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You searched for subject:(Endoplasmic Reticulum Stress). Showing records 1 – 30 of 125 total matches.

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University of Toronto

1. Hartley, Taila. Endoplasmic Reticulum Stress in Pancreatic Beta-cells.

Degree: 2009, University of Toronto

Endoplasmic reticulum (ER) stress has been implicated in pancreatic beta-cell loss contributing to diabetes mellitus, however the molecular mechanisms of ER stress-induced apoptosis are unclear.… (more)

Subjects/Keywords: Endoplasmic Reticulum Stress; Beta Cells; 0379

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APA (6th Edition):

Hartley, T. (2009). Endoplasmic Reticulum Stress in Pancreatic Beta-cells. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/18337

Chicago Manual of Style (16th Edition):

Hartley, Taila. “Endoplasmic Reticulum Stress in Pancreatic Beta-cells.” 2009. Masters Thesis, University of Toronto. Accessed April 19, 2019. http://hdl.handle.net/1807/18337.

MLA Handbook (7th Edition):

Hartley, Taila. “Endoplasmic Reticulum Stress in Pancreatic Beta-cells.” 2009. Web. 19 Apr 2019.

Vancouver:

Hartley T. Endoplasmic Reticulum Stress in Pancreatic Beta-cells. [Internet] [Masters thesis]. University of Toronto; 2009. [cited 2019 Apr 19]. Available from: http://hdl.handle.net/1807/18337.

Council of Science Editors:

Hartley T. Endoplasmic Reticulum Stress in Pancreatic Beta-cells. [Masters Thesis]. University of Toronto; 2009. Available from: http://hdl.handle.net/1807/18337


University of Louisville

2. Ngoh, Gladys Afor. The role of O-GlcNAc signaling in acute myocardial ischemia.

Degree: PhD, 2009, University of Louisville

 O -linked ß-N-acetylglucosamine ( O -GlcNAc) is an inducible, dynamically cycling, and reversible post-translational modification of serine/threonine amino acid residues of nucleocytoplasmic and mitochondrial proteins.… (more)

Subjects/Keywords: Myocardial ischemia; O-GlcNAc; Oxidative stress; Endoplasmic reticulum stress

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APA (6th Edition):

Ngoh, G. A. (2009). The role of O-GlcNAc signaling in acute myocardial ischemia. (Doctoral Dissertation). University of Louisville. Retrieved from 10.18297/etd/1056 ; https://ir.library.louisville.edu/etd/1056

Chicago Manual of Style (16th Edition):

Ngoh, Gladys Afor. “The role of O-GlcNAc signaling in acute myocardial ischemia.” 2009. Doctoral Dissertation, University of Louisville. Accessed April 19, 2019. 10.18297/etd/1056 ; https://ir.library.louisville.edu/etd/1056.

MLA Handbook (7th Edition):

Ngoh, Gladys Afor. “The role of O-GlcNAc signaling in acute myocardial ischemia.” 2009. Web. 19 Apr 2019.

Vancouver:

Ngoh GA. The role of O-GlcNAc signaling in acute myocardial ischemia. [Internet] [Doctoral dissertation]. University of Louisville; 2009. [cited 2019 Apr 19]. Available from: 10.18297/etd/1056 ; https://ir.library.louisville.edu/etd/1056.

Council of Science Editors:

Ngoh GA. The role of O-GlcNAc signaling in acute myocardial ischemia. [Doctoral Dissertation]. University of Louisville; 2009. Available from: 10.18297/etd/1056 ; https://ir.library.louisville.edu/etd/1056


Université de Bordeaux I

3. Bouchecareilh, Marion. Régulation de l’activité biologique de la protéine IRE1 : rôle dans le développement des cancers : The effects of exergames training on cognitive aging : a study of learning transfer.

Degree: Docteur es, Biologie cellulaire et physiopathologie, 2008, Université de Bordeaux I

Le Réticulum endoplasmique (RE) est le premier compartiment intracellulaire traversé par les protéines sécrétées. Au sein de cet organite, les protéines acquièrent une conformation native,… (more)

Subjects/Keywords: Réticulum Endoplasmique; Stress; Cancer; Ire1; Endoplasmic Reticulum; Stress; Cancer; Ire1

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APA (6th Edition):

Bouchecareilh, M. (2008). Régulation de l’activité biologique de la protéine IRE1 : rôle dans le développement des cancers : The effects of exergames training on cognitive aging : a study of learning transfer. (Doctoral Dissertation). Université de Bordeaux I. Retrieved from http://www.theses.fr/2008BOR13711

Chicago Manual of Style (16th Edition):

Bouchecareilh, Marion. “Régulation de l’activité biologique de la protéine IRE1 : rôle dans le développement des cancers : The effects of exergames training on cognitive aging : a study of learning transfer.” 2008. Doctoral Dissertation, Université de Bordeaux I. Accessed April 19, 2019. http://www.theses.fr/2008BOR13711.

MLA Handbook (7th Edition):

Bouchecareilh, Marion. “Régulation de l’activité biologique de la protéine IRE1 : rôle dans le développement des cancers : The effects of exergames training on cognitive aging : a study of learning transfer.” 2008. Web. 19 Apr 2019.

Vancouver:

Bouchecareilh M. Régulation de l’activité biologique de la protéine IRE1 : rôle dans le développement des cancers : The effects of exergames training on cognitive aging : a study of learning transfer. [Internet] [Doctoral dissertation]. Université de Bordeaux I; 2008. [cited 2019 Apr 19]. Available from: http://www.theses.fr/2008BOR13711.

Council of Science Editors:

Bouchecareilh M. Régulation de l’activité biologique de la protéine IRE1 : rôle dans le développement des cancers : The effects of exergames training on cognitive aging : a study of learning transfer. [Doctoral Dissertation]. Université de Bordeaux I; 2008. Available from: http://www.theses.fr/2008BOR13711


Colorado State University

4. Estrada, Andrea Lee. Role of fatty acids on endoplasmic reticulum proteostasis in non-alcoholic fatty liver disease, The.

Degree: PhD, Food Science and Human Nutrition, 2018, Colorado State University

 Non-alcoholic fatty liver disease (NAFLD) is currently a significant health concern in both adults and children. NAFLD is a disease characterized by accumulation of fat… (more)

Subjects/Keywords: Endoplasmic reticulum stress; Protein synthesis; Saturated fatty acids; Non-alcoholic fatty liver disease; Endoplasmic reticulum; Proteostasis

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APA (6th Edition):

Estrada, A. L. (2018). Role of fatty acids on endoplasmic reticulum proteostasis in non-alcoholic fatty liver disease, The. (Doctoral Dissertation). Colorado State University. Retrieved from http://hdl.handle.net/10217/185714

Chicago Manual of Style (16th Edition):

Estrada, Andrea Lee. “Role of fatty acids on endoplasmic reticulum proteostasis in non-alcoholic fatty liver disease, The.” 2018. Doctoral Dissertation, Colorado State University. Accessed April 19, 2019. http://hdl.handle.net/10217/185714.

MLA Handbook (7th Edition):

Estrada, Andrea Lee. “Role of fatty acids on endoplasmic reticulum proteostasis in non-alcoholic fatty liver disease, The.” 2018. Web. 19 Apr 2019.

Vancouver:

Estrada AL. Role of fatty acids on endoplasmic reticulum proteostasis in non-alcoholic fatty liver disease, The. [Internet] [Doctoral dissertation]. Colorado State University; 2018. [cited 2019 Apr 19]. Available from: http://hdl.handle.net/10217/185714.

Council of Science Editors:

Estrada AL. Role of fatty acids on endoplasmic reticulum proteostasis in non-alcoholic fatty liver disease, The. [Doctoral Dissertation]. Colorado State University; 2018. Available from: http://hdl.handle.net/10217/185714


University of Alberta

5. Lara, Carlos J. The Herp and HRD1-dependent degradation of TRPP2.

Degree: MS, Department of Physiology, 2012, University of Alberta

 Autosomal Dominant Polycystic Kidney Disease (ADPKD) is a prevalent genetic disorder where multiple fluid-filled cysts destroy kidney architecture, eventually requiring hemodialysis or kidney transplant. Approximately… (more)

Subjects/Keywords: calcium signaling; endoplasmic reticulum stress; polycystic kidney disease; Herp; HRD1; TRPP2

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APA (6th Edition):

Lara, C. J. (2012). The Herp and HRD1-dependent degradation of TRPP2. (Masters Thesis). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/p8418n98g

Chicago Manual of Style (16th Edition):

Lara, Carlos J. “The Herp and HRD1-dependent degradation of TRPP2.” 2012. Masters Thesis, University of Alberta. Accessed April 19, 2019. https://era.library.ualberta.ca/files/p8418n98g.

MLA Handbook (7th Edition):

Lara, Carlos J. “The Herp and HRD1-dependent degradation of TRPP2.” 2012. Web. 19 Apr 2019.

Vancouver:

Lara CJ. The Herp and HRD1-dependent degradation of TRPP2. [Internet] [Masters thesis]. University of Alberta; 2012. [cited 2019 Apr 19]. Available from: https://era.library.ualberta.ca/files/p8418n98g.

Council of Science Editors:

Lara CJ. The Herp and HRD1-dependent degradation of TRPP2. [Masters Thesis]. University of Alberta; 2012. Available from: https://era.library.ualberta.ca/files/p8418n98g


University of Alberta

6. Deslauriers, Andre. Endoplasmic reticulum stress induction by an endogenous retrovirus glycoprotein during neuroinflammation: regulation by a free radical scavenger.

Degree: MS, Department of Medical Microbiology and Immunology, 2010, University of Alberta

Endoplasmic reticulum (ER) stress is a homeostatic mechanism, which is utilized by cells to adapt to inter- and intra-cellular changes. There is a burgeoning literature… (more)

Subjects/Keywords: Human Endougenous Retroviruses; Endoplasmic Reticulum Stress; Multiple Sclerosis

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APA (6th Edition):

Deslauriers, A. (2010). Endoplasmic reticulum stress induction by an endogenous retrovirus glycoprotein during neuroinflammation: regulation by a free radical scavenger. (Masters Thesis). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/bg257g06z

Chicago Manual of Style (16th Edition):

Deslauriers, Andre. “Endoplasmic reticulum stress induction by an endogenous retrovirus glycoprotein during neuroinflammation: regulation by a free radical scavenger.” 2010. Masters Thesis, University of Alberta. Accessed April 19, 2019. https://era.library.ualberta.ca/files/bg257g06z.

MLA Handbook (7th Edition):

Deslauriers, Andre. “Endoplasmic reticulum stress induction by an endogenous retrovirus glycoprotein during neuroinflammation: regulation by a free radical scavenger.” 2010. Web. 19 Apr 2019.

Vancouver:

Deslauriers A. Endoplasmic reticulum stress induction by an endogenous retrovirus glycoprotein during neuroinflammation: regulation by a free radical scavenger. [Internet] [Masters thesis]. University of Alberta; 2010. [cited 2019 Apr 19]. Available from: https://era.library.ualberta.ca/files/bg257g06z.

Council of Science Editors:

Deslauriers A. Endoplasmic reticulum stress induction by an endogenous retrovirus glycoprotein during neuroinflammation: regulation by a free radical scavenger. [Masters Thesis]. University of Alberta; 2010. Available from: https://era.library.ualberta.ca/files/bg257g06z


University of Otago

7. Seo, Benedict Lloyd. Endoplasmic Reticulum Stress and Russell Bodies: Study of the Relationship Using a Periodontal Inflammation Model .

Degree: 2011, University of Otago

 The endoplasmic reticulum (ER) is an organelle of great importance. It represents the intracellular site for protein synthesis, folding, and post-translational modification. Intricately related processes… (more)

Subjects/Keywords: Endoplasmic reticulum stress; Russell Bodies; Unfolded protein response

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APA (6th Edition):

Seo, B. L. (2011). Endoplasmic Reticulum Stress and Russell Bodies: Study of the Relationship Using a Periodontal Inflammation Model . (Doctoral Dissertation). University of Otago. Retrieved from http://hdl.handle.net/10523/2041

Chicago Manual of Style (16th Edition):

Seo, Benedict Lloyd. “Endoplasmic Reticulum Stress and Russell Bodies: Study of the Relationship Using a Periodontal Inflammation Model .” 2011. Doctoral Dissertation, University of Otago. Accessed April 19, 2019. http://hdl.handle.net/10523/2041.

MLA Handbook (7th Edition):

Seo, Benedict Lloyd. “Endoplasmic Reticulum Stress and Russell Bodies: Study of the Relationship Using a Periodontal Inflammation Model .” 2011. Web. 19 Apr 2019.

Vancouver:

Seo BL. Endoplasmic Reticulum Stress and Russell Bodies: Study of the Relationship Using a Periodontal Inflammation Model . [Internet] [Doctoral dissertation]. University of Otago; 2011. [cited 2019 Apr 19]. Available from: http://hdl.handle.net/10523/2041.

Council of Science Editors:

Seo BL. Endoplasmic Reticulum Stress and Russell Bodies: Study of the Relationship Using a Periodontal Inflammation Model . [Doctoral Dissertation]. University of Otago; 2011. Available from: http://hdl.handle.net/10523/2041


Universiteit Utrecht

8. Renne, M.F. Endoplasmic Reticulum Stress and lipid metabolism.

Degree: 2014, Universiteit Utrecht

 Upon endoplasmic reticulum (ER) stress, the unfolded protein response (UPR) triggers cellular mechanisms to restore ER homeostasis. Aberrancies in lipid homeostasis can cause alterations in… (more)

Subjects/Keywords: Unfolded protein response; lipid metabolism; endoplasmic reticulum stress; membrane fluidity

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APA (6th Edition):

Renne, M. F. (2014). Endoplasmic Reticulum Stress and lipid metabolism. (Masters Thesis). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/296878

Chicago Manual of Style (16th Edition):

Renne, M F. “Endoplasmic Reticulum Stress and lipid metabolism.” 2014. Masters Thesis, Universiteit Utrecht. Accessed April 19, 2019. http://dspace.library.uu.nl:8080/handle/1874/296878.

MLA Handbook (7th Edition):

Renne, M F. “Endoplasmic Reticulum Stress and lipid metabolism.” 2014. Web. 19 Apr 2019.

Vancouver:

Renne MF. Endoplasmic Reticulum Stress and lipid metabolism. [Internet] [Masters thesis]. Universiteit Utrecht; 2014. [cited 2019 Apr 19]. Available from: http://dspace.library.uu.nl:8080/handle/1874/296878.

Council of Science Editors:

Renne MF. Endoplasmic Reticulum Stress and lipid metabolism. [Masters Thesis]. Universiteit Utrecht; 2014. Available from: http://dspace.library.uu.nl:8080/handle/1874/296878


National University of Ireland – Galway

9. Saveljeva, Svetlana. Cellular responses to endoplasmic reticulum stress: Role of autophagy and cell death .

Degree: 2014, National University of Ireland – Galway

 This PhD thesis describes cellular responses to the induction of endoplasmic reticulum (ER) stress, focusing on the role of autophagy and cell death. Pro-survival role… (more)

Subjects/Keywords: Endoplasmic reticulum stress; Cell death; Autophagy; Apoptosis; Necroptosis; Biochemistry

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APA (6th Edition):

Saveljeva, S. (2014). Cellular responses to endoplasmic reticulum stress: Role of autophagy and cell death . (Thesis). National University of Ireland – Galway. Retrieved from http://hdl.handle.net/10379/4786

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

Chicago Manual of Style (16th Edition):

Saveljeva, Svetlana. “Cellular responses to endoplasmic reticulum stress: Role of autophagy and cell death .” 2014. Thesis, National University of Ireland – Galway. Accessed April 19, 2019. http://hdl.handle.net/10379/4786.

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

MLA Handbook (7th Edition):

Saveljeva, Svetlana. “Cellular responses to endoplasmic reticulum stress: Role of autophagy and cell death .” 2014. Web. 19 Apr 2019.

Vancouver:

Saveljeva S. Cellular responses to endoplasmic reticulum stress: Role of autophagy and cell death . [Internet] [Thesis]. National University of Ireland – Galway; 2014. [cited 2019 Apr 19]. Available from: http://hdl.handle.net/10379/4786.

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

Council of Science Editors:

Saveljeva S. Cellular responses to endoplasmic reticulum stress: Role of autophagy and cell death . [Thesis]. National University of Ireland – Galway; 2014. Available from: http://hdl.handle.net/10379/4786

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


University of Hong Kong

10. Lam, Dennis. A study of biological role of reactive oxygen species in cellular response in stress.

Degree: PhD, 2012, University of Hong Kong

 When proteins are unable to fold properly in the endoplasmic reticulum (ER), the resultant formation of misfolded proteins causes stress of the ER. Cells with… (more)

Subjects/Keywords: Active oxygen.; Endoplasmic reticulum.; Protein folding.; Stress (Physiology)

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APA (6th Edition):

Lam, D. (2012). A study of biological role of reactive oxygen species in cellular response in stress. (Doctoral Dissertation). University of Hong Kong. Retrieved from Lam, D. [林勁行]. (2012). A study of biological role of reactive oxygen species in cellular response in stress. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4786960 ; http://dx.doi.org/10.5353/th_b4786960 ; http://hdl.handle.net/10722/161520

Chicago Manual of Style (16th Edition):

Lam, Dennis. “A study of biological role of reactive oxygen species in cellular response in stress.” 2012. Doctoral Dissertation, University of Hong Kong. Accessed April 19, 2019. Lam, D. [林勁行]. (2012). A study of biological role of reactive oxygen species in cellular response in stress. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4786960 ; http://dx.doi.org/10.5353/th_b4786960 ; http://hdl.handle.net/10722/161520.

MLA Handbook (7th Edition):

Lam, Dennis. “A study of biological role of reactive oxygen species in cellular response in stress.” 2012. Web. 19 Apr 2019.

Vancouver:

Lam D. A study of biological role of reactive oxygen species in cellular response in stress. [Internet] [Doctoral dissertation]. University of Hong Kong; 2012. [cited 2019 Apr 19]. Available from: Lam, D. [林勁行]. (2012). A study of biological role of reactive oxygen species in cellular response in stress. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4786960 ; http://dx.doi.org/10.5353/th_b4786960 ; http://hdl.handle.net/10722/161520.

Council of Science Editors:

Lam D. A study of biological role of reactive oxygen species in cellular response in stress. [Doctoral Dissertation]. University of Hong Kong; 2012. Available from: Lam, D. [林勁行]. (2012). A study of biological role of reactive oxygen species in cellular response in stress. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4786960 ; http://dx.doi.org/10.5353/th_b4786960 ; http://hdl.handle.net/10722/161520


University of Southern California

11. Ashish Anshu, Fnu. Anti-cancer effects of novel glidobactin type proteasome inhibitors.

Degree: MS, Molecular Microbiology & Immunology, 2011, University of Southern California

 Proteasome inhibitors are widely used today as an important tool for anti-cancer treatment, which has led to a wide search of novel proteasome inhibitors. Proteasome… (more)

Subjects/Keywords: apoptosis; autophagy; endoplasmic reticulum stress; glidobactin A; hematological malignancy; proteasome

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APA (6th Edition):

Ashish Anshu, F. (2011). Anti-cancer effects of novel glidobactin type proteasome inhibitors. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/456326/rec/839

Chicago Manual of Style (16th Edition):

Ashish Anshu, Fnu. “Anti-cancer effects of novel glidobactin type proteasome inhibitors.” 2011. Masters Thesis, University of Southern California. Accessed April 19, 2019. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/456326/rec/839.

MLA Handbook (7th Edition):

Ashish Anshu, Fnu. “Anti-cancer effects of novel glidobactin type proteasome inhibitors.” 2011. Web. 19 Apr 2019.

Vancouver:

Ashish Anshu F. Anti-cancer effects of novel glidobactin type proteasome inhibitors. [Internet] [Masters thesis]. University of Southern California; 2011. [cited 2019 Apr 19]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/456326/rec/839.

Council of Science Editors:

Ashish Anshu F. Anti-cancer effects of novel glidobactin type proteasome inhibitors. [Masters Thesis]. University of Southern California; 2011. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/456326/rec/839


University of Saskatchewan

12. Rafiei, Hossein 1981-. Molecular mechanisms of protection by dietary polyphenols against free fatty acid-induced mitochondrial dysfunction and endoplasmic reticulum stress in an in vitro model of non-alcoholic fatty liver disease.

Degree: 2017, University of Saskatchewan

 Non-alcoholic fatty liver disease (NAFLD) is a public health burden. Steatosis as the “first hit”, and oxidative stress, inflammation, mitochondrial dysfunction, and endoplasmic reticulum stress(more)

Subjects/Keywords: Non-alcoholic fatty liver disease; Mitochondrial dysfunction; endoplasmic reticulum stress; Steatosis

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APA (6th Edition):

Rafiei, H. 1. (2017). Molecular mechanisms of protection by dietary polyphenols against free fatty acid-induced mitochondrial dysfunction and endoplasmic reticulum stress in an in vitro model of non-alcoholic fatty liver disease. (Thesis). University of Saskatchewan. Retrieved from http://hdl.handle.net/10388/7946

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

Chicago Manual of Style (16th Edition):

Rafiei, Hossein 1981-. “Molecular mechanisms of protection by dietary polyphenols against free fatty acid-induced mitochondrial dysfunction and endoplasmic reticulum stress in an in vitro model of non-alcoholic fatty liver disease.” 2017. Thesis, University of Saskatchewan. Accessed April 19, 2019. http://hdl.handle.net/10388/7946.

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

MLA Handbook (7th Edition):

Rafiei, Hossein 1981-. “Molecular mechanisms of protection by dietary polyphenols against free fatty acid-induced mitochondrial dysfunction and endoplasmic reticulum stress in an in vitro model of non-alcoholic fatty liver disease.” 2017. Web. 19 Apr 2019.

Vancouver:

Rafiei H1. Molecular mechanisms of protection by dietary polyphenols against free fatty acid-induced mitochondrial dysfunction and endoplasmic reticulum stress in an in vitro model of non-alcoholic fatty liver disease. [Internet] [Thesis]. University of Saskatchewan; 2017. [cited 2019 Apr 19]. Available from: http://hdl.handle.net/10388/7946.

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

Council of Science Editors:

Rafiei H1. Molecular mechanisms of protection by dietary polyphenols against free fatty acid-induced mitochondrial dysfunction and endoplasmic reticulum stress in an in vitro model of non-alcoholic fatty liver disease. [Thesis]. University of Saskatchewan; 2017. Available from: http://hdl.handle.net/10388/7946

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


McMaster University

13. Tat, Victor. THE ROLE OF THE IRE1α PATHWAY IN VASCULAR STIFFENING AND FIBROSIS.

Degree: MSc, 2017, McMaster University

Background: Vascular stiffening develops with both hypertension and aging, and is a strong predictor of end-organ damage. Excessive deposition of collagen by vascular smooth muscle… (more)

Subjects/Keywords: Hypertension; Unfolded Protein Response; Endoplasmic Reticulum Stress; Vascular Stiffening; Fibrosis

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APA (6th Edition):

Tat, V. (2017). THE ROLE OF THE IRE1α PATHWAY IN VASCULAR STIFFENING AND FIBROSIS. (Masters Thesis). McMaster University. Retrieved from http://hdl.handle.net/11375/21052

Chicago Manual of Style (16th Edition):

Tat, Victor. “THE ROLE OF THE IRE1α PATHWAY IN VASCULAR STIFFENING AND FIBROSIS.” 2017. Masters Thesis, McMaster University. Accessed April 19, 2019. http://hdl.handle.net/11375/21052.

MLA Handbook (7th Edition):

Tat, Victor. “THE ROLE OF THE IRE1α PATHWAY IN VASCULAR STIFFENING AND FIBROSIS.” 2017. Web. 19 Apr 2019.

Vancouver:

Tat V. THE ROLE OF THE IRE1α PATHWAY IN VASCULAR STIFFENING AND FIBROSIS. [Internet] [Masters thesis]. McMaster University; 2017. [cited 2019 Apr 19]. Available from: http://hdl.handle.net/11375/21052.

Council of Science Editors:

Tat V. THE ROLE OF THE IRE1α PATHWAY IN VASCULAR STIFFENING AND FIBROSIS. [Masters Thesis]. McMaster University; 2017. Available from: http://hdl.handle.net/11375/21052


McMaster University

14. Carlisle, Rachel E. Inhibiting endoplasmic reticulum stress prevents the development of hypertensive nephrosclerosis.

Degree: PhD, 2017, McMaster University

Endoplasmic reticulum (ER) stress, which results from the aggregation of misfolded proteins in the ER, has been implicated in many forms of kidney injury, including… (more)

Subjects/Keywords: endoplasmic reticulum stress; chronic kidney disease; 4-phenylbutyrate; hypertension

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APA (6th Edition):

Carlisle, R. E. (2017). Inhibiting endoplasmic reticulum stress prevents the development of hypertensive nephrosclerosis. (Doctoral Dissertation). McMaster University. Retrieved from http://hdl.handle.net/11375/22040

Chicago Manual of Style (16th Edition):

Carlisle, Rachel E. “Inhibiting endoplasmic reticulum stress prevents the development of hypertensive nephrosclerosis.” 2017. Doctoral Dissertation, McMaster University. Accessed April 19, 2019. http://hdl.handle.net/11375/22040.

MLA Handbook (7th Edition):

Carlisle, Rachel E. “Inhibiting endoplasmic reticulum stress prevents the development of hypertensive nephrosclerosis.” 2017. Web. 19 Apr 2019.

Vancouver:

Carlisle RE. Inhibiting endoplasmic reticulum stress prevents the development of hypertensive nephrosclerosis. [Internet] [Doctoral dissertation]. McMaster University; 2017. [cited 2019 Apr 19]. Available from: http://hdl.handle.net/11375/22040.

Council of Science Editors:

Carlisle RE. Inhibiting endoplasmic reticulum stress prevents the development of hypertensive nephrosclerosis. [Doctoral Dissertation]. McMaster University; 2017. Available from: http://hdl.handle.net/11375/22040


McMaster University

15. Assee, Samantha. Role of the GABARAP Tumor Suppressor in the Control of E.R. Stress and Cell Apoptosis.

Degree: 2018, McMaster University

In response to starvation, mis-folded proteins accumulate in the endoplasmic reticulum (E.R.) causing E.R. stress. This triggers a series of signaling pathways known as the… (more)

Subjects/Keywords: GABARAP; Endoplasmic Reticulum; Unfolded Protein Response; Stress; Autophagy; CHOP; Apoptosis

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APA (6th Edition):

Assee, S. (2018). Role of the GABARAP Tumor Suppressor in the Control of E.R. Stress and Cell Apoptosis. (Thesis). McMaster University. Retrieved from http://hdl.handle.net/11375/22747

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

Chicago Manual of Style (16th Edition):

Assee, Samantha. “Role of the GABARAP Tumor Suppressor in the Control of E.R. Stress and Cell Apoptosis.” 2018. Thesis, McMaster University. Accessed April 19, 2019. http://hdl.handle.net/11375/22747.

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

MLA Handbook (7th Edition):

Assee, Samantha. “Role of the GABARAP Tumor Suppressor in the Control of E.R. Stress and Cell Apoptosis.” 2018. Web. 19 Apr 2019.

Vancouver:

Assee S. Role of the GABARAP Tumor Suppressor in the Control of E.R. Stress and Cell Apoptosis. [Internet] [Thesis]. McMaster University; 2018. [cited 2019 Apr 19]. Available from: http://hdl.handle.net/11375/22747.

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

Council of Science Editors:

Assee S. Role of the GABARAP Tumor Suppressor in the Control of E.R. Stress and Cell Apoptosis. [Thesis]. McMaster University; 2018. Available from: http://hdl.handle.net/11375/22747

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


University of the Western Cape

16. Pillay, Leeshan. The integrated effects of selected inducers of endoplasmic reticulum stress, the unfolded protein response and apoptosis on P-Glycoprotein mediated drug resistance in MCF-7 breast carcinoma cells .

Degree: 2015, University of the Western Cape

 Purpose: One of the leading causes of death reported in women worldwide is breast cancer. Manytumours, including breast cancer, associated with poor prognosis, have received… (more)

Subjects/Keywords: Breast cancer; P-Glycoprotein; Apoptosis; Endoplasmic reticulum stress; Multidrug resistance

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APA (6th Edition):

Pillay, L. (2015). The integrated effects of selected inducers of endoplasmic reticulum stress, the unfolded protein response and apoptosis on P-Glycoprotein mediated drug resistance in MCF-7 breast carcinoma cells . (Thesis). University of the Western Cape. Retrieved from http://hdl.handle.net/11394/4459

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

Chicago Manual of Style (16th Edition):

Pillay, Leeshan. “The integrated effects of selected inducers of endoplasmic reticulum stress, the unfolded protein response and apoptosis on P-Glycoprotein mediated drug resistance in MCF-7 breast carcinoma cells .” 2015. Thesis, University of the Western Cape. Accessed April 19, 2019. http://hdl.handle.net/11394/4459.

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

MLA Handbook (7th Edition):

Pillay, Leeshan. “The integrated effects of selected inducers of endoplasmic reticulum stress, the unfolded protein response and apoptosis on P-Glycoprotein mediated drug resistance in MCF-7 breast carcinoma cells .” 2015. Web. 19 Apr 2019.

Vancouver:

Pillay L. The integrated effects of selected inducers of endoplasmic reticulum stress, the unfolded protein response and apoptosis on P-Glycoprotein mediated drug resistance in MCF-7 breast carcinoma cells . [Internet] [Thesis]. University of the Western Cape; 2015. [cited 2019 Apr 19]. Available from: http://hdl.handle.net/11394/4459.

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

Council of Science Editors:

Pillay L. The integrated effects of selected inducers of endoplasmic reticulum stress, the unfolded protein response and apoptosis on P-Glycoprotein mediated drug resistance in MCF-7 breast carcinoma cells . [Thesis]. University of the Western Cape; 2015. Available from: http://hdl.handle.net/11394/4459

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


NSYSU

17. Tsai, Tsung-Chang. Discovery of New Natural Products from Cultrued Soft Coral Sinularia sandensis and Investigation of Molecular Mechanisms of Apoptosis Induced by 7-Acetylsinumaximol B and Anti-metastasis of Dihydroaustrasulfone Alcohol on Cancer Cells.

Degree: PhD, Institute Of Marine Biotechnology And Resources, 2018, NSYSU

 Cultured soft coral Sinularia sandensis has led to the isolation of elenven natural compounds, including two new cembranoids, 4-carbomethoxyl-10-epigyrosanoldie E (1) and 7-acetylsinumaximol B (2);… (more)

Subjects/Keywords: apoptosis; endoplasmic reticulum stress; configuration; autophagy; migration; invasion

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APA (6th Edition):

Tsai, T. (2018). Discovery of New Natural Products from Cultrued Soft Coral Sinularia sandensis and Investigation of Molecular Mechanisms of Apoptosis Induced by 7-Acetylsinumaximol B and Anti-metastasis of Dihydroaustrasulfone Alcohol on Cancer Cells. (Doctoral Dissertation). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0715118-003404

Chicago Manual of Style (16th Edition):

Tsai, Tsung-Chang. “Discovery of New Natural Products from Cultrued Soft Coral Sinularia sandensis and Investigation of Molecular Mechanisms of Apoptosis Induced by 7-Acetylsinumaximol B and Anti-metastasis of Dihydroaustrasulfone Alcohol on Cancer Cells.” 2018. Doctoral Dissertation, NSYSU. Accessed April 19, 2019. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0715118-003404.

MLA Handbook (7th Edition):

Tsai, Tsung-Chang. “Discovery of New Natural Products from Cultrued Soft Coral Sinularia sandensis and Investigation of Molecular Mechanisms of Apoptosis Induced by 7-Acetylsinumaximol B and Anti-metastasis of Dihydroaustrasulfone Alcohol on Cancer Cells.” 2018. Web. 19 Apr 2019.

Vancouver:

Tsai T. Discovery of New Natural Products from Cultrued Soft Coral Sinularia sandensis and Investigation of Molecular Mechanisms of Apoptosis Induced by 7-Acetylsinumaximol B and Anti-metastasis of Dihydroaustrasulfone Alcohol on Cancer Cells. [Internet] [Doctoral dissertation]. NSYSU; 2018. [cited 2019 Apr 19]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0715118-003404.

Council of Science Editors:

Tsai T. Discovery of New Natural Products from Cultrued Soft Coral Sinularia sandensis and Investigation of Molecular Mechanisms of Apoptosis Induced by 7-Acetylsinumaximol B and Anti-metastasis of Dihydroaustrasulfone Alcohol on Cancer Cells. [Doctoral Dissertation]. NSYSU; 2018. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0715118-003404


Stellenbosch University

18. Benade, Janina. Are early proteomic and metabolic changes induced by long-term sugar-sweetened beverage consumption the key to unlocking the cardio-metabolic pandemic?.

Degree: MSc, Physiological Sciences, 2017, Stellenbosch University

 ENGLISH ABSTRACT: INTRODUCTION: Cardio-metabolic diseases (e.g. type 2 diabetes mellitus) are a major cause of mortality worldwide. The incidence of cardio-metabolic diseases continues to increase,… (more)

Subjects/Keywords: Sugar-sweetened beverages; Diabetes; Cardiovascular disease; Endoplasmic reticulum stress; Proteomics; UCTD

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APA (6th Edition):

Benade, J. (2017). Are early proteomic and metabolic changes induced by long-term sugar-sweetened beverage consumption the key to unlocking the cardio-metabolic pandemic?. (Masters Thesis). Stellenbosch University. Retrieved from http://hdl.handle.net/10019.1/101368

Chicago Manual of Style (16th Edition):

Benade, Janina. “Are early proteomic and metabolic changes induced by long-term sugar-sweetened beverage consumption the key to unlocking the cardio-metabolic pandemic?.” 2017. Masters Thesis, Stellenbosch University. Accessed April 19, 2019. http://hdl.handle.net/10019.1/101368.

MLA Handbook (7th Edition):

Benade, Janina. “Are early proteomic and metabolic changes induced by long-term sugar-sweetened beverage consumption the key to unlocking the cardio-metabolic pandemic?.” 2017. Web. 19 Apr 2019.

Vancouver:

Benade J. Are early proteomic and metabolic changes induced by long-term sugar-sweetened beverage consumption the key to unlocking the cardio-metabolic pandemic?. [Internet] [Masters thesis]. Stellenbosch University; 2017. [cited 2019 Apr 19]. Available from: http://hdl.handle.net/10019.1/101368.

Council of Science Editors:

Benade J. Are early proteomic and metabolic changes induced by long-term sugar-sweetened beverage consumption the key to unlocking the cardio-metabolic pandemic?. [Masters Thesis]. Stellenbosch University; 2017. Available from: http://hdl.handle.net/10019.1/101368


University of Texas – Austin

19. Lu, Na, 1978-. The anticancer effects of vitamin E derivative alpha-tea in human hematological malignancies.

Degree: Nutritional Sciences, 2010, University of Texas – Austin

 alpha-TEA (alpha-tocopherol ether linked acetic acid) has been shown to induce apoptosis in human prostate, ovarian and breast cancer cells in culture and in xenograft… (more)

Subjects/Keywords: alpha-TEA; Apoptosis; Human hematological malignancies; Ceramide; Endoplasmic reticulum stress

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APA (6th Edition):

Lu, Na, 1. (2010). The anticancer effects of vitamin E derivative alpha-tea in human hematological malignancies. (Thesis). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/ETD-UT-2010-12-2289

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

Chicago Manual of Style (16th Edition):

Lu, Na, 1978-. “The anticancer effects of vitamin E derivative alpha-tea in human hematological malignancies.” 2010. Thesis, University of Texas – Austin. Accessed April 19, 2019. http://hdl.handle.net/2152/ETD-UT-2010-12-2289.

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

MLA Handbook (7th Edition):

Lu, Na, 1978-. “The anticancer effects of vitamin E derivative alpha-tea in human hematological malignancies.” 2010. Web. 19 Apr 2019.

Vancouver:

Lu, Na 1. The anticancer effects of vitamin E derivative alpha-tea in human hematological malignancies. [Internet] [Thesis]. University of Texas – Austin; 2010. [cited 2019 Apr 19]. Available from: http://hdl.handle.net/2152/ETD-UT-2010-12-2289.

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

Council of Science Editors:

Lu, Na 1. The anticancer effects of vitamin E derivative alpha-tea in human hematological malignancies. [Thesis]. University of Texas – Austin; 2010. Available from: http://hdl.handle.net/2152/ETD-UT-2010-12-2289

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


University of Minnesota

20. Dauer, Patricia. Endoplasmic Reticulum Stress-Mediated Signaling in Pancreatic Cancer.

Degree: PhD, Pharmacology, 2018, University of Minnesota

 Pancreatic ductal adenocarcinoma (PDAC) ranks among the poorest prognoses for cancer patients, with an estimated 5-year survival of just 8%. The stagnant survival rates are… (more)

Subjects/Keywords: Chemoresistance; Endoplasmic Reticulum Stress; GRP78; Pancreatic Cancer; SP1; Tumor microenvironment

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APA (6th Edition):

Dauer, P. (2018). Endoplasmic Reticulum Stress-Mediated Signaling in Pancreatic Cancer. (Doctoral Dissertation). University of Minnesota. Retrieved from http://hdl.handle.net/11299/198397

Chicago Manual of Style (16th Edition):

Dauer, Patricia. “Endoplasmic Reticulum Stress-Mediated Signaling in Pancreatic Cancer.” 2018. Doctoral Dissertation, University of Minnesota. Accessed April 19, 2019. http://hdl.handle.net/11299/198397.

MLA Handbook (7th Edition):

Dauer, Patricia. “Endoplasmic Reticulum Stress-Mediated Signaling in Pancreatic Cancer.” 2018. Web. 19 Apr 2019.

Vancouver:

Dauer P. Endoplasmic Reticulum Stress-Mediated Signaling in Pancreatic Cancer. [Internet] [Doctoral dissertation]. University of Minnesota; 2018. [cited 2019 Apr 19]. Available from: http://hdl.handle.net/11299/198397.

Council of Science Editors:

Dauer P. Endoplasmic Reticulum Stress-Mediated Signaling in Pancreatic Cancer. [Doctoral Dissertation]. University of Minnesota; 2018. Available from: http://hdl.handle.net/11299/198397

21. Lhomond, Stephanie. Impact fonctionnel de mutations somatiques dans le gène ERN1 (IRE1ΑLPHA) dans les glioblastomes : Impact of functional somatic mutations in the gene ERN1 (IRE1ALPHA) in glioblastomas.

Degree: Docteur es, Biologie Cellulaire et Physiopathologie, 2014, Bordeaux

Dans les cellules eucaryotes, des altérations du microenvironnement cellulaire ou desmutations des protéines de la voie de sécrétion induisent un stress du RE et activent… (more)

Subjects/Keywords: Réticulum endoplasmique; Stress; IRE1α; ERN1; Cancer; Glioblastome; Endoplasmic reticulum; Stress; IRE1α; ERN1; Cancer; Glioblastoma

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APA (6th Edition):

Lhomond, S. (2014). Impact fonctionnel de mutations somatiques dans le gène ERN1 (IRE1ΑLPHA) dans les glioblastomes : Impact of functional somatic mutations in the gene ERN1 (IRE1ALPHA) in glioblastomas. (Doctoral Dissertation). Bordeaux. Retrieved from http://www.theses.fr/2014BORD0038

Chicago Manual of Style (16th Edition):

Lhomond, Stephanie. “Impact fonctionnel de mutations somatiques dans le gène ERN1 (IRE1ΑLPHA) dans les glioblastomes : Impact of functional somatic mutations in the gene ERN1 (IRE1ALPHA) in glioblastomas.” 2014. Doctoral Dissertation, Bordeaux. Accessed April 19, 2019. http://www.theses.fr/2014BORD0038.

MLA Handbook (7th Edition):

Lhomond, Stephanie. “Impact fonctionnel de mutations somatiques dans le gène ERN1 (IRE1ΑLPHA) dans les glioblastomes : Impact of functional somatic mutations in the gene ERN1 (IRE1ALPHA) in glioblastomas.” 2014. Web. 19 Apr 2019.

Vancouver:

Lhomond S. Impact fonctionnel de mutations somatiques dans le gène ERN1 (IRE1ΑLPHA) dans les glioblastomes : Impact of functional somatic mutations in the gene ERN1 (IRE1ALPHA) in glioblastomas. [Internet] [Doctoral dissertation]. Bordeaux; 2014. [cited 2019 Apr 19]. Available from: http://www.theses.fr/2014BORD0038.

Council of Science Editors:

Lhomond S. Impact fonctionnel de mutations somatiques dans le gène ERN1 (IRE1ΑLPHA) dans les glioblastomes : Impact of functional somatic mutations in the gene ERN1 (IRE1ALPHA) in glioblastomas. [Doctoral Dissertation]. Bordeaux; 2014. Available from: http://www.theses.fr/2014BORD0038


University of Toronto

22. Tang, Christine. Mechanisms of High Glucose-induced Decrease in β-cell Function.

Degree: 2010, University of Toronto

Chronic hyperglycemia, a hallmark of type 2 diabetes, can decrease β-cell function and mass (β-cell glucotoxicity); however, the mechanisms are incompletely understood. The objective was… (more)

Subjects/Keywords: Glucotoxicity; Oxidative Stress; Type 2 Diabetes; Endoplasmic Reticulum Stress; c-jun N-terminal kinase; 0719

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APA (6th Edition):

Tang, C. (2010). Mechanisms of High Glucose-induced Decrease in β-cell Function. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/26331

Chicago Manual of Style (16th Edition):

Tang, Christine. “Mechanisms of High Glucose-induced Decrease in β-cell Function.” 2010. Doctoral Dissertation, University of Toronto. Accessed April 19, 2019. http://hdl.handle.net/1807/26331.

MLA Handbook (7th Edition):

Tang, Christine. “Mechanisms of High Glucose-induced Decrease in β-cell Function.” 2010. Web. 19 Apr 2019.

Vancouver:

Tang C. Mechanisms of High Glucose-induced Decrease in β-cell Function. [Internet] [Doctoral dissertation]. University of Toronto; 2010. [cited 2019 Apr 19]. Available from: http://hdl.handle.net/1807/26331.

Council of Science Editors:

Tang C. Mechanisms of High Glucose-induced Decrease in β-cell Function. [Doctoral Dissertation]. University of Toronto; 2010. Available from: http://hdl.handle.net/1807/26331


University of Utah

23. Moore, Kristin A. The mechanisms and function of regulated ire1-dependent decay during endoplasmic reticulum stress.

Degree: PhD, Biology, 2016, University of Utah

 The endoplasmic reticulum (ER) is a dynamic organelle that is responsible for the folding and quality control of proteins within the endomembrane system. Both physiological… (more)

Subjects/Keywords: Blos1; Endoplasmic reticulum (ER); ER stress; mRNA degradation; Regulated-Ire1 Dependent Decay; Unfolded Protein Response

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APA (6th Edition):

Moore, K. A. (2016). The mechanisms and function of regulated ire1-dependent decay during endoplasmic reticulum stress. (Doctoral Dissertation). University of Utah. Retrieved from http://content.lib.utah.edu/cdm/singleitem/collection/etd3/id/4104/rec/2602

Chicago Manual of Style (16th Edition):

Moore, Kristin A. “The mechanisms and function of regulated ire1-dependent decay during endoplasmic reticulum stress.” 2016. Doctoral Dissertation, University of Utah. Accessed April 19, 2019. http://content.lib.utah.edu/cdm/singleitem/collection/etd3/id/4104/rec/2602.

MLA Handbook (7th Edition):

Moore, Kristin A. “The mechanisms and function of regulated ire1-dependent decay during endoplasmic reticulum stress.” 2016. Web. 19 Apr 2019.

Vancouver:

Moore KA. The mechanisms and function of regulated ire1-dependent decay during endoplasmic reticulum stress. [Internet] [Doctoral dissertation]. University of Utah; 2016. [cited 2019 Apr 19]. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd3/id/4104/rec/2602.

Council of Science Editors:

Moore KA. The mechanisms and function of regulated ire1-dependent decay during endoplasmic reticulum stress. [Doctoral Dissertation]. University of Utah; 2016. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd3/id/4104/rec/2602


RMIT University

24. Sun, R. The role of ER stress in lipogenesis and insulin resistance in response to over nutrition.

Degree: 2014, RMIT University

 Insulin resistance is one of the major defect of type 2 diabetes. Excess lipid and endoplasmic reticulum (ER) stress have been suggested to induce hepatic… (more)

Subjects/Keywords: Fields of Research; Hepatic insulin resistance; Endoplasmic reticulum stress; lipid metabolism; Fructose; Liver

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APA (6th Edition):

Sun, R. (2014). The role of ER stress in lipogenesis and insulin resistance in response to over nutrition. (Thesis). RMIT University. Retrieved from http://researchbank.rmit.edu.au/view/rmit:161524

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

Chicago Manual of Style (16th Edition):

Sun, R. “The role of ER stress in lipogenesis and insulin resistance in response to over nutrition.” 2014. Thesis, RMIT University. Accessed April 19, 2019. http://researchbank.rmit.edu.au/view/rmit:161524.

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

MLA Handbook (7th Edition):

Sun, R. “The role of ER stress in lipogenesis and insulin resistance in response to over nutrition.” 2014. Web. 19 Apr 2019.

Vancouver:

Sun R. The role of ER stress in lipogenesis and insulin resistance in response to over nutrition. [Internet] [Thesis]. RMIT University; 2014. [cited 2019 Apr 19]. Available from: http://researchbank.rmit.edu.au/view/rmit:161524.

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

Council of Science Editors:

Sun R. The role of ER stress in lipogenesis and insulin resistance in response to over nutrition. [Thesis]. RMIT University; 2014. Available from: http://researchbank.rmit.edu.au/view/rmit:161524

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


University of Toledo Health Science Campus

25. Kaul, Aparna. Mechanisms of Non-Conventional Cell Death in Brain Tumor Cells.

Degree: PhD, College of Medicine, 2009, University of Toledo Health Science Campus

 The concept of programmed cell death has evolved over the years to include bothapoptotic and non-apoptotic death mechanisms. This study describes a novel form ofnon-apoptotic… (more)

Subjects/Keywords: Cellular Biology; Molecular Biology; Apoptosis; methuosis; endoplasmic reticulum-stress; macropinocytosis; non-apoptotic; glioblastoma

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APA (6th Edition):

Kaul, A. (2009). Mechanisms of Non-Conventional Cell Death in Brain Tumor Cells. (Doctoral Dissertation). University of Toledo Health Science Campus. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=mco1243364096

Chicago Manual of Style (16th Edition):

Kaul, Aparna. “Mechanisms of Non-Conventional Cell Death in Brain Tumor Cells.” 2009. Doctoral Dissertation, University of Toledo Health Science Campus. Accessed April 19, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=mco1243364096.

MLA Handbook (7th Edition):

Kaul, Aparna. “Mechanisms of Non-Conventional Cell Death in Brain Tumor Cells.” 2009. Web. 19 Apr 2019.

Vancouver:

Kaul A. Mechanisms of Non-Conventional Cell Death in Brain Tumor Cells. [Internet] [Doctoral dissertation]. University of Toledo Health Science Campus; 2009. [cited 2019 Apr 19]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=mco1243364096.

Council of Science Editors:

Kaul A. Mechanisms of Non-Conventional Cell Death in Brain Tumor Cells. [Doctoral Dissertation]. University of Toledo Health Science Campus; 2009. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=mco1243364096

26. 정, 익락. The effect of iron metabolism on palmitate-induced INS-1 cell death.

Degree: 2015, Ajou University

Ⅰ. INTRODUCTION 1 Ⅱ. MATERIALS AND METHODS 24 A. MATERIALS 24 1. Reagents 24 B. METHODS 25 1. Cell Culture 25 2. Preparation of palmitate… (more)

Subjects/Keywords: Apoptosis; Endoplasmic reticulum(ER) stress; Lipotoxicity; Iron; INS-1 Cell; Palmitate; Transferrin receptor; Soduim fluorocitrate

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APA (6th Edition):

정, . (2015). The effect of iron metabolism on palmitate-induced INS-1 cell death. (Thesis). Ajou University. Retrieved from http://repository.ajou.ac.kr/handle/201003/11837 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000020143

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

Chicago Manual of Style (16th Edition):

정, 익락. “The effect of iron metabolism on palmitate-induced INS-1 cell death.” 2015. Thesis, Ajou University. Accessed April 19, 2019. http://repository.ajou.ac.kr/handle/201003/11837 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000020143.

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

MLA Handbook (7th Edition):

정, 익락. “The effect of iron metabolism on palmitate-induced INS-1 cell death.” 2015. Web. 19 Apr 2019.

Vancouver:

정 . The effect of iron metabolism on palmitate-induced INS-1 cell death. [Internet] [Thesis]. Ajou University; 2015. [cited 2019 Apr 19]. Available from: http://repository.ajou.ac.kr/handle/201003/11837 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000020143.

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

Council of Science Editors:

정 . The effect of iron metabolism on palmitate-induced INS-1 cell death. [Thesis]. Ajou University; 2015. Available from: http://repository.ajou.ac.kr/handle/201003/11837 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000020143

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


Vanderbilt University

27. Leamy, Alexandra Kathlene. Role of lipid metabolic pathways in the progression of hepatic lipotoxicity.

Degree: PhD, Chemical Engineering, 2015, Vanderbilt University

 The steady rise in Western obesity rates has been closely linked to significant increases in a multitude of accompanying health problems including obesity, type II… (more)

Subjects/Keywords: phospholipids; triglyceride synthesis; endoplasmic reticulum stress; saturated fatty acids; lipotoxicity; lipid metabolism

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APA (6th Edition):

Leamy, A. K. (2015). Role of lipid metabolic pathways in the progression of hepatic lipotoxicity. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu//available/etd-03222015-205527/ ;

Chicago Manual of Style (16th Edition):

Leamy, Alexandra Kathlene. “Role of lipid metabolic pathways in the progression of hepatic lipotoxicity.” 2015. Doctoral Dissertation, Vanderbilt University. Accessed April 19, 2019. http://etd.library.vanderbilt.edu//available/etd-03222015-205527/ ;.

MLA Handbook (7th Edition):

Leamy, Alexandra Kathlene. “Role of lipid metabolic pathways in the progression of hepatic lipotoxicity.” 2015. Web. 19 Apr 2019.

Vancouver:

Leamy AK. Role of lipid metabolic pathways in the progression of hepatic lipotoxicity. [Internet] [Doctoral dissertation]. Vanderbilt University; 2015. [cited 2019 Apr 19]. Available from: http://etd.library.vanderbilt.edu//available/etd-03222015-205527/ ;.

Council of Science Editors:

Leamy AK. Role of lipid metabolic pathways in the progression of hepatic lipotoxicity. [Doctoral Dissertation]. Vanderbilt University; 2015. Available from: http://etd.library.vanderbilt.edu//available/etd-03222015-205527/ ;


Cornell University

28. Krumm, Christopher Steven. Tales of Metabolic Regulation: Adiponectin in the Cow and Sel1L in the Mouse .

Degree: 2017, Cornell University

 The first part of this dissertation assessed factors regulating the insulin sensitizing hormone adiponectin in dairy cows. Plasma adiponectin is reduced during the transition from… (more)

Subjects/Keywords: Endocrinology; Biology; Adiponectin; endoplasmic reticulum stress; Metabolism; Sel1L; Transition Dairy Cow; Animal sciences

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APA (6th Edition):

Krumm, C. S. (2017). Tales of Metabolic Regulation: Adiponectin in the Cow and Sel1L in the Mouse . (Thesis). Cornell University. Retrieved from http://hdl.handle.net/1813/47862

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

Chicago Manual of Style (16th Edition):

Krumm, Christopher Steven. “Tales of Metabolic Regulation: Adiponectin in the Cow and Sel1L in the Mouse .” 2017. Thesis, Cornell University. Accessed April 19, 2019. http://hdl.handle.net/1813/47862.

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

MLA Handbook (7th Edition):

Krumm, Christopher Steven. “Tales of Metabolic Regulation: Adiponectin in the Cow and Sel1L in the Mouse .” 2017. Web. 19 Apr 2019.

Vancouver:

Krumm CS. Tales of Metabolic Regulation: Adiponectin in the Cow and Sel1L in the Mouse . [Internet] [Thesis]. Cornell University; 2017. [cited 2019 Apr 19]. Available from: http://hdl.handle.net/1813/47862.

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

Council of Science Editors:

Krumm CS. Tales of Metabolic Regulation: Adiponectin in the Cow and Sel1L in the Mouse . [Thesis]. Cornell University; 2017. Available from: http://hdl.handle.net/1813/47862

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


University of New South Wales

29. Akerfeldt, Mia. Pathways leading to β-cell dysfunction and death in type 1 and type 2 diabetes.

Degree: Garvan Institute of Medical Research, 2011, University of New South Wales

 The failure of β-cells to provide sufficient amounts of insulin to maintain blood glucose levels within a narrow physiological range is central to the development… (more)

Subjects/Keywords: Insulin secretion; β; -cell apoptosis; Endoplasmic reticulum stress; Helix-loop-helix transcription factor

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

APA (6th Edition):

Akerfeldt, M. (2011). Pathways leading to β-cell dysfunction and death in type 1 and type 2 diabetes. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/51610 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10277/SOURCE02?view=true

Chicago Manual of Style (16th Edition):

Akerfeldt, Mia. “Pathways leading to β-cell dysfunction and death in type 1 and type 2 diabetes.” 2011. Doctoral Dissertation, University of New South Wales. Accessed April 19, 2019. http://handle.unsw.edu.au/1959.4/51610 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10277/SOURCE02?view=true.

MLA Handbook (7th Edition):

Akerfeldt, Mia. “Pathways leading to β-cell dysfunction and death in type 1 and type 2 diabetes.” 2011. Web. 19 Apr 2019.

Vancouver:

Akerfeldt M. Pathways leading to β-cell dysfunction and death in type 1 and type 2 diabetes. [Internet] [Doctoral dissertation]. University of New South Wales; 2011. [cited 2019 Apr 19]. Available from: http://handle.unsw.edu.au/1959.4/51610 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10277/SOURCE02?view=true.

Council of Science Editors:

Akerfeldt M. Pathways leading to β-cell dysfunction and death in type 1 and type 2 diabetes. [Doctoral Dissertation]. University of New South Wales; 2011. Available from: http://handle.unsw.edu.au/1959.4/51610 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10277/SOURCE02?view=true


University of Illinois – Urbana-Champaign

30. Knezevic, Claire. Development of poly(ADP-ribose) glycohydrolase inhibitors and tetracyclic indoles as anticancer compounds.

Degree: PhD, 0335, 2014, University of Illinois – Urbana-Champaign

 In the quest for novel anticancer small molecules, one of two major complementary strategies, either a target- or phenotype-based approach, is generally utilized. Target-based approaches,… (more)

Subjects/Keywords: anticancer; poly(ADP-ribose) glycohydrolase (PARG); endoplasmic reticulum (ER) stress; lead hopping; phenotypic screen

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

APA (6th Edition):

Knezevic, C. (2014). Development of poly(ADP-ribose) glycohydrolase inhibitors and tetracyclic indoles as anticancer compounds. (Doctoral Dissertation). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/50439

Chicago Manual of Style (16th Edition):

Knezevic, Claire. “Development of poly(ADP-ribose) glycohydrolase inhibitors and tetracyclic indoles as anticancer compounds.” 2014. Doctoral Dissertation, University of Illinois – Urbana-Champaign. Accessed April 19, 2019. http://hdl.handle.net/2142/50439.

MLA Handbook (7th Edition):

Knezevic, Claire. “Development of poly(ADP-ribose) glycohydrolase inhibitors and tetracyclic indoles as anticancer compounds.” 2014. Web. 19 Apr 2019.

Vancouver:

Knezevic C. Development of poly(ADP-ribose) glycohydrolase inhibitors and tetracyclic indoles as anticancer compounds. [Internet] [Doctoral dissertation]. University of Illinois – Urbana-Champaign; 2014. [cited 2019 Apr 19]. Available from: http://hdl.handle.net/2142/50439.

Council of Science Editors:

Knezevic C. Development of poly(ADP-ribose) glycohydrolase inhibitors and tetracyclic indoles as anticancer compounds. [Doctoral Dissertation]. University of Illinois – Urbana-Champaign; 2014. Available from: http://hdl.handle.net/2142/50439

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