendante de la voie Wnt. L'inhibition de l'expression des Arrbs partielle ou totale dans des souris ApcΔ14/+ montre que seules les souris invalidées pour l'Arrb2 développent 33% des tumeurs détectées chez les souris ApcΔ14/+ ; Arrb2+/+. Ces tumeurs ont une croissance normale. Cependant, l'analyse de leur transcriptome montre qu'elles expriment notamment certains gènes liés au système immunitaire, alors que les tumeurs dépendantes de l'Arrb2 expriment des gènes différents impliqués entre autres dans la voie Wnt. L'invalidation de l'Arrb2 réduit l'expression de gènes cibles de la voie Wnt dans les cellules isolées de 12 sur 18 tumeurs de souris ApcΔ14/+, et inhibe l'augmentation d'activité Wnt et la formation de colonies en agar mou induite par l'invalidation d'Apc dans des cellules murines ApcMin/+. L'Arrb2 est donc essentielle pour l'initiation et la croissance des tumeurs intestinales présentant une activité Wnt élevée. Pour comprendre les mécanismes régulés par l'Arrb2 dans ce contexte, les complexes protéiques associés à l'Arrb2 ont été analysés par protéomique dans des cellules humaines de cancer colorectal SW480 exprimant ou non un dominant négatif de Tcf4. 132 partenaires de l'Arrb2 potentiellement imbriqués dans un réseau de 917 protéines, ont été identifiés dans les cellules où la voie Wnt est active. Une baisse de 80% de l'activité Wnt entraine la disparition de 41 protéines avec 256 interactions potentielles alors que 42 protéines apparaissent avec 244 interactions potentielles. Le rôle clé d'Arrb2 dans le cancer colorectal s'expliquerait par la connexion d'au moins une quarantaine de protéines dépendantes de l'activité Wnt à un réseau de signalisation complexe dont l'analyse est en cours.

Β-arrestins (Arrbs) participate in the regulation of multiple signaling pathways, including Wnt/β-catenin (Wnt), the major actor in human colorectal cancer. The aim of my project was to study the involvement of Arrbs and the mechanisms they regulate in Wnt-dependent intestinal tumorigenesis. The partial or total inhibition of Arrbs in ApcΔ14/+ mice showed that only mice with Arrb2 depletion developed only 33% of the tumors detected in their Arrb2-WT littermates. These remaining tumors grow normally and are Arrb2–independent. Transcriptomic analysis showed that they overexpressed genes that reflect a high interaction with the immune system, whereas those overexpressed in Arrb2–dependent tumors are predominantly involved in Wnt signaling. Moreover, Arrb2 siRNAs decreased the expression of Wnt target genes in cells isolated from 12 of 18 tumors from ApcΔ14/+ mice, completely reversed the increased Wnt activity and colony formation in soft agar induced by Apc siRNA treatment in ApcMin/+ cells. Therefore, Arrb2 is essential for the initiation and growth of…

Advisors/Committee Members: Joubert, Dominique (thesis director).

Subjects/Keywords: Β-arrestine2; Cancer colorectal; Voie Wnt/β-caténine; Tumorigenèse intestinale; Β-arrestin2; Colorectal cancer; Wnt/β-catenin pathway; Intestinal tumorigenesis

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

APA (6^th Edition):

Flacelière, M. (2012). La β-arrestine2, un acteur majeur de la tumorigenèse intestinale dépendante de la voie Wnt/β-caténine. : β-arrestine2, a major actor of the Wnt/β-catenin-dependent intestinal tumorigenesis. (Doctoral Dissertation). Université Montpellier II. Retrieved from http://www.theses.fr/2012MON20012

Chicago Manual of Style (16^th Edition):

Flacelière, Maud. “La β-arrestine2, un acteur majeur de la tumorigenèse intestinale dépendante de la voie Wnt/β-caténine. : β-arrestine2, a major actor of the Wnt/β-catenin-dependent intestinal tumorigenesis.” 2012. Doctoral Dissertation, Université Montpellier II. Accessed February 28, 2021. http://www.theses.fr/2012MON20012.

MLA Handbook (7^th Edition):

Flacelière, Maud. “La β-arrestine2, un acteur majeur de la tumorigenèse intestinale dépendante de la voie Wnt/β-caténine. : β-arrestine2, a major actor of the Wnt/β-catenin-dependent intestinal tumorigenesis.” 2012. Web. 28 Feb 2021.

Vancouver:

Flacelière M. La β-arrestine2, un acteur majeur de la tumorigenèse intestinale dépendante de la voie Wnt/β-caténine. : β-arrestine2, a major actor of the Wnt/β-catenin-dependent intestinal tumorigenesis. [Internet] [Doctoral dissertation]. Université Montpellier II; 2012. [cited 2021 Feb 28]. Available from: http://www.theses.fr/2012MON20012.

Council of Science Editors:

Flacelière M. La β-arrestine2, un acteur majeur de la tumorigenèse intestinale dépendante de la voie Wnt/β-caténine. : β-arrestine2, a major actor of the Wnt/β-catenin-dependent intestinal tumorigenesis. [Doctoral Dissertation]. Université Montpellier II; 2012. Available from: http://www.theses.fr/2012MON20012

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

22. Sklavos, Argyrios. Ο ρόλος του Wnt/β-catenin και του εκλεκτικού αναστολέα του στη μετάδοση του σήματος του ηπατοκυτταρικού καρκίνου: πειραματική μελέτη σε μύες.

Degree: 2018, Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ)

URL: http://hdl.handle.net/10442/hedi/43345

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Recent evidence has suggested that downregulation of the Wnt/βcatenin signaling pathway may contribute to the development and growth of HCC. Consequently, elements of this pathway… (more)

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Recent evidence has suggested that downregulation of the Wnt/βcatenin signaling pathway may contribute to the development and growth of HCC. Consequently, elements of this pathway have begun to emerge as potential targets for improving outcomes of antiHCC. Thus, the present study sought to examine the effects of Wnt1 blockade using the classical diethylnitrosamine (DEN)induced chemical carcinogenesis mouse model of HCC. The depletion of Wnt1 using neutralizing antisera was done for ten consecutive days at the age of 9 months and mice were examined for the following 20 days. At that time, DENtreated mice had multiple variablysized hepatic cell adenomas. AntiWnt1 was particularly potent in suppressing the expression of critical elements of the Wnt/βcatenin signaling pathway, such as βcatenin and Frizzled1 receptor, however, not Dickkopfrelated protein 1. This effect coexisted with the suppression of Cyclin D1, FOXM1, NFκΒ and cJun commensurate with proliferation and apoptosis blockade in hepatocellular adenomas, and reduced Bcl2 and cMet in the serum of mice. Nonetheless, tumor size and multiplicity were found to be unaffected, suggesting that apoptosis may be equally important to proliferation in the context of counteracting DEN induced hepatocellular adenomas of mice.

Πρόσφατα δεδομένα υποδεικνύουν ότι η μειορρύθμιση του μονοπατιού μοριακής σηματοδότησης Wnt/β-catenin μπορεί να παίζει ρόλο στη δημιουργία και ανάπτυξη του ηπατοκυτταρικού καρκίνου. Κατά συνέπεια τα στοιχεία που εμπλέκονται στο μονοπάτι θεωρήθηκαν ως πιθανοί στόχοι για τη βελτίωση των αποτελεσμάτων της αντιμετώπισης και θεραπείας του ηπατοκυτταρικού καρκίνου. Υπό το φως αυτών των δεδομένων η παρούσα εργασία εξετάζει τα αποτελέσματα της αναστολής του σήματος του Wnt/β-catenin, σε ένα κλασσικό χημικά επαγόμενο (DEN) μοντέλο καρκινογένεσης –δημιουργίας ηπατοκυτταρικού καρκίνου σε μύες. Η εξάλειψη του Wnt/β-catenin επιτεύχθηκε με τη χορήγηση αντι-ορού (Anti-Wnt-1) για 10 συνεχόμενες ημέρες στην ηλικία των 9 μηνών και οι μύες εξετάστηκαν 20 ημέρες μετά. Σ’ αυτό το χρονικό σημείο οι μύες στους οποίους είχε χορηγηθεί DEN εξετάστηκαν και διαπιστώθηκε ότι είχαν αναπτύξει πολλαπλά και ποικίλων μεγεθών ηπατοκυτταρικά αδενώματα. Η χορήγηση του Anti-Wnt-1 είχε σαν αποτέλεσμα την καταστολή σημαντικών στοιχείων του μοριακού μονοπατιού Wnt/β-catenin όπως η β-catenin και ο υποδοχέας Frizzled-1, όχι όμως και την Dickkopf σχετιζόμενη πρωτεΐνη 1. Αυτό το αποτέλεσμα συνυπήρχε με την καταστολή της Cyclin D1, του FOXM1, του NF-κΒ και του c-Jun, αντίστοιχα με την καταστολή του πολλαπλασιασμού και της απόπτωσης στα ηπατοκυτταρικά αδενώματα και τη μείωση των Bcl-2 και c-Met στον ορό των μυών. Εν τούτοις το μέγεθος και ο αριθμός των όγκων δεν επηράστηκαν, γεγονός που υποδεικνύει ότι η απόπτωση είναι εξίσου σημαντική με τον πολλαπλασιασμό, στο πλαίσιο της δράσης εναντίων των επαγόμενων μετά από χορήγηση DEN, ηπατοκυτταρικών αδενωμάτων σε μύες.

Subjects/Keywords: Μοριακό μονοπάτι Wnt/β-catenin; Μειορρύθμιση; Πολλαπλασιασμός; Απόπτωση; Wnt/β-catenin molecular pathway; Downregulation; Proliferation; Apoptosis

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

APA (6^th Edition):

Sklavos, A. (2018). Ο ρόλος του Wnt/β-catenin και του εκλεκτικού αναστολέα του στη μετάδοση του σήματος του ηπατοκυτταρικού καρκίνου: πειραματική μελέτη σε μύες. (Thesis). Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ). Retrieved from http://hdl.handle.net/10442/hedi/43345

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):

Sklavos, Argyrios. “Ο ρόλος του Wnt/β-catenin και του εκλεκτικού αναστολέα του στη μετάδοση του σήματος του ηπατοκυτταρικού καρκίνου: πειραματική μελέτη σε μύες.” 2018. Thesis, Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ). Accessed February 28, 2021. http://hdl.handle.net/10442/hedi/43345.

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

MLA Handbook (7^th Edition):

Sklavos, Argyrios. “Ο ρόλος του Wnt/β-catenin και του εκλεκτικού αναστολέα του στη μετάδοση του σήματος του ηπατοκυτταρικού καρκίνου: πειραματική μελέτη σε μύες.” 2018. Web. 28 Feb 2021.

Vancouver:

Sklavos A. Ο ρόλος του Wnt/β-catenin και του εκλεκτικού αναστολέα του στη μετάδοση του σήματος του ηπατοκυτταρικού καρκίνου: πειραματική μελέτη σε μύες. [Internet] [Thesis]. Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ); 2018. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/10442/hedi/43345.

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

Council of Science Editors:

Sklavos A. Ο ρόλος του Wnt/β-catenin και του εκλεκτικού αναστολέα του στη μετάδοση του σήματος του ηπατοκυτταρικού καρκίνου: πειραματική μελέτη σε μύες. [Thesis]. Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ); 2018. Available from: http://hdl.handle.net/10442/hedi/43345

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

University of Vienna

23. Vonbrüll, Matthias. Manipulation of Wnt signaling in tumorcells with antisense molecules.

Degree: 2018, University of Vienna

URL: http://othes.univie.ac.at/53305/

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Seit der Erfindung von Antisense Molekülen gab es zahlreiche Versuche diese therapeutisch anzuwenden. Die FDA Zulassungen von Fomivirsen, Pegaptanib und Mipomersen heben das große Potential… (more)

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Seit der Erfindung von Antisense Molekülen gab es zahlreiche Versuche diese therapeutisch anzuwenden. Die FDA Zulassungen von Fomivirsen, Pegaptanib und Mipomersen heben das große Potential von Antisense Molekülen hervor. Trotzdem war die Ausbeute an Anwendungen, gemessen an den unternommenen Anstrengungen, bescheiden. Durch die stetige Entwicklung neuer Targeting-Strategien und Modifikationen der Moleküle ist ein Bedarf an zuverlässigen Assays entstanden. In Bezug auf neue Tumortherapien ist der Wnt Signalweg von großem Interesse, da er in viele Erkrankungen, unter anderem Krebs, involviert ist. β-catenin spielt eine Schlüsselrolle in diesem Signalweg und ist bei vielen Krebsarten aktiv. In diesem Projekt wurde eine Antisense Strategie mit Peptide Nucleic Acids (PNAs) für das Targeting des Splicings von β-catenin gewählt. Dafür wurde ein splice-basierter Reporterassay entwickelt und optimiert. Nachdem der Assay eine zuverlässige Quantifizierung der Effekte von Antisense Molekülen erlaubte, wurde er verwendet um verschiedene PNAs zu testen, mit Zielsequenzen auf β-catenin. Dabei erwies sich der Splicedonor von Exon 13 auf β-catenin als ideal, da dies zu einer verkürzten Version von β-catenin führt. Diese behält ihre Interaktion mit Tcf/Lef Proteinen, verliert jedoch die Transaktivierungsfunktion des C-Terminus. Dadurch konkurriert das Protein mit der Wildtyp-Version von β-catenin und führt somit zu einem dominant negativen Effekt. In dieser Strategie liegt großes Potential für zukünftige Projekte mit β-catenin als Target-Gen. Diese Arbeit zeigt einen neuartigen Reporterassay zur genauen Detektion von Antisense Effekten sowie eine interessante Targeting-Strategie für β-catenin, die für zukünftige Projekte anwendbar ist.

Since the invention of antisense molecules there have been numerous attempts to apply them therapeutically. The FDA approvals of Fomivirsen, Pegaptanib and Mipomersen point out the great potential of antisense molecules. However, compared to the efforts made the output has been modest so far. But new targeting strategies have been developed and new modifications to the molecules are available thereby creating a demand on reliable assays to test them. When it comes to potential new tumor therapies the canonical Wnt signaling pathway is of great interest since it is involved in a number of diseases including cancer. β-catenin is a key player in this pathway and is found to be activated in many cancer types. In this project, an antisense strategy was selected targeting the splicing of β-catenin with peptide nucleic acids (PNAs). For this purpose, a splice based reporter assay was designed and optimised in this project. After the essay enabled a reliable quantification of the effect of antisense molecules, we used it to screen different PNAs targeting multiple sites within β-catenin. Targeting of the splice donor of exon 13 of β-catenin turned out to be ideal, because it leads to a truncated version of the protein that retains its interaction with Tcf/Lef proteins, but lacks the C-terminally…

Subjects/Keywords: 42.13 Molekularbiologie; Antisense Molekül / β-catenin / Morpholino / PNA / Wnt Signalweg; Antisense / β-catenin / Morpholino / PNA / Wnt signaling

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

APA (6^th Edition):

Vonbrüll, M. (2018). Manipulation of Wnt signaling in tumorcells with antisense molecules. (Thesis). University of Vienna. Retrieved from http://othes.univie.ac.at/53305/

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):

Vonbrüll, Matthias. “Manipulation of Wnt signaling in tumorcells with antisense molecules.” 2018. Thesis, University of Vienna. Accessed February 28, 2021. http://othes.univie.ac.at/53305/.

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

MLA Handbook (7^th Edition):

Vonbrüll, Matthias. “Manipulation of Wnt signaling in tumorcells with antisense molecules.” 2018. Web. 28 Feb 2021.

Vancouver:

Vonbrüll M. Manipulation of Wnt signaling in tumorcells with antisense molecules. [Internet] [Thesis]. University of Vienna; 2018. [cited 2021 Feb 28]. Available from: http://othes.univie.ac.at/53305/.

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

Council of Science Editors:

Vonbrüll M. Manipulation of Wnt signaling in tumorcells with antisense molecules. [Thesis]. University of Vienna; 2018. Available from: http://othes.univie.ac.at/53305/

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

24. Le Rolle, Morgane. Voie de signalisation WNT/ β-catenin et différenciation des cellules germinales chez les mammifères : WNT/β-catenin signaling pathway and germ cell differentiation in mammals.

Degree: Docteur es, Sciences de la vie et de la santé, 2019, Université Côte d'Azur (ComUE)

URL: http://www.theses.fr/2019AZUR6014

► La préservation de la fertilité suscite une inquiétude croissante. Depuis les dernières décennies, la fertilité a diminué dans les pays industrialisés. En conséquence, un nombre… (more)

▼ La préservation de la fertilité suscite une inquiétude croissante. Depuis les dernières décennies, la fertilité a diminué dans les pays industrialisés. En conséquence, un nombre croissant de couples a recours à la procréation médicalement assistée, sans grand succès par manque de connaissances sur les cellules reproductrices (cellules germinales). L’étude de ces cellules constitue un socle essentiel pour des applications médicales, mais jusqu’à présent, les mécanismes moléculaires qui régissent leur développement restent peu compris en raison de l’absence de modèles d'étude physiologiques.Les cellules germinales sont produites au cours du développement embryonnaire, se multiplient pour constituer un stock suffisant, se différencient dans la gonade en fonction du sexe de l'embryon, puis entrent en méiose pour devenir des gamètes fertiles, les ovocytes (femelles) et les spermatozoïdes (mâles). Mon laboratoire d’accueil a démontré que la voie de signalisation canonique WNT/β-catenin est nécessaire au développement de l'ovaire in vivo et qu'en absence d'activation de cette voie dans l'ovaire embryonnaire de souris, la prolifération et la différenciation des cellules germinales primordiales sont perturbées.Tirant partie de notre expertise dans l'analyse de modèles de différenciation gonadique, nous nous sommes intéressés au mécanisme d'action de la voie WNT/β-catenin dans la différenciation des cellules germinales, en analysant au moyen de modèles murins de perte et gain de fonction de β-catenin les conséquences de la modification de son expression dans les cellules de la gonade.Dans un premier temps, nous avons démontré que le maintien, après la naissance, de l'activité de la voie WNT/β-catenin dans les cellules souches spermatogoniales du testicule de souris stimule leur prolifération de manière massive, provoquant un défaut de différenciation en spermatozoïdes. Dans un deuxième temps, nous avons montré que l'ablation génétique du gène Ctnnb1 (codant pour β-catenin) dans les cellules germinales primordiales in vivo entraîne une perte précoce de leur pluripotence et une différenciation prématurée en ovogonies. Nous avons démontré, pour la première fois in vivo, que tandis que le développement ovarien progresse, β-catenin forme des complexes protéiques avec POU5F1 et CDH1 qui transitent du noyau des cellules germinales à leur membrane, permettant ainsi leur sortie de pluripotence et leur différenciation. Nos résultats indiquent que l'E3-ubiquitine ligase ZNRF3 régule la pluripotence des cellules germinales par une boucle de rétroaction négative.Ces données indiquent que dans l'ovaire comme dans le testicule, une régulation fine de l'activité de la voie de signalisation WNT/β-catenin est requise pour déterminer la fenêtre de différenciation des cellules germinales primordiales in vivo. De plus, la voie WNT/β-catenin contrôle la sortie de pluripotence des cellules germinales primordiales via une activité non-transcriptionnelle de β-catenin, permettant à terme de coordonner le développement des cellules somatiques et… Advisors/Committee Members: Chassot, Anne-Amandine (thesis director).

Subjects/Keywords: Cellules germinales; Ovaire; WNT/β-catenin; POU5F1; Fertilité; Germ cells; Ovary; WNT/β-catenin; POU5F1; Pluripotency; Fertility

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

APA (6^th Edition):

Le Rolle, M. (2019). Voie de signalisation WNT/ β-catenin et différenciation des cellules germinales chez les mammifères : WNT/β-catenin signaling pathway and germ cell differentiation in mammals. (Doctoral Dissertation). Université Côte d'Azur (ComUE). Retrieved from http://www.theses.fr/2019AZUR6014

Chicago Manual of Style (16^th Edition):

Le Rolle, Morgane. “Voie de signalisation WNT/ β-catenin et différenciation des cellules germinales chez les mammifères : WNT/β-catenin signaling pathway and germ cell differentiation in mammals.” 2019. Doctoral Dissertation, Université Côte d'Azur (ComUE). Accessed February 28, 2021. http://www.theses.fr/2019AZUR6014.

MLA Handbook (7^th Edition):

Le Rolle, Morgane. “Voie de signalisation WNT/ β-catenin et différenciation des cellules germinales chez les mammifères : WNT/β-catenin signaling pathway and germ cell differentiation in mammals.” 2019. Web. 28 Feb 2021.

Vancouver:

Le Rolle M. Voie de signalisation WNT/ β-catenin et différenciation des cellules germinales chez les mammifères : WNT/β-catenin signaling pathway and germ cell differentiation in mammals. [Internet] [Doctoral dissertation]. Université Côte d'Azur (ComUE); 2019. [cited 2021 Feb 28]. Available from: http://www.theses.fr/2019AZUR6014.

Council of Science Editors:

Le Rolle M. Voie de signalisation WNT/ β-catenin et différenciation des cellules germinales chez les mammifères : WNT/β-catenin signaling pathway and germ cell differentiation in mammals. [Doctoral Dissertation]. Université Côte d'Azur (ComUE); 2019. Available from: http://www.theses.fr/2019AZUR6014

University of Helsinki

25. Diaz, Heli. Ravintotekijöiden vaikutus β-kateniinin aminohappotähteiden fosforylaatioon paksusuolisyöpämalleissa: The effect of dietary components on phosphorylation of β-catenin in colon cancer models.

Degree: Department of Food and Environmental Sciences; Helsingfors universitet, Agrikultur- och forstvetenskapliga fakulteten, Institutionen för livsmedels- och miljövetenskaper, 2014, University of Helsinki

URL: http://hdl.handle.net/10138/45423

► Background Protein called ?-catenin has the key role in the Wnt signaling pathway which induces cell division and growth. The disruption of the ?-catenin degradation… (more)

▼ Background Protein called ?-catenin has the key role in the Wnt signaling pathway which induces cell division and growth. The disruption of the ?-catenin degradation can lead to uncontrolled cell division and development of colon cancer due to ?-catenin´s ability to enhance the expression of the proto-oncogenes in Wnt singaling pathway. Cells control ?-catenin by degradation and phosphorylation. Phosphorylated ?-catenin at serine675 and serine552 residues increases proto-oncogene expression, and thereby promotes colon cancer formation. At present, only few research articles have addressed whether diet can affect the phosphorylation status of ?-catenin in the intestinal mucosa. Objective The objective of the master´s thesis was to develop fluorescence-based western blotting method to analyze phosphorylated ?-catenin forms from colon cancer cell and intestinal mucosa tissue samples. Optimized method was used to analyze phospho-Ser675- and phospho-Ser552-?-catenin from samples derived from two dietary studies conducted with ApcMin mice. The aim of this was to determine whether dietary components have effect on phosphorylation of ?-catenin in the intestinal mucosa tissue and whether phosphorylated ?-catenin correlated with intestinal adenoma number and size. Materials and methods Fluorescence-based western blotting method was developed to analyze all the ?-catenin phosphorylation forms that can be detected by using commercially available antibodies (Ser33/37/Thr41, Thr41/Ser45, Ser552, Ser675 and Tyr654). Phospho-?-catenin was measured from samples obtained from colon cancer cells lines and intestinal mucosa tissue of ApcMin mice (a model of colon cancer). Optimized method was used to analyze ?-catenin, phospho-Ser675- and phospho-Ser552-?-catenin levels from normal intestinal mucosa samples of ApcMin mice originated from two dietary studies. In the first study mice were fed 0,8 % plant stanol diet and in the second study mice were fed western type diet which contained high levels of fat and saturated fat and low levels of calcium and vitamin D3. The aim of the two studies was to determine whether plant stanol and western type diet have effect on tumor formation. Statistical analyses were made by using Mann-Whitney U test and Spearman correlation (PASW Statistics 18.0 software). Results By using fluorescence-based western blotting method phospho-Ser675- and phospho-Ser552-?-catenin were detected in cell and mouse samples as well as phospho-Ser33/37/Thr41-?-catenin in cell samples. The method could not be optimized for the detection of phospho-Tyr654- and phospho-Thr41/Ser45-?-catenin in cell and mouse samples and phospho-Ser33/37/Thr41-?-catenin in mouse samples. However, phospho-Thr41/Ser45-?-catenin was detected in cell samples but not in mouse samples by using the chemiluminescence-based western blotting method. The adenoma number was significantly higher in mice fed plant stanol diet than in control mice (p=0,002). Plant stanol diet resulted in significantly higher levels of ?-catenin…

Subjects/Keywords: Ser675; Ser552; β-catenin; phosphorylation; colon cancer; β-kateniini; fosforylaatio; suolistosyöpä; Näringslära; Nutrition; Ravitsemustiede

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

APA (6^th Edition):

Diaz, H. (2014). Ravintotekijöiden vaikutus β-kateniinin aminohappotähteiden fosforylaatioon paksusuolisyöpämalleissa: The effect of dietary components on phosphorylation of β-catenin in colon cancer models. (Masters Thesis). University of Helsinki. Retrieved from http://hdl.handle.net/10138/45423

Chicago Manual of Style (16^th Edition):

Diaz, Heli. “Ravintotekijöiden vaikutus β-kateniinin aminohappotähteiden fosforylaatioon paksusuolisyöpämalleissa: The effect of dietary components on phosphorylation of β-catenin in colon cancer models.” 2014. Masters Thesis, University of Helsinki. Accessed February 28, 2021. http://hdl.handle.net/10138/45423.

MLA Handbook (7^th Edition):

Diaz, Heli. “Ravintotekijöiden vaikutus β-kateniinin aminohappotähteiden fosforylaatioon paksusuolisyöpämalleissa: The effect of dietary components on phosphorylation of β-catenin in colon cancer models.” 2014. Web. 28 Feb 2021.

Vancouver:

Diaz H. Ravintotekijöiden vaikutus β-kateniinin aminohappotähteiden fosforylaatioon paksusuolisyöpämalleissa: The effect of dietary components on phosphorylation of β-catenin in colon cancer models. [Internet] [Masters thesis]. University of Helsinki; 2014. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/10138/45423.

Council of Science Editors:

Diaz H. Ravintotekijöiden vaikutus β-kateniinin aminohappotähteiden fosforylaatioon paksusuolisyöpämalleissa: The effect of dietary components on phosphorylation of β-catenin in colon cancer models. [Masters Thesis]. University of Helsinki; 2014. Available from: http://hdl.handle.net/10138/45423

Université Paris-Sud – Paris XI

26. Sartor, Chiara. Hnf4α and Choline Metabolism Role in β-catenin Activated Liver Carcinogenesis : Le rôle d’Hnfα et du métabolisme de la choline dans les carcinomes hépatocellulaires activés pas la β-caténine.

Degree: Docteur es, Aspects moléculaires et cellulaires de la biologie, 2015, Université Paris-Sud – Paris XI

URL: http://www.theses.fr/2015PA11T046

► La voie de signalisation WNT/β-caténine est impliquée dans de nombreuses processi cellulaires, du développement à la physiologie. Dans le foie adulte, elle est nécessaire pour… (more)

▼ La voie de signalisation WNT/β-caténine est impliquée dans de nombreuses processi cellulaires, du développement à la physiologie. Dans le foie adulte, elle est nécessaire pour établir et maintenir la zonation métabolique, condition préalable pour la fonctionnalité de l’organe, mais elle est aussi cause d’un pourcentage non négligeable (11-32%) de carcinomes hépatocellulaires (CHC), qui surviennent après mutation activatrice du gène codant la β-caténine. Mes travaux se sont inscrits dans la continuité de travaux de l’équipe auxquels j’ai participé , et ont eu pour principaux objectifs : (1) d’explorer le rôle du facteur de transcription Hnf4α dans la physiologie et les cancers du foie, en lien avec la signalisation β-caténine ; (2) de déterminer si une imagerie tumorale par tomographie par émission de positrons (TEP) spécifique de la captation de choline pouvait prédire les CHC mutés pour la β-caténine et si le métabolisme de la choline pouvait présenter une piste thérapeutique des cancers du foie.Pour ces deux projets, j’ai eu accès à des cohortes de patients atteints de cancers du foie, mais j’ai également pu bénéficier du modèle gain-de-fonction de la β-caténine développé au laboratoire, qui consiste en une perte du suppresseur de tumeur Apc, frein majeur de la voie β-caténine conduisant à des cancers du foie. Grâce à un modèle d’invalidation hepato-spécifique et conditionnelle du gène Hnf4α, j’ai pu prouver que la perte de Hnf4α mène à une augmentation de la prolifération, du stockage des lipides dans le foie et à une désorganisation de l’architecture zonale hépatique, en particulier celle de la triade portale. J’ai aussi démontré que dans un contexte de carcinome murin invalidé par Apc, le rôle suppresseur de tumeur d’Hnf4α était mineur.Une approche métabolomique avait montré qu’un signal β-caténine perturbait le métabolisme des phospholipides dérivant de la choline. Grâce à une étude parallèle réalisée chez des patients porteurs de CHC d’une part, et dans nos modèles murins d’autre part, nous avons pu mettre en évidence par TEP une fixation accrue de la F-choline dans les tumeurs activées β-caténine. Ce phénotype est spécifique d’une signalisation β-caténine active puisque cette captation accrue n’était pas présente chez les patients porteurs de carcinome hépatocellulaire non mutés ou chez les souris présentant une cancérogenèse indépendante de la β-caténine (modèle DEN). J’ai ensuite étudié le devenir intracellulaire de la choline. En utilisant de la choline radiomarquée j’ai montré in vitro qu’un signal β-caténine aberrant accroit l’incorporation de choline dans les phospholipides, et accroit également son rôle de donneur de groupements méthyles, participant à la méthylation de l’ADN. Cela pourrait expliquer pourquoi l’ADN est hyperméthylé chez les souris avec la perte d’Apc, puisque l’administration d’un régime sans choline et methionine à ces souris réverse le phénotype d’hyperméthylation. L’ensemble de ces résultats suggère que la choline pourrait jouer un rôle important dans la cancérogenèse liée à la… Advisors/Committee Members: Colnot, Sabine (thesis director).

Subjects/Keywords: Foie; Carcinome hépatocellulaire; Β-caténine; Hnf4α; Liver; Hepatocellular carcinoma; Β-catenin; Hnf4α

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

APA (6^th Edition):

Sartor, C. (2015). Hnf4α and Choline Metabolism Role in β-catenin Activated Liver Carcinogenesis : Le rôle d’Hnfα et du métabolisme de la choline dans les carcinomes hépatocellulaires activés pas la β-caténine. (Doctoral Dissertation). Université Paris-Sud – Paris XI. Retrieved from http://www.theses.fr/2015PA11T046

Chicago Manual of Style (16^th Edition):

Sartor, Chiara. “Hnf4α and Choline Metabolism Role in β-catenin Activated Liver Carcinogenesis : Le rôle d’Hnfα et du métabolisme de la choline dans les carcinomes hépatocellulaires activés pas la β-caténine.” 2015. Doctoral Dissertation, Université Paris-Sud – Paris XI. Accessed February 28, 2021. http://www.theses.fr/2015PA11T046.

MLA Handbook (7^th Edition):

Sartor, Chiara. “Hnf4α and Choline Metabolism Role in β-catenin Activated Liver Carcinogenesis : Le rôle d’Hnfα et du métabolisme de la choline dans les carcinomes hépatocellulaires activés pas la β-caténine.” 2015. Web. 28 Feb 2021.

Vancouver:

Sartor C. Hnf4α and Choline Metabolism Role in β-catenin Activated Liver Carcinogenesis : Le rôle d’Hnfα et du métabolisme de la choline dans les carcinomes hépatocellulaires activés pas la β-caténine. [Internet] [Doctoral dissertation]. Université Paris-Sud – Paris XI; 2015. [cited 2021 Feb 28]. Available from: http://www.theses.fr/2015PA11T046.

Council of Science Editors:

Sartor C. Hnf4α and Choline Metabolism Role in β-catenin Activated Liver Carcinogenesis : Le rôle d’Hnfα et du métabolisme de la choline dans les carcinomes hépatocellulaires activés pas la β-caténine. [Doctoral Dissertation]. Université Paris-Sud – Paris XI; 2015. Available from: http://www.theses.fr/2015PA11T046

27. Bertrand, Juliette. Rôle de Dicer dans la pigmentation et sa régulation par les UVB dans le lignage mélanocytaire : Role of Dicer in pigmentation and its regulation by UVB in the melanocyte lineage.

Degree: Docteur es, Biologie cellulaire et moléculaire, 2017, Sorbonne Paris Cité

URL: http://www.theses.fr/2017USPCB019

►

Les mélanocytes, cellules responsables de la pigmentation de la peau et des poils, protègent les cellules des stress environnementaux, en particulier des rayonnements ultra-violets (UV)… (more)

▼

Les mélanocytes, cellules responsables de la pigmentation de la peau et des poils, protègent les cellules des stress environnementaux, en particulier des rayonnements ultra-violets (UV) présents à la surface de la Terre. Les UV induisent des dommages moléculaires et régulent de nombreuses voies de signalisation en aval de MC1R, MAPK, PI3K, ou PKC. A court terme, les UV peuvent induire la mélanogenèse et à long terme participent à la mélanomagenèse. Dicer, protéine clef de la maturation des microARN, est régulée par différents stress. La protéine multifonctionnelle β-caténine est impliquée dans le développement des mélanocytes. Ces deux protéines participent à la régulation fine de l'expression génique. L'objectif de cette thèse est de mettre en évidence le rôle et la régulation de Dicer dans le lignage mélanocytaire dans des conditions normales et de stress (UVB). Dans une première partie, nous nous sommes intéressés au rôle de Dicer dans la pigmentation et sa régulation dans le lignage mélanocytaire. Nous avons montré, in vivo dans un modèle murin, que Dicer est nécessaire à la fois à la mise en place du lignage mélanocytaire et au fonctionnement de ce lignage chez l'adulte. L'absence de Dicer dans le lignage mélanocytaire affecte la localisation des mélanocytes de la papille dermique du follicule pileux et empêche la pigmentation du poil. In vitro, la transcription de Dicer est régulée par différentes voies, en particulier par les protéines PI3K, RSK, GSK3β et β-caténine. L'activité répressive de β-caténine sur la transcription de Dicer est dépendante de sites LEF/TCF. Dans une deuxième partie, nous nous sommes intéressés à l'implication de Dicer, en relation avec β-caténine, dans la réponse aux UVB. Nous avons mis en évidence in vivo et in vitro la relocalisation nucléaire et l'activation transcriptionnelle de β-caténine induites par les UV. Tout comme β-caténine, les UVB répriment la migration des mélanocytes in vitro. Nous avons montré in vitro que les UVB répriment l'expression de Dicer et que cette répression est dépendante de sites de fixation de facteurs de transcription, dont LEF/TCF, présents dans la région promotrice de Dicer. Une diminution de Dicer participe à la protection des mélanocytes contre les UVB. Ce travail de thèse a donc permis de montrer le rôle de Dicer dans la pigmentation adulte et de mettre en évidence des voies de régulation de l'expression de Dicer dans les mélanocytes non stressés et dans les mélanocytes soumis à un stress UVB.

Melanocytes, cells responsible for pigmentation of the skin and hair, protect cells from environmental stress, especially ultra-violet radiations (UV) present on Earth floor. UV induce molecular damages and regulate many signaling pathways downstream of MC1R, MAPK, PI3K, or PKC. In the short term, UV can increase melanogenesis and in the long term, participate in melanomagenesis. Dicer, a key protein involved in microRNA maturation, is regulated by different types of stress. The multifunctional protein β-catenin is implicated in melanocyte development. These…

Advisors/Committee Members: Larue, Lionel (thesis director).

Subjects/Keywords: Mélanocyte; Pigmentation; UVB; Β-caténine; Dicer; Melanocyte; Pigmentation; UVB; Β-catenin; Dicer; 616.989

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

APA (6^th Edition):

Bertrand, J. (2017). Rôle de Dicer dans la pigmentation et sa régulation par les UVB dans le lignage mélanocytaire : Role of Dicer in pigmentation and its regulation by UVB in the melanocyte lineage. (Doctoral Dissertation). Sorbonne Paris Cité. Retrieved from http://www.theses.fr/2017USPCB019

Chicago Manual of Style (16^th Edition):

Bertrand, Juliette. “Rôle de Dicer dans la pigmentation et sa régulation par les UVB dans le lignage mélanocytaire : Role of Dicer in pigmentation and its regulation by UVB in the melanocyte lineage.” 2017. Doctoral Dissertation, Sorbonne Paris Cité. Accessed February 28, 2021. http://www.theses.fr/2017USPCB019.

MLA Handbook (7^th Edition):

Bertrand, Juliette. “Rôle de Dicer dans la pigmentation et sa régulation par les UVB dans le lignage mélanocytaire : Role of Dicer in pigmentation and its regulation by UVB in the melanocyte lineage.” 2017. Web. 28 Feb 2021.

Vancouver:

Bertrand J. Rôle de Dicer dans la pigmentation et sa régulation par les UVB dans le lignage mélanocytaire : Role of Dicer in pigmentation and its regulation by UVB in the melanocyte lineage. [Internet] [Doctoral dissertation]. Sorbonne Paris Cité; 2017. [cited 2021 Feb 28]. Available from: http://www.theses.fr/2017USPCB019.

Council of Science Editors:

Bertrand J. Rôle de Dicer dans la pigmentation et sa régulation par les UVB dans le lignage mélanocytaire : Role of Dicer in pigmentation and its regulation by UVB in the melanocyte lineage. [Doctoral Dissertation]. Sorbonne Paris Cité; 2017. Available from: http://www.theses.fr/2017USPCB019

28. Parisi, Alice. Defining the role of APC and canonical WNT signaling in embryonic and adult myogenesis : Etude du rôle d'APC et de la voie de signalisation WNT au cours de la myogenèse embryonnaire et adulte.

Degree: Docteur es, Biologie cellulaire, 2014, Université Paris Descartes – Paris V

URL: http://www.theses.fr/2014PA05T033

► La voie de signalisation Wnt/β-caténine (Wnt canonique) est impliquée dans une grande variété de fonctions biologiques, entre autres dans l’établissement des axes embryonnaires, l’organogenèse et… (more)

▼ La voie de signalisation Wnt/β-caténine (Wnt canonique) est impliquée dans une grande variété de fonctions biologiques, entre autres dans l’établissement des axes embryonnaires, l’organogenèse et l’homéostasie de cellules souches adultes. En absence de signaux Wnt, un complexe multiprotéique comprenant le suppresseur de tumeur Adenomatous Polyposis Coli (APC) marque la β-caténine pour la dégradation protéasomique. L’activation de la voie Wnt canonique induit un arrêt de la dégradation de la β-caténine, qui s’accumule dans le noyau, où elle active l’expression de gènes cibles de Wnt. Au cours de la myogenèse embryonnaire, processus pendant lequel le muscle squelettique est formé, une partie des cellules pluripotentes du dermomyotome acquièrt l’identité musculaire, se différencie et forme les myofibres, les unités fonctionnelles du muscle squelettique. La myogenèse n’est pas confinée qu’à la période embryonnaire. En effet, elle peut être réactivée dans le muscle adulte suite à une lésion ou dans certaines conditions pathologiques. Dans ce contexte, les cellules souches du muscle squelettique, appelées cellules satellites, sortent de leur quiescence et génèrent des progéniteurs myogéniques qui prolifèrent et se différencient en formant de nouvelles myofibres pour réparer le tissu. De plus, une partie des progéniteurs myogéniques retournent à l’état quiescent, renouvelant ainsi la population de cellules souches résidentes. Le rôle de la voie de signalisation Wnt/β-caténine dans l’engagement des cellules pluripotentes du dermomyotome vers le destin myogénique demeure méconnu. De même, la fonction de la voie Wnt canonique dans les cellules satellites au cours de la régénération du muscle squelettique adulte reste à l’heure actuelle controversée, car différentes approches sont parvenues à des conclusions contradictoires. Grâce à des modèles génétiques murins, nous avons caractérisé le rôle précis de la voie Wnt canonique au cours de la myogenèse embryonnaire et adulte. Nous montrons in vivo que l’hyperactivation constitutive de la voie de signalisation Wnt/β-caténine induite par l’inactivation conditionnelle d’APC, le principal régulateur négatif de la cascade, se traduit par un défaut majeur de formation et de régénération du muscle squelettique. Nos résultats ex vivo et in vitro démontrent que l’hyperactivation de la voie Wnt canonique altère la progression du cycle cellulaire et entraîne la mort par apoptose. De plus, l’inactivation conditionnelle de la β-caténine n’affecte pas la prolifération des progéniteurs myogéniques mais perturbe leur différenciation. Globalement, nos résultats suggèrent deux rôles différents de la voie de signalisation Wnt/β-caténine dans le muscle squelettique. D’une part, l’inhibition de la voie Wnt canonique est nécessaire au cours de l’initiation de la myogenèse pour permettre l’engagement myogénique des cellules pluripotentes du dermomyotome et l’activation des cellules satellites. D’autre part, la voie de signalisation Wnt/β-caténine est requise à la fois dans les progéniteurs musculaires… Advisors/Committee Members: Le Grand, Fabien (thesis director).

Subjects/Keywords: Muscle squelettique; APC; WNT; Β-caténine; Skeletal muscle; APC; WNT; Β-catenin; 571.6

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

APA (6^th Edition):

Parisi, A. (2014). Defining the role of APC and canonical WNT signaling in embryonic and adult myogenesis : Etude du rôle d'APC et de la voie de signalisation WNT au cours de la myogenèse embryonnaire et adulte. (Doctoral Dissertation). Université Paris Descartes – Paris V. Retrieved from http://www.theses.fr/2014PA05T033

Chicago Manual of Style (16^th Edition):

Parisi, Alice. “Defining the role of APC and canonical WNT signaling in embryonic and adult myogenesis : Etude du rôle d'APC et de la voie de signalisation WNT au cours de la myogenèse embryonnaire et adulte.” 2014. Doctoral Dissertation, Université Paris Descartes – Paris V. Accessed February 28, 2021. http://www.theses.fr/2014PA05T033.

MLA Handbook (7^th Edition):

Parisi, Alice. “Defining the role of APC and canonical WNT signaling in embryonic and adult myogenesis : Etude du rôle d'APC et de la voie de signalisation WNT au cours de la myogenèse embryonnaire et adulte.” 2014. Web. 28 Feb 2021.

Vancouver:

Parisi A. Defining the role of APC and canonical WNT signaling in embryonic and adult myogenesis : Etude du rôle d'APC et de la voie de signalisation WNT au cours de la myogenèse embryonnaire et adulte. [Internet] [Doctoral dissertation]. Université Paris Descartes – Paris V; 2014. [cited 2021 Feb 28]. Available from: http://www.theses.fr/2014PA05T033.

Council of Science Editors:

Parisi A. Defining the role of APC and canonical WNT signaling in embryonic and adult myogenesis : Etude du rôle d'APC et de la voie de signalisation WNT au cours de la myogenèse embryonnaire et adulte. [Doctoral Dissertation]. Université Paris Descartes – Paris V; 2014. Available from: http://www.theses.fr/2014PA05T033

University of North Texas

29. Subedi, Ashok. Roles of Primary Cilia in the Oligodendrocyte Lineage.

Degree: 2018, University of North Texas

URL: https://digital.library.unt.edu/ark:/67531/metadc1404594/

► Primary cilia are nonmotile, hair-shaped organelles that extend from the basal body in the centrosome. The present study is the first investigation of this organelle… (more)

▼ Primary cilia are nonmotile, hair-shaped organelles that extend from the basal body in the centrosome. The present study is the first investigation of this organelle in the oligodendrocyte lineage in vivo. I used immunohistochemical approaches in normal and cilia-deficient mutant mice to study cilia in relation to oligodendrogenesis and myelination. Primary cilia immunoreactive for Arl13b and ACIII were commonly present in NG2+ oligodendrocyte progenitor cells (OPCs), in which cilia-associated pathways control proliferation, differentiation, and migration. The loss of primary cilia is generally associated with enhanced Wnt/β-catenin signaling, and Wnt/β-catenin signaling has been shown to promote myelin gene expression. I examined whether the lack of cilia in the oligodendrocyte lineage is associated with elevated Wnt/β-catenin activity. I found that absence of a primary cilium was associated with with higher levels of TCF3, and with β-galactosidase in Axin2-lacZ Wnt reporter mice. This evidence supports the proposal that cilia loss in oligodendrocytes leads to enhanced Wnt/β-catenin activity, which promotes myelination. Cilia are dependent on the centrosome, which assembles microtubules for the cilium, the cytoskeleton, and the mitotic spindle. Centrosomes are the organizing center for microtubule assembly in OPCs, but this function is decentralized in oligodendrocytes. I found that the intensity of centrosomal pericentrin was reduced in oligodendrocytes relative to OPCs, and γ-tubulin was evident in centrosomes of OPCs but not in mature oligodendrocytes. These decreases in centrosomal proteins might contribute to functional differences between OPCs and oligodendrocytes. The importance of cilia in the oligodendrocyte lineage was examined in Tg737orpk mice, which have a hypomorphic IFT88 mutation resulting in decreased cilia numbers and lengths. These mice showed marked, differential decreases in numbers of oligodendrocytes and myelin, yet little or no change in OPC populations. It appears that sufficient cells were available for maturation, but lineage progression was stalled. There were no evident effects of the mutation on Wnt/β-catenin. Factors that might contribute to the abnormalities in the oligodendrocyte lineage of Tg737orpk mice include decreased cilia-dependent Shh mitogenic signaling and dysregulation in cilia-associated pathways such as Notch and Wnt/β-catenin. Advisors/Committee Members: Fuchs, Jannon L., Lund, Amie K., Jagadeeswaren, Pudur, Root, Douglas D., Schwark, Harris D..

Subjects/Keywords: Oligodendrocyte; Primary Cilia; Wnt/β-catenin; Myelination; Centrosome

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

APA (6^th Edition):

Subedi, A. (2018). Roles of Primary Cilia in the Oligodendrocyte Lineage. (Thesis). University of North Texas. Retrieved from https://digital.library.unt.edu/ark:/67531/metadc1404594/

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):

Subedi, Ashok. “Roles of Primary Cilia in the Oligodendrocyte Lineage.” 2018. Thesis, University of North Texas. Accessed February 28, 2021. https://digital.library.unt.edu/ark:/67531/metadc1404594/.

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

MLA Handbook (7^th Edition):

Subedi, Ashok. “Roles of Primary Cilia in the Oligodendrocyte Lineage.” 2018. Web. 28 Feb 2021.

Vancouver:

Subedi A. Roles of Primary Cilia in the Oligodendrocyte Lineage. [Internet] [Thesis]. University of North Texas; 2018. [cited 2021 Feb 28]. Available from: https://digital.library.unt.edu/ark:/67531/metadc1404594/.

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

Council of Science Editors:

Subedi A. Roles of Primary Cilia in the Oligodendrocyte Lineage. [Thesis]. University of North Texas; 2018. Available from: https://digital.library.unt.edu/ark:/67531/metadc1404594/

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

30. 吉田, 直裕. Analysis of Wnt and β-catenin Expression in Advanced Colorectal Cancer : 進行大腸直腸癌におけるWntおよびβカテニン発現の解析.

Degree: 博士（医学）, 2018, Kurume University / 久留米大学

URL: http://hdl.handle.net/11316/710

2015年度

Subjects/Keywords: Wnt; colorectal cancer; β-catenin

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

APA (6^th Edition):

吉田, �. (2018). Analysis of Wnt and β-catenin Expression in Advanced Colorectal Cancer : 進行大腸直腸癌におけるWntおよびβカテニン発現の解析. (Thesis). Kurume University / 久留米大学. Retrieved from http://hdl.handle.net/11316/710

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):

吉田, 直裕. “Analysis of Wnt and β-catenin Expression in Advanced Colorectal Cancer : 進行大腸直腸癌におけるWntおよびβカテニン発現の解析.” 2018. Thesis, Kurume University / 久留米大学. Accessed February 28, 2021. http://hdl.handle.net/11316/710.

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

MLA Handbook (7^th Edition):

吉田, 直裕. “Analysis of Wnt and β-catenin Expression in Advanced Colorectal Cancer : 進行大腸直腸癌におけるWntおよびβカテニン発現の解析.” 2018. Web. 28 Feb 2021.

Vancouver:

吉田 �. Analysis of Wnt and β-catenin Expression in Advanced Colorectal Cancer : 進行大腸直腸癌におけるWntおよびβカテニン発現の解析. [Internet] [Thesis]. Kurume University / 久留米大学; 2018. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/11316/710.

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

Council of Science Editors:

吉田 �. Analysis of Wnt and β-catenin Expression in Advanced Colorectal Cancer : 進行大腸直腸癌におけるWntおよびβカテニン発現の解析. [Thesis]. Kurume University / 久留米大学; 2018. Available from: http://hdl.handle.net/11316/710

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

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Open Access Theses and Dissertations