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You searched for subject:(beta cell proliferation). Showing records 1 – 30 of 47 total matches.

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University of Southern California

1. Yang, Kai-Ting. Pten deletion in adult pancreatic beta-cells induces cell proliferation and G1/S cell cycle progression.

Degree: MS, Biochemistry and Molecular Biology, 2013, University of Southern California

 β-cells, which produce and release insulin play a major role in maintaining glucose homeostasis. PTEN is a lipid phosphatase that antagonizes PI3K/AKT signaling pathway and… (more)

Subjects/Keywords: Pten; beta-cell; cell proliferation

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APA (6th Edition):

Yang, K. (2013). Pten deletion in adult pancreatic beta-cells induces cell proliferation and G1/S cell cycle progression. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/316863/rec/5321

Chicago Manual of Style (16th Edition):

Yang, Kai-Ting. “Pten deletion in adult pancreatic beta-cells induces cell proliferation and G1/S cell cycle progression.” 2013. Masters Thesis, University of Southern California. Accessed April 14, 2021. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/316863/rec/5321.

MLA Handbook (7th Edition):

Yang, Kai-Ting. “Pten deletion in adult pancreatic beta-cells induces cell proliferation and G1/S cell cycle progression.” 2013. Web. 14 Apr 2021.

Vancouver:

Yang K. Pten deletion in adult pancreatic beta-cells induces cell proliferation and G1/S cell cycle progression. [Internet] [Masters thesis]. University of Southern California; 2013. [cited 2021 Apr 14]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/316863/rec/5321.

Council of Science Editors:

Yang K. Pten deletion in adult pancreatic beta-cells induces cell proliferation and G1/S cell cycle progression. [Masters Thesis]. University of Southern California; 2013. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/316863/rec/5321


Vanderbilt University

2. Carboneau, Bethany Ann. Regulation of Beta-Cell Mass Expansion by Prostaglandin E2 Signaling.

Degree: PhD, Molecular Physiology and Biophysics, 2017, Vanderbilt University

 Type 2 diabetes is a major healthcare concern and is characterized by chronic hyperglycemia and low-grade inflammation. Hyperglycemia and systemic inflammation can induce the production… (more)

Subjects/Keywords: pancreatic beta cell; prostaglandins; proliferation; cell death; beta-cell mass

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APA (6th Edition):

Carboneau, B. A. (2017). Regulation of Beta-Cell Mass Expansion by Prostaglandin E2 Signaling. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/13906

Chicago Manual of Style (16th Edition):

Carboneau, Bethany Ann. “Regulation of Beta-Cell Mass Expansion by Prostaglandin E2 Signaling.” 2017. Doctoral Dissertation, Vanderbilt University. Accessed April 14, 2021. http://hdl.handle.net/1803/13906.

MLA Handbook (7th Edition):

Carboneau, Bethany Ann. “Regulation of Beta-Cell Mass Expansion by Prostaglandin E2 Signaling.” 2017. Web. 14 Apr 2021.

Vancouver:

Carboneau BA. Regulation of Beta-Cell Mass Expansion by Prostaglandin E2 Signaling. [Internet] [Doctoral dissertation]. Vanderbilt University; 2017. [cited 2021 Apr 14]. Available from: http://hdl.handle.net/1803/13906.

Council of Science Editors:

Carboneau BA. Regulation of Beta-Cell Mass Expansion by Prostaglandin E2 Signaling. [Doctoral Dissertation]. Vanderbilt University; 2017. Available from: http://hdl.handle.net/1803/13906


Vanderbilt University

3. Riley, Kimberly Ann Gooding. Modulation of Beta-Cell Intrinsic and Extrinsic Characteristics by CTGF to Promote Beta-Cell Mass Regeneration.

Degree: PhD, Cell and Developmental Biology, 2015, Vanderbilt University

 As diabetes continues to affect millions of people within the United States, identification of novel factors that may enhance beta-cell proliferation and mass regeneration in… (more)

Subjects/Keywords: diabetes; regeneration; beta-cell; CTGF; pancreas; proliferation

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APA (6th Edition):

Riley, K. A. G. (2015). Modulation of Beta-Cell Intrinsic and Extrinsic Characteristics by CTGF to Promote Beta-Cell Mass Regeneration. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/10722

Chicago Manual of Style (16th Edition):

Riley, Kimberly Ann Gooding. “Modulation of Beta-Cell Intrinsic and Extrinsic Characteristics by CTGF to Promote Beta-Cell Mass Regeneration.” 2015. Doctoral Dissertation, Vanderbilt University. Accessed April 14, 2021. http://hdl.handle.net/1803/10722.

MLA Handbook (7th Edition):

Riley, Kimberly Ann Gooding. “Modulation of Beta-Cell Intrinsic and Extrinsic Characteristics by CTGF to Promote Beta-Cell Mass Regeneration.” 2015. Web. 14 Apr 2021.

Vancouver:

Riley KAG. Modulation of Beta-Cell Intrinsic and Extrinsic Characteristics by CTGF to Promote Beta-Cell Mass Regeneration. [Internet] [Doctoral dissertation]. Vanderbilt University; 2015. [cited 2021 Apr 14]. Available from: http://hdl.handle.net/1803/10722.

Council of Science Editors:

Riley KAG. Modulation of Beta-Cell Intrinsic and Extrinsic Characteristics by CTGF to Promote Beta-Cell Mass Regeneration. [Doctoral Dissertation]. Vanderbilt University; 2015. Available from: http://hdl.handle.net/1803/10722


Virginia Tech

4. Li, Xiaoxiao. Ranolazine: a Potential Anti-diabetic Drug.

Degree: MS, Human Nutrition, Foods, and Exercise, 2012, Virginia Tech

 Diabetes is a life-long chronic disease that affects more than 24 million Americans. Loss of pancreatic beta-cell mass and function is central to the development… (more)

Subjects/Keywords: Ranolazine; Beta-cell; Apoptosis; Proliferation; Diabetes

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APA (6th Edition):

Li, X. (2012). Ranolazine: a Potential Anti-diabetic Drug. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/19202

Chicago Manual of Style (16th Edition):

Li, Xiaoxiao. “Ranolazine: a Potential Anti-diabetic Drug.” 2012. Masters Thesis, Virginia Tech. Accessed April 14, 2021. http://hdl.handle.net/10919/19202.

MLA Handbook (7th Edition):

Li, Xiaoxiao. “Ranolazine: a Potential Anti-diabetic Drug.” 2012. Web. 14 Apr 2021.

Vancouver:

Li X. Ranolazine: a Potential Anti-diabetic Drug. [Internet] [Masters thesis]. Virginia Tech; 2012. [cited 2021 Apr 14]. Available from: http://hdl.handle.net/10919/19202.

Council of Science Editors:

Li X. Ranolazine: a Potential Anti-diabetic Drug. [Masters Thesis]. Virginia Tech; 2012. Available from: http://hdl.handle.net/10919/19202


University of California – San Diego

5. Benthuysen, Jacqueline. Regulation of pancreatic beta cell proliferation and aging.

Degree: Biomedical Sciences, 2016, University of California – San Diego

 The replicative capacity of insulin-producing pancreatic beta cells is dynamically regulated during development, maturation, and aging. Early in life, beta cells proliferate rapidly to expand… (more)

Subjects/Keywords: Molecular biology; Genetics; Beta cell; Beta cell aging; Beta cell proliferation; Glucose; MAPK; Nkx6.1

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APA (6th Edition):

Benthuysen, J. (2016). Regulation of pancreatic beta cell proliferation and aging. (Thesis). University of California – San Diego. Retrieved from http://www.escholarship.org/uc/item/1k9844q3

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):

Benthuysen, Jacqueline. “Regulation of pancreatic beta cell proliferation and aging.” 2016. Thesis, University of California – San Diego. Accessed April 14, 2021. http://www.escholarship.org/uc/item/1k9844q3.

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

MLA Handbook (7th Edition):

Benthuysen, Jacqueline. “Regulation of pancreatic beta cell proliferation and aging.” 2016. Web. 14 Apr 2021.

Vancouver:

Benthuysen J. Regulation of pancreatic beta cell proliferation and aging. [Internet] [Thesis]. University of California – San Diego; 2016. [cited 2021 Apr 14]. Available from: http://www.escholarship.org/uc/item/1k9844q3.

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

Council of Science Editors:

Benthuysen J. Regulation of pancreatic beta cell proliferation and aging. [Thesis]. University of California – San Diego; 2016. Available from: http://www.escholarship.org/uc/item/1k9844q3

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


University of Illinois – Chicago

6. Rady, Brian. Transcription Factors E2F Have a Role in Proliferation of Beta-Cells and Development of Type-2 Diabetes.

Degree: 2013, University of Illinois – Chicago

 This work pertains to the search for genetic targets to induce beta-cell proliferation. This proliferation was intended to support the advancement of islet cell transplant… (more)

Subjects/Keywords: Diabetes; cell therapy; beta-cell proliferation; cell-cycle

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APA (6th Edition):

Rady, B. (2013). Transcription Factors E2F Have a Role in Proliferation of Beta-Cells and Development of Type-2 Diabetes. (Thesis). University of Illinois – Chicago. Retrieved from http://hdl.handle.net/10027/10071

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):

Rady, Brian. “Transcription Factors E2F Have a Role in Proliferation of Beta-Cells and Development of Type-2 Diabetes.” 2013. Thesis, University of Illinois – Chicago. Accessed April 14, 2021. http://hdl.handle.net/10027/10071.

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

MLA Handbook (7th Edition):

Rady, Brian. “Transcription Factors E2F Have a Role in Proliferation of Beta-Cells and Development of Type-2 Diabetes.” 2013. Web. 14 Apr 2021.

Vancouver:

Rady B. Transcription Factors E2F Have a Role in Proliferation of Beta-Cells and Development of Type-2 Diabetes. [Internet] [Thesis]. University of Illinois – Chicago; 2013. [cited 2021 Apr 14]. Available from: http://hdl.handle.net/10027/10071.

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

Council of Science Editors:

Rady B. Transcription Factors E2F Have a Role in Proliferation of Beta-Cells and Development of Type-2 Diabetes. [Thesis]. University of Illinois – Chicago; 2013. Available from: http://hdl.handle.net/10027/10071

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

7. Coelho, Marisa. Expanding our therapeutic options: β-blockers for colon cancer?.

Degree: 2013, Instituto Politécnico do Porto

Supported by U. Porto/Santander Totta (IJUP) (PP-IJUP2011-320)

Colon cancer is the fourth and third most common cancer, respectively in men and women worldwide and its… (more)

Subjects/Keywords: Stress; Catecholamines; Adrenergic receptors; β-blockers; Cell proliferation; Catecolaminas; Recetores adrenérgicos; β-bloqueadores; Proliferação celular

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APA (6th Edition):

Coelho, M. (2013). Expanding our therapeutic options: β-blockers for colon cancer?. (Thesis). Instituto Politécnico do Porto. Retrieved from https://www.rcaap.pt/detail.jsp?id=oai:recipp.ipp.pt:10400.22/3471

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):

Coelho, Marisa. “Expanding our therapeutic options: β-blockers for colon cancer?.” 2013. Thesis, Instituto Politécnico do Porto. Accessed April 14, 2021. https://www.rcaap.pt/detail.jsp?id=oai:recipp.ipp.pt:10400.22/3471.

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

MLA Handbook (7th Edition):

Coelho, Marisa. “Expanding our therapeutic options: β-blockers for colon cancer?.” 2013. Web. 14 Apr 2021.

Vancouver:

Coelho M. Expanding our therapeutic options: β-blockers for colon cancer?. [Internet] [Thesis]. Instituto Politécnico do Porto; 2013. [cited 2021 Apr 14]. Available from: https://www.rcaap.pt/detail.jsp?id=oai:recipp.ipp.pt:10400.22/3471.

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

Council of Science Editors:

Coelho M. Expanding our therapeutic options: β-blockers for colon cancer?. [Thesis]. Instituto Politécnico do Porto; 2013. Available from: https://www.rcaap.pt/detail.jsp?id=oai:recipp.ipp.pt:10400.22/3471

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


Brigham Young University

8. Draney, Carrie. Overexpression of HDAC1 Induces Functional β-cell Mass.

Degree: MS, 2016, Brigham Young University

 Type 2 diabetes is a metabolic disorder that results in β-cell dysfunction and ultimate destruction, and leads to impaired glucose homeostasis. High rates of proliferation(more)

Subjects/Keywords: diabetes; β-cell; proliferation; HDAC1; p15/INK4b; Nutrition

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APA (6th Edition):

Draney, C. (2016). Overexpression of HDAC1 Induces Functional β-cell Mass. (Masters Thesis). Brigham Young University. Retrieved from https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=7573&context=etd

Chicago Manual of Style (16th Edition):

Draney, Carrie. “Overexpression of HDAC1 Induces Functional β-cell Mass.” 2016. Masters Thesis, Brigham Young University. Accessed April 14, 2021. https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=7573&context=etd.

MLA Handbook (7th Edition):

Draney, Carrie. “Overexpression of HDAC1 Induces Functional β-cell Mass.” 2016. Web. 14 Apr 2021.

Vancouver:

Draney C. Overexpression of HDAC1 Induces Functional β-cell Mass. [Internet] [Masters thesis]. Brigham Young University; 2016. [cited 2021 Apr 14]. Available from: https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=7573&context=etd.

Council of Science Editors:

Draney C. Overexpression of HDAC1 Induces Functional β-cell Mass. [Masters Thesis]. Brigham Young University; 2016. Available from: https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=7573&context=etd


University of Toronto

9. Xu, Songyi. Valve Interstitial Cell Activation and Proliferation are Associated with Changes in Beta-catenin.

Degree: 2012, University of Toronto

Heart valve interstitial cells (VICs) undergo activation and proliferation in repair and disease, but the mechanisms are not fully understood. We hypothesize that the establishment… (more)

Subjects/Keywords: heart valve interstitial cell; beta-catenin; activation; proliferation; 0571

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APA (6th Edition):

Xu, S. (2012). Valve Interstitial Cell Activation and Proliferation are Associated with Changes in Beta-catenin. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/32290

Chicago Manual of Style (16th Edition):

Xu, Songyi. “Valve Interstitial Cell Activation and Proliferation are Associated with Changes in Beta-catenin.” 2012. Masters Thesis, University of Toronto. Accessed April 14, 2021. http://hdl.handle.net/1807/32290.

MLA Handbook (7th Edition):

Xu, Songyi. “Valve Interstitial Cell Activation and Proliferation are Associated with Changes in Beta-catenin.” 2012. Web. 14 Apr 2021.

Vancouver:

Xu S. Valve Interstitial Cell Activation and Proliferation are Associated with Changes in Beta-catenin. [Internet] [Masters thesis]. University of Toronto; 2012. [cited 2021 Apr 14]. Available from: http://hdl.handle.net/1807/32290.

Council of Science Editors:

Xu S. Valve Interstitial Cell Activation and Proliferation are Associated with Changes in Beta-catenin. [Masters Thesis]. University of Toronto; 2012. Available from: http://hdl.handle.net/1807/32290

10. Bianca de Fatima Borim Pulino. Expressão imuno-histoquímica da beta-catenina, p-Akt, CD44 e vimentina nos ameloblastomas.

Degree: 2013, University of São Paulo

O ameloblastoma é definido como um tumor odontogênico epitelial de crescimento lento e localmente invasivo, que acomete os maxilares com alta taxa de recorrência quando… (more)

Subjects/Keywords: Ameloblastoma; beta-Catenina; Imuno-histoquímica; Proliferação de células; Ameloblastoma; beta-Catenin; Cell proliferation; Immunohistochemistry

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APA (6th Edition):

Pulino, B. d. F. B. (2013). Expressão imuno-histoquímica da beta-catenina, p-Akt, CD44 e vimentina nos ameloblastomas. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/23/23141/tde-17102013-200337/

Chicago Manual of Style (16th Edition):

Pulino, Bianca de Fatima Borim. “Expressão imuno-histoquímica da beta-catenina, p-Akt, CD44 e vimentina nos ameloblastomas.” 2013. Masters Thesis, University of São Paulo. Accessed April 14, 2021. http://www.teses.usp.br/teses/disponiveis/23/23141/tde-17102013-200337/.

MLA Handbook (7th Edition):

Pulino, Bianca de Fatima Borim. “Expressão imuno-histoquímica da beta-catenina, p-Akt, CD44 e vimentina nos ameloblastomas.” 2013. Web. 14 Apr 2021.

Vancouver:

Pulino BdFB. Expressão imuno-histoquímica da beta-catenina, p-Akt, CD44 e vimentina nos ameloblastomas. [Internet] [Masters thesis]. University of São Paulo; 2013. [cited 2021 Apr 14]. Available from: http://www.teses.usp.br/teses/disponiveis/23/23141/tde-17102013-200337/.

Council of Science Editors:

Pulino BdFB. Expressão imuno-histoquímica da beta-catenina, p-Akt, CD44 e vimentina nos ameloblastomas. [Masters Thesis]. University of São Paulo; 2013. Available from: http://www.teses.usp.br/teses/disponiveis/23/23141/tde-17102013-200337/


University of Toronto

11. Gohil, Himaben Pravinsinh. GABA: a Potential Agent of Beta-Cell Proliferation.

Degree: 2018, University of Toronto

Studies have shown that GABA can increase the β-cell mass and improve glucose tolerance in normal and STZ treated mouse models. Herein we explored the… (more)

Subjects/Keywords: Beta-cell mass; Cell proliferation; GABA; Glucose tolerance; Metabolism; Pre-diabetes; 0719

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APA (6th Edition):

Gohil, H. P. (2018). GABA: a Potential Agent of Beta-Cell Proliferation. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/91730

Chicago Manual of Style (16th Edition):

Gohil, Himaben Pravinsinh. “GABA: a Potential Agent of Beta-Cell Proliferation.” 2018. Masters Thesis, University of Toronto. Accessed April 14, 2021. http://hdl.handle.net/1807/91730.

MLA Handbook (7th Edition):

Gohil, Himaben Pravinsinh. “GABA: a Potential Agent of Beta-Cell Proliferation.” 2018. Web. 14 Apr 2021.

Vancouver:

Gohil HP. GABA: a Potential Agent of Beta-Cell Proliferation. [Internet] [Masters thesis]. University of Toronto; 2018. [cited 2021 Apr 14]. Available from: http://hdl.handle.net/1807/91730.

Council of Science Editors:

Gohil HP. GABA: a Potential Agent of Beta-Cell Proliferation. [Masters Thesis]. University of Toronto; 2018. Available from: http://hdl.handle.net/1807/91730


Vanderbilt University

12. Zhang, Jia. The role of Foxm1 in growth factor-mediated pancreatic beta-cell proliferation.

Degree: PhD, Cell and Developmental Biology, 2010, Vanderbilt University

 THE ROLE OF FOXM1 IN GROWTH FACTOR-MEDIATED PANCREATIC BETA-CELL PROLIFERATION JIA ZHANG Dissertation under the direction of Professor Maureen A. Gannon Both type I and… (more)

Subjects/Keywords: gestational diabetes; beta-cell proliferation; Foxm1

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APA (6th Edition):

Zhang, J. (2010). The role of Foxm1 in growth factor-mediated pancreatic beta-cell proliferation. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/11861

Chicago Manual of Style (16th Edition):

Zhang, Jia. “The role of Foxm1 in growth factor-mediated pancreatic beta-cell proliferation.” 2010. Doctoral Dissertation, Vanderbilt University. Accessed April 14, 2021. http://hdl.handle.net/1803/11861.

MLA Handbook (7th Edition):

Zhang, Jia. “The role of Foxm1 in growth factor-mediated pancreatic beta-cell proliferation.” 2010. Web. 14 Apr 2021.

Vancouver:

Zhang J. The role of Foxm1 in growth factor-mediated pancreatic beta-cell proliferation. [Internet] [Doctoral dissertation]. Vanderbilt University; 2010. [cited 2021 Apr 14]. Available from: http://hdl.handle.net/1803/11861.

Council of Science Editors:

Zhang J. The role of Foxm1 in growth factor-mediated pancreatic beta-cell proliferation. [Doctoral Dissertation]. Vanderbilt University; 2010. Available from: http://hdl.handle.net/1803/11861


Penn State University

13. Wang, Rong. PERK eIF2alpha kinase regulates cell proliferation, insulin synthesis and secretion in pancreatic beta cells.

Degree: 2014, Penn State University

 Insulin synthesis and secretion, as well as cell proliferation are under tight regulation in pancreatic β-cells to maintain glucose homeostasis. Dysfunction in any of these… (more)

Subjects/Keywords: PERK eIF2alpha kinase; Ca2+ dynamics; insulin secretion; insulin biosynthesis; diabetes; ER stress; beta cell proliferation

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APA (6th Edition):

Wang, R. (2014). PERK eIF2alpha kinase regulates cell proliferation, insulin synthesis and secretion in pancreatic beta cells. (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/21417

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):

Wang, Rong. “PERK eIF2alpha kinase regulates cell proliferation, insulin synthesis and secretion in pancreatic beta cells.” 2014. Thesis, Penn State University. Accessed April 14, 2021. https://submit-etda.libraries.psu.edu/catalog/21417.

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

MLA Handbook (7th Edition):

Wang, Rong. “PERK eIF2alpha kinase regulates cell proliferation, insulin synthesis and secretion in pancreatic beta cells.” 2014. Web. 14 Apr 2021.

Vancouver:

Wang R. PERK eIF2alpha kinase regulates cell proliferation, insulin synthesis and secretion in pancreatic beta cells. [Internet] [Thesis]. Penn State University; 2014. [cited 2021 Apr 14]. Available from: https://submit-etda.libraries.psu.edu/catalog/21417.

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

Council of Science Editors:

Wang R. PERK eIF2alpha kinase regulates cell proliferation, insulin synthesis and secretion in pancreatic beta cells. [Thesis]. Penn State University; 2014. Available from: https://submit-etda.libraries.psu.edu/catalog/21417

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


Penn State University

14. Matsui, Yurika. THE FUNCTION AND REGULATION OF A TRANSCRIPTIONAL CO-ACTIVATOR YAP IN GROWTH CONTROL AND TISSUE HOMEOSTASIS.

Degree: 2017, Penn State University

 In each organ, cells employ intricate mechanisms in order to control their turnover for the maintenance of overall organ size and function. Many factors involved… (more)

Subjects/Keywords: Hippo pathway; Yes-associated protein (YAP); cell proliferation; apoptosis; isoform; pancreatic beta-cell; large tumor suppressor kinase 1 (LATS1)

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APA (6th Edition):

Matsui, Y. (2017). THE FUNCTION AND REGULATION OF A TRANSCRIPTIONAL CO-ACTIVATOR YAP IN GROWTH CONTROL AND TISSUE HOMEOSTASIS. (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/14713yum111

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):

Matsui, Yurika. “THE FUNCTION AND REGULATION OF A TRANSCRIPTIONAL CO-ACTIVATOR YAP IN GROWTH CONTROL AND TISSUE HOMEOSTASIS.” 2017. Thesis, Penn State University. Accessed April 14, 2021. https://submit-etda.libraries.psu.edu/catalog/14713yum111.

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

MLA Handbook (7th Edition):

Matsui, Yurika. “THE FUNCTION AND REGULATION OF A TRANSCRIPTIONAL CO-ACTIVATOR YAP IN GROWTH CONTROL AND TISSUE HOMEOSTASIS.” 2017. Web. 14 Apr 2021.

Vancouver:

Matsui Y. THE FUNCTION AND REGULATION OF A TRANSCRIPTIONAL CO-ACTIVATOR YAP IN GROWTH CONTROL AND TISSUE HOMEOSTASIS. [Internet] [Thesis]. Penn State University; 2017. [cited 2021 Apr 14]. Available from: https://submit-etda.libraries.psu.edu/catalog/14713yum111.

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

Council of Science Editors:

Matsui Y. THE FUNCTION AND REGULATION OF A TRANSCRIPTIONAL CO-ACTIVATOR YAP IN GROWTH CONTROL AND TISSUE HOMEOSTASIS. [Thesis]. Penn State University; 2017. Available from: https://submit-etda.libraries.psu.edu/catalog/14713yum111

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


University of Manchester

15. Salisbury, Rachel. Gene expression and cell cycle regulation in human pancreas development and congenital hyperinsulinism.

Degree: 2015, University of Manchester

 The dynamics of β-cell mass are at the focus of an extensive international effort to develop β-cell replacement therapies for type 1 diabetes. During normal… (more)

Subjects/Keywords: Human Development; Pancreas; Fetal; Congenital Hyperinsulinism Infancy; Hyperinsulinism; Beta Cell; Islets; Proliferation; Neurogenin3; Endocrine; Differentiation; Cell Cycle; Transcription Factor; Gene

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APA (6th Edition):

Salisbury, R. (2015). Gene expression and cell cycle regulation in human pancreas development and congenital hyperinsulinism. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:244755

Chicago Manual of Style (16th Edition):

Salisbury, Rachel. “Gene expression and cell cycle regulation in human pancreas development and congenital hyperinsulinism.” 2015. Doctoral Dissertation, University of Manchester. Accessed April 14, 2021. http://www.manchester.ac.uk/escholar/uk-ac-man-scw:244755.

MLA Handbook (7th Edition):

Salisbury, Rachel. “Gene expression and cell cycle regulation in human pancreas development and congenital hyperinsulinism.” 2015. Web. 14 Apr 2021.

Vancouver:

Salisbury R. Gene expression and cell cycle regulation in human pancreas development and congenital hyperinsulinism. [Internet] [Doctoral dissertation]. University of Manchester; 2015. [cited 2021 Apr 14]. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:244755.

Council of Science Editors:

Salisbury R. Gene expression and cell cycle regulation in human pancreas development and congenital hyperinsulinism. [Doctoral Dissertation]. University of Manchester; 2015. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:244755

16. Lubaczeuski, Camila. Participação do sistema nervoso parassimpático no metabolismo energético e na proliferação celular em ilhotas pancreáticas de ratos obesos-MSG.

Degree: 2013, Universidade Estadual do Oeste do Parana; Programa de Pós-Graduação Stricto Sensu em Biociências e Saúde; UNIOESTE; BR; Biologia, processo saúde-doença e políticas da saúde

Made available in DSpace on 2017-07-10T14:17:01Z (GMT). No. of bitstreams: 1 Camila.pdf: 1579699 bytes, checksum: 81aed6e2676f0085056d80a67c1ae83e (MD5) Previous issue date: 2013-08-01

The growing number of… (more)

Subjects/Keywords: Obesidade; Sistema nervoso parassimpático; Proliferação de células β; MSG-obesity; Vagus nerve; Parasympathetic nervous system; β; -cell proliferation; CNPQ::CIENCIAS DA SAUDE

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APA (6th Edition):

Lubaczeuski, C. (2013). Participação do sistema nervoso parassimpático no metabolismo energético e na proliferação celular em ilhotas pancreáticas de ratos obesos-MSG. (Masters Thesis). Universidade Estadual do Oeste do Parana; Programa de Pós-Graduação Stricto Sensu em Biociências e Saúde; UNIOESTE; BR; Biologia, processo saúde-doença e políticas da saúde. Retrieved from http://tede.unioeste.br:8080/tede/handle/tede/627

Chicago Manual of Style (16th Edition):

Lubaczeuski, Camila. “Participação do sistema nervoso parassimpático no metabolismo energético e na proliferação celular em ilhotas pancreáticas de ratos obesos-MSG.” 2013. Masters Thesis, Universidade Estadual do Oeste do Parana; Programa de Pós-Graduação Stricto Sensu em Biociências e Saúde; UNIOESTE; BR; Biologia, processo saúde-doença e políticas da saúde. Accessed April 14, 2021. http://tede.unioeste.br:8080/tede/handle/tede/627.

MLA Handbook (7th Edition):

Lubaczeuski, Camila. “Participação do sistema nervoso parassimpático no metabolismo energético e na proliferação celular em ilhotas pancreáticas de ratos obesos-MSG.” 2013. Web. 14 Apr 2021.

Vancouver:

Lubaczeuski C. Participação do sistema nervoso parassimpático no metabolismo energético e na proliferação celular em ilhotas pancreáticas de ratos obesos-MSG. [Internet] [Masters thesis]. Universidade Estadual do Oeste do Parana; Programa de Pós-Graduação Stricto Sensu em Biociências e Saúde; UNIOESTE; BR; Biologia, processo saúde-doença e políticas da saúde; 2013. [cited 2021 Apr 14]. Available from: http://tede.unioeste.br:8080/tede/handle/tede/627.

Council of Science Editors:

Lubaczeuski C. Participação do sistema nervoso parassimpático no metabolismo energético e na proliferação celular em ilhotas pancreáticas de ratos obesos-MSG. [Masters Thesis]. Universidade Estadual do Oeste do Parana; Programa de Pós-Graduação Stricto Sensu em Biociências e Saúde; UNIOESTE; BR; Biologia, processo saúde-doença e políticas da saúde; 2013. Available from: http://tede.unioeste.br:8080/tede/handle/tede/627


Universidade Estadual de Campinas

17. Maschio, Daniela Aparecida, 1983-. Possível ativação da via de sinalização Wnt/beta-catenina no processo de hiperplasia compensatória da célula beta pancreática em modelo animal de resistência periférica à insulina.

Degree: Instituto de Biologia; Programa de Pós-Graduação em Biologia Celular e Estrutural, 2014, Universidade Estadual de Campinas

Orientador: Carla Beatriz Collares Buzato

Dissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia

Made available in DSpace on 2018-08-24T14:09:15Z (GMT). No. of bitstreams:… (more)

Subjects/Keywords: Pré-diabetes; Células secretoras de insulina; Via Wnt/beta-catenina; Proliferação celular; Prediabetes; Pancreatic beta cells; Wnt/beta-catenin pathway; Cell proliferation

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

APA (6th Edition):

Maschio, Daniela Aparecida, 1. (2014). Possível ativação da via de sinalização Wnt/beta-catenina no processo de hiperplasia compensatória da célula beta pancreática em modelo animal de resistência periférica à insulina. (Masters Thesis). Universidade Estadual de Campinas. Retrieved from MASCHIO, Daniela Aparecida. Possível ativação da via de sinalização Wnt/beta-catenina no processo de hiperplasia compensatória da célula beta pancreática em modelo animal de resistência periférica à insulina. 2014. 83 f. Dissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia, Campinas, SP. Disponível em: <http://www.repositorio.unicamp.br/handle/REPOSIP/317123>. Acesso em: 24 ago. 2018. ; http://repositorio.unicamp.br/jspui/handle/REPOSIP/317123

Chicago Manual of Style (16th Edition):

Maschio, Daniela Aparecida, 1983-. “Possível ativação da via de sinalização Wnt/beta-catenina no processo de hiperplasia compensatória da célula beta pancreática em modelo animal de resistência periférica à insulina.” 2014. Masters Thesis, Universidade Estadual de Campinas. Accessed April 14, 2021. MASCHIO, Daniela Aparecida. Possível ativação da via de sinalização Wnt/beta-catenina no processo de hiperplasia compensatória da célula beta pancreática em modelo animal de resistência periférica à insulina. 2014. 83 f. Dissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia, Campinas, SP. Disponível em: <http://www.repositorio.unicamp.br/handle/REPOSIP/317123>. Acesso em: 24 ago. 2018. ; http://repositorio.unicamp.br/jspui/handle/REPOSIP/317123.

MLA Handbook (7th Edition):

Maschio, Daniela Aparecida, 1983-. “Possível ativação da via de sinalização Wnt/beta-catenina no processo de hiperplasia compensatória da célula beta pancreática em modelo animal de resistência periférica à insulina.” 2014. Web. 14 Apr 2021.

Vancouver:

Maschio, Daniela Aparecida 1. Possível ativação da via de sinalização Wnt/beta-catenina no processo de hiperplasia compensatória da célula beta pancreática em modelo animal de resistência periférica à insulina. [Internet] [Masters thesis]. Universidade Estadual de Campinas; 2014. [cited 2021 Apr 14]. Available from: MASCHIO, Daniela Aparecida. Possível ativação da via de sinalização Wnt/beta-catenina no processo de hiperplasia compensatória da célula beta pancreática em modelo animal de resistência periférica à insulina. 2014. 83 f. Dissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia, Campinas, SP. Disponível em: <http://www.repositorio.unicamp.br/handle/REPOSIP/317123>. Acesso em: 24 ago. 2018. ; http://repositorio.unicamp.br/jspui/handle/REPOSIP/317123.

Council of Science Editors:

Maschio, Daniela Aparecida 1. Possível ativação da via de sinalização Wnt/beta-catenina no processo de hiperplasia compensatória da célula beta pancreática em modelo animal de resistência periférica à insulina. [Masters Thesis]. Universidade Estadual de Campinas; 2014. Available from: MASCHIO, Daniela Aparecida. Possível ativação da via de sinalização Wnt/beta-catenina no processo de hiperplasia compensatória da célula beta pancreática em modelo animal de resistência periférica à insulina. 2014. 83 f. Dissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia, Campinas, SP. Disponível em: <http://www.repositorio.unicamp.br/handle/REPOSIP/317123>. Acesso em: 24 ago. 2018. ; http://repositorio.unicamp.br/jspui/handle/REPOSIP/317123


Universidade Estadual de Campinas

18. Garcia-Fossa, Fernanda, 1995-. Inter-relação entre nanopartículas lipídicas sólidas, a via do TGF-B e transição epitélio-mesenquimal em células de próstata tumorais e não tumorais.

Degree: Instituto de Biologia; Programa de Pós-Graduação em Biologia Funcional e Molecular, 2020, Universidade Estadual de Campinas

Orientador: Marcelo Bispo de Jesus

Dissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia

Made available in DSpace on 2020-05-20T19:55:09Z (GMT). No. of bitstreams:… (more)

Subjects/Keywords: Movimento celular; Proliferação celular; Metástase; Cicatrização de feridas; Fator de crescimento transformador beta; Cell movement; Cell proliferation; Neoplasm metastasis; Wound healing; Transforming growth factor beta

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

APA (6th Edition):

Garcia-Fossa, Fernanda, 1. (2020). Inter-relação entre nanopartículas lipídicas sólidas, a via do TGF-B e transição epitélio-mesenquimal em células de próstata tumorais e não tumorais. (Masters Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/341842

Chicago Manual of Style (16th Edition):

Garcia-Fossa, Fernanda, 1995-. “Inter-relação entre nanopartículas lipídicas sólidas, a via do TGF-B e transição epitélio-mesenquimal em células de próstata tumorais e não tumorais.” 2020. Masters Thesis, Universidade Estadual de Campinas. Accessed April 14, 2021. http://repositorio.unicamp.br/jspui/handle/REPOSIP/341842.

MLA Handbook (7th Edition):

Garcia-Fossa, Fernanda, 1995-. “Inter-relação entre nanopartículas lipídicas sólidas, a via do TGF-B e transição epitélio-mesenquimal em células de próstata tumorais e não tumorais.” 2020. Web. 14 Apr 2021.

Vancouver:

Garcia-Fossa, Fernanda 1. Inter-relação entre nanopartículas lipídicas sólidas, a via do TGF-B e transição epitélio-mesenquimal em células de próstata tumorais e não tumorais. [Internet] [Masters thesis]. Universidade Estadual de Campinas; 2020. [cited 2021 Apr 14]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/341842.

Council of Science Editors:

Garcia-Fossa, Fernanda 1. Inter-relação entre nanopartículas lipídicas sólidas, a via do TGF-B e transição epitélio-mesenquimal em células de próstata tumorais e não tumorais. [Masters Thesis]. Universidade Estadual de Campinas; 2020. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/341842


Kyoto University / 京都大学

19. Bando, Mika. Studies on pathophysiological significance of intraislet ghrelin using transgenic animal model. : 遺伝子改変動物を用いた膵島由来グレリンの病態生理学的意義の検討.

Degree: 博士(人間健康科学), 2014, Kyoto University / 京都大学

新制・課程博士

甲第18197号

人健博第14号

Subjects/Keywords: ghrelin; insulin secretion; glucose metabolism; diabetes; beta cell proliferation

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

APA (6th Edition):

Bando, M. (2014). Studies on pathophysiological significance of intraislet ghrelin using transgenic animal model. : 遺伝子改変動物を用いた膵島由来グレリンの病態生理学的意義の検討. (Thesis). Kyoto University / 京都大学. Retrieved from http://hdl.handle.net/2433/188712 ; http://dx.doi.org/10.14989/doctor.k18197

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):

Bando, Mika. “Studies on pathophysiological significance of intraislet ghrelin using transgenic animal model. : 遺伝子改変動物を用いた膵島由来グレリンの病態生理学的意義の検討.” 2014. Thesis, Kyoto University / 京都大学. Accessed April 14, 2021. http://hdl.handle.net/2433/188712 ; http://dx.doi.org/10.14989/doctor.k18197.

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

MLA Handbook (7th Edition):

Bando, Mika. “Studies on pathophysiological significance of intraislet ghrelin using transgenic animal model. : 遺伝子改変動物を用いた膵島由来グレリンの病態生理学的意義の検討.” 2014. Web. 14 Apr 2021.

Vancouver:

Bando M. Studies on pathophysiological significance of intraislet ghrelin using transgenic animal model. : 遺伝子改変動物を用いた膵島由来グレリンの病態生理学的意義の検討. [Internet] [Thesis]. Kyoto University / 京都大学; 2014. [cited 2021 Apr 14]. Available from: http://hdl.handle.net/2433/188712 ; http://dx.doi.org/10.14989/doctor.k18197.

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

Council of Science Editors:

Bando M. Studies on pathophysiological significance of intraislet ghrelin using transgenic animal model. : 遺伝子改変動物を用いた膵島由来グレリンの病態生理学的意義の検討. [Thesis]. Kyoto University / 京都大学; 2014. Available from: http://hdl.handle.net/2433/188712 ; http://dx.doi.org/10.14989/doctor.k18197

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

20. ALHERZ, MOHAMMAD. The metabolic determinants of the response to ketone bodies in SH-SY5Y neuroblastoma cells.

Degree: School of Medicine. Discipline of Anatomy, 2020, Trinity College Dublin

 Neuroblastoma (NB) is a childhood malignancy of the sympathetic nervous system. Its mutual neoplastic and neurodevelopmental underpinnings are characterised by an excessive glucose demand as… (more)

Subjects/Keywords: Cancer; Neuroblastoma; Metformin; Ketogenic Diet; Warburg Effect; Metabolism; Proliferation; Morphology; Beta-Hydroxybutyrate; Cell Culture; Neurodevelopment; Pyruvate; Lactate; Glucose; Glutamine

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APA (6th Edition):

ALHERZ, M. (2020). The metabolic determinants of the response to ketone bodies in SH-SY5Y neuroblastoma cells. (Thesis). Trinity College Dublin. Retrieved from http://hdl.handle.net/2262/94130

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):

ALHERZ, MOHAMMAD. “The metabolic determinants of the response to ketone bodies in SH-SY5Y neuroblastoma cells.” 2020. Thesis, Trinity College Dublin. Accessed April 14, 2021. http://hdl.handle.net/2262/94130.

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

MLA Handbook (7th Edition):

ALHERZ, MOHAMMAD. “The metabolic determinants of the response to ketone bodies in SH-SY5Y neuroblastoma cells.” 2020. Web. 14 Apr 2021.

Vancouver:

ALHERZ M. The metabolic determinants of the response to ketone bodies in SH-SY5Y neuroblastoma cells. [Internet] [Thesis]. Trinity College Dublin; 2020. [cited 2021 Apr 14]. Available from: http://hdl.handle.net/2262/94130.

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

Council of Science Editors:

ALHERZ M. The metabolic determinants of the response to ketone bodies in SH-SY5Y neuroblastoma cells. [Thesis]. Trinity College Dublin; 2020. Available from: http://hdl.handle.net/2262/94130

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


Kyoto University

21. Bando, Mika. Studies on pathophysiological significance of intraislet ghrelin using transgenic animal model.

Degree: 2014, Kyoto University

Subjects/Keywords: ghrelin; insulin secretion; glucose metabolism; diabetes; beta cell proliferation

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

APA (6th Edition):

Bando, M. (2014). Studies on pathophysiological significance of intraislet ghrelin using transgenic animal model. (Thesis). Kyoto University. Retrieved from http://hdl.handle.net/2433/188712

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):

Bando, Mika. “Studies on pathophysiological significance of intraislet ghrelin using transgenic animal model. ” 2014. Thesis, Kyoto University. Accessed April 14, 2021. http://hdl.handle.net/2433/188712.

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

MLA Handbook (7th Edition):

Bando, Mika. “Studies on pathophysiological significance of intraislet ghrelin using transgenic animal model. ” 2014. Web. 14 Apr 2021.

Vancouver:

Bando M. Studies on pathophysiological significance of intraislet ghrelin using transgenic animal model. [Internet] [Thesis]. Kyoto University; 2014. [cited 2021 Apr 14]. Available from: http://hdl.handle.net/2433/188712.

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

Council of Science Editors:

Bando M. Studies on pathophysiological significance of intraislet ghrelin using transgenic animal model. [Thesis]. Kyoto University; 2014. Available from: http://hdl.handle.net/2433/188712

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


University of Pennsylvania

22. Rieck, Sebastian. The Generation of Fully Functional β-Cells by Proliferation: Lessons From Pregnancy and HNF4α.

Degree: 2011, University of Pennsylvania

 Diabetes mellitus is an increasingly prevalent metabolic disorder that is estimated to affect over 300 million people by 2025. Common to either type 1 or… (more)

Subjects/Keywords: beta-cell proliferation; diabetes mellitus; regeneration; Endocrinology; Medical Cell Biology; Medical Genetics; Medical Molecular Biology; Medical Physiology; Medical Sciences; Pharmacology; Physiological Processes

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APA (6th Edition):

Rieck, S. (2011). The Generation of Fully Functional β-Cells by Proliferation: Lessons From Pregnancy and HNF4α. (Thesis). University of Pennsylvania. Retrieved from https://repository.upenn.edu/edissertations/984

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):

Rieck, Sebastian. “The Generation of Fully Functional β-Cells by Proliferation: Lessons From Pregnancy and HNF4α.” 2011. Thesis, University of Pennsylvania. Accessed April 14, 2021. https://repository.upenn.edu/edissertations/984.

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

MLA Handbook (7th Edition):

Rieck, Sebastian. “The Generation of Fully Functional β-Cells by Proliferation: Lessons From Pregnancy and HNF4α.” 2011. Web. 14 Apr 2021.

Vancouver:

Rieck S. The Generation of Fully Functional β-Cells by Proliferation: Lessons From Pregnancy and HNF4α. [Internet] [Thesis]. University of Pennsylvania; 2011. [cited 2021 Apr 14]. Available from: https://repository.upenn.edu/edissertations/984.

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

Council of Science Editors:

Rieck S. The Generation of Fully Functional β-Cells by Proliferation: Lessons From Pregnancy and HNF4α. [Thesis]. University of Pennsylvania; 2011. Available from: https://repository.upenn.edu/edissertations/984

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


IUPUI

23. Maganti Vijaykumar, Aarthi. Mechanisms of transcriptional regulation in the maintenance of β cell function.

Degree: 2015, IUPUI

Indiana University-Purdue University Indianapolis (IUPUI) Indiana University School of Medicine

The islet β cell is central to the maintenance of glucose homeostasis as the β… (more)

Subjects/Keywords: Transcription; Islet; Pdx1; Diabetes; ER Stress; Methylation; Pancreatic beta cells; Cell proliferation; DNA  – Genetics; DNA  – Metabolism; Insulin  – Genetics; Diabetes  – Treatment; Mice as laboratory animals

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

APA (6th Edition):

Maganti Vijaykumar, A. (2015). Mechanisms of transcriptional regulation in the maintenance of β cell function. (Thesis). IUPUI. Retrieved from http://hdl.handle.net/1805/7944

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):

Maganti Vijaykumar, Aarthi. “Mechanisms of transcriptional regulation in the maintenance of β cell function.” 2015. Thesis, IUPUI. Accessed April 14, 2021. http://hdl.handle.net/1805/7944.

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

MLA Handbook (7th Edition):

Maganti Vijaykumar, Aarthi. “Mechanisms of transcriptional regulation in the maintenance of β cell function.” 2015. Web. 14 Apr 2021.

Vancouver:

Maganti Vijaykumar A. Mechanisms of transcriptional regulation in the maintenance of β cell function. [Internet] [Thesis]. IUPUI; 2015. [cited 2021 Apr 14]. Available from: http://hdl.handle.net/1805/7944.

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

Council of Science Editors:

Maganti Vijaykumar A. Mechanisms of transcriptional regulation in the maintenance of β cell function. [Thesis]. IUPUI; 2015. Available from: http://hdl.handle.net/1805/7944

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

24. Guez, Fanny. Etude des mécanismes moléculaires impliqués dans le cycle cellulaire des cellules β pancréatiques humaines : Molecular mechanisms involved in the cell cycle of human pancreatic beta cells.

Degree: Docteur es, Biologie moléculaire et cellulaire, 2013, Université Paris Descartes – Paris V

Le diabète est une maladie qui touche 347 millions de personnes dans le monde (90% ayant un diabète de type 2) (OMS, septembre 2012). Elle… (more)

Subjects/Keywords: Pancréas; Cellules bêta; Humain; Diabète; Cycle cellulaire; Prolifération; Facteurs de croissances; Hormones; Autophagie; Pancreas; Beta cells; Human; Diabetes; Cell cycle; Proliferation; Growth factors; Hormones; Autophagy; 616.462

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APA (6th Edition):

Guez, F. (2013). Etude des mécanismes moléculaires impliqués dans le cycle cellulaire des cellules β pancréatiques humaines : Molecular mechanisms involved in the cell cycle of human pancreatic beta cells. (Doctoral Dissertation). Université Paris Descartes – Paris V. Retrieved from http://www.theses.fr/2013PA05T094

Chicago Manual of Style (16th Edition):

Guez, Fanny. “Etude des mécanismes moléculaires impliqués dans le cycle cellulaire des cellules β pancréatiques humaines : Molecular mechanisms involved in the cell cycle of human pancreatic beta cells.” 2013. Doctoral Dissertation, Université Paris Descartes – Paris V. Accessed April 14, 2021. http://www.theses.fr/2013PA05T094.

MLA Handbook (7th Edition):

Guez, Fanny. “Etude des mécanismes moléculaires impliqués dans le cycle cellulaire des cellules β pancréatiques humaines : Molecular mechanisms involved in the cell cycle of human pancreatic beta cells.” 2013. Web. 14 Apr 2021.

Vancouver:

Guez F. Etude des mécanismes moléculaires impliqués dans le cycle cellulaire des cellules β pancréatiques humaines : Molecular mechanisms involved in the cell cycle of human pancreatic beta cells. [Internet] [Doctoral dissertation]. Université Paris Descartes – Paris V; 2013. [cited 2021 Apr 14]. Available from: http://www.theses.fr/2013PA05T094.

Council of Science Editors:

Guez F. Etude des mécanismes moléculaires impliqués dans le cycle cellulaire des cellules β pancréatiques humaines : Molecular mechanisms involved in the cell cycle of human pancreatic beta cells. [Doctoral Dissertation]. Université Paris Descartes – Paris V; 2013. Available from: http://www.theses.fr/2013PA05T094


Georgia State University

25. Wang, Haizhen. The C-Phycocyanin/Beta Protein Inhibits Cancer Cell Proliferation.

Degree: MS, Biology, 2008, Georgia State University

 C-Phycocyanin (C-PC) from blue-green algae has been reported to have various pharmacological characteristics, including anti-inflammatory and anti-cancer activities. In this study, the beta-subunit of C-PC… (more)

Subjects/Keywords: beta-subunit of C-Phycocyanin; Apoptosis; Cell cycle; Proliferation; GAPDH; caspase; beta-tubulin; Biology

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

APA (6th Edition):

Wang, H. (2008). The C-Phycocyanin/Beta Protein Inhibits Cancer Cell Proliferation. (Thesis). Georgia State University. Retrieved from https://scholarworks.gsu.edu/biology_theses/15

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):

Wang, Haizhen. “The C-Phycocyanin/Beta Protein Inhibits Cancer Cell Proliferation.” 2008. Thesis, Georgia State University. Accessed April 14, 2021. https://scholarworks.gsu.edu/biology_theses/15.

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

MLA Handbook (7th Edition):

Wang, Haizhen. “The C-Phycocyanin/Beta Protein Inhibits Cancer Cell Proliferation.” 2008. Web. 14 Apr 2021.

Vancouver:

Wang H. The C-Phycocyanin/Beta Protein Inhibits Cancer Cell Proliferation. [Internet] [Thesis]. Georgia State University; 2008. [cited 2021 Apr 14]. Available from: https://scholarworks.gsu.edu/biology_theses/15.

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

Council of Science Editors:

Wang H. The C-Phycocyanin/Beta Protein Inhibits Cancer Cell Proliferation. [Thesis]. Georgia State University; 2008. Available from: https://scholarworks.gsu.edu/biology_theses/15

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

26. Wong, Victor Shing Chi. Role of R-spondin-1 in the Regulation of β-cell Behaviour.

Degree: 2011, University of Toronto

R-spondin-1 (Rspo1) is an intestinal growth factor known to exert its effects through activation of the canonical Wnt (cWnt) pathway, but its function in the… (more)

Subjects/Keywords: R-spondin-1; β-cell; Proliferation; Apoptosis; Insulin secretion; Islet; 0719

…Rspo1 stimulates β-cell proliferation ….77 Figure 2.4. Rspo1 inhibits cytokine… …rates of proliferation, apoptosis and/or neogenesis. 1.2.2 Adaptive β-cell growth and function… …in the murine β-cell similarly causes a dramatic increase in β-cell proliferation and β… …cell proliferation, decreased β-cell size and mass, and impaired glucose tolerance (77… …Wnt (cWnt) signaling network ...35 Chapter 2: R-spondin-1 is a novel β-cell… 

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

APA (6th Edition):

Wong, V. S. C. (2011). Role of R-spondin-1 in the Regulation of β-cell Behaviour. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/29914

Chicago Manual of Style (16th Edition):

Wong, Victor Shing Chi. “Role of R-spondin-1 in the Regulation of β-cell Behaviour.” 2011. Doctoral Dissertation, University of Toronto. Accessed April 14, 2021. http://hdl.handle.net/1807/29914.

MLA Handbook (7th Edition):

Wong, Victor Shing Chi. “Role of R-spondin-1 in the Regulation of β-cell Behaviour.” 2011. Web. 14 Apr 2021.

Vancouver:

Wong VSC. Role of R-spondin-1 in the Regulation of β-cell Behaviour. [Internet] [Doctoral dissertation]. University of Toronto; 2011. [cited 2021 Apr 14]. Available from: http://hdl.handle.net/1807/29914.

Council of Science Editors:

Wong VSC. Role of R-spondin-1 in the Regulation of β-cell Behaviour. [Doctoral Dissertation]. University of Toronto; 2011. Available from: http://hdl.handle.net/1807/29914

27. Jiao, Yang. Regulators of Mouse and Human Beta Cell Proliferation.

Degree: 2013, University of Pennsylvania

 Diabetes mellitus is an increasingly prevalent metabolic disorder that is estimated to affect over 300 million people by 2025. Common to either type 1 or… (more)

Subjects/Keywords: Beta cell proliferation; Betatrophin; CISH; Diabetes; HNF4-alpha; SOCS2; Cell Biology; Genetics; Molecular Biology

…betatrophin on beta-cell proliferation… …of beta cell proliferation… …57 4.5.2 Beta cell proliferation during pregnancy… …58 4.5.3 Molecular mechanisms for beta cell proliferation during… …glucose homeostasis or beta cell proliferation during pregnancy in… 

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

APA (6th Edition):

Jiao, Y. (2013). Regulators of Mouse and Human Beta Cell Proliferation. (Thesis). University of Pennsylvania. Retrieved from https://repository.upenn.edu/edissertations/877

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):

Jiao, Yang. “Regulators of Mouse and Human Beta Cell Proliferation.” 2013. Thesis, University of Pennsylvania. Accessed April 14, 2021. https://repository.upenn.edu/edissertations/877.

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

MLA Handbook (7th Edition):

Jiao, Yang. “Regulators of Mouse and Human Beta Cell Proliferation.” 2013. Web. 14 Apr 2021.

Vancouver:

Jiao Y. Regulators of Mouse and Human Beta Cell Proliferation. [Internet] [Thesis]. University of Pennsylvania; 2013. [cited 2021 Apr 14]. Available from: https://repository.upenn.edu/edissertations/877.

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

Council of Science Editors:

Jiao Y. Regulators of Mouse and Human Beta Cell Proliferation. [Thesis]. University of Pennsylvania; 2013. Available from: https://repository.upenn.edu/edissertations/877

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


University of Gothenburg / Göteborgs Universitet

28. Falk, Peter. Experimental Models of the Human Peritoneal Environment: Effects of TGF-beta and Hyaluronan.

Degree: 2008, University of Gothenburg / Göteborgs Universitet

 BACKGROUND Post surgical adhesion formation is still an unsolved problem and occurs when there is an imbalance between fibrin deposition and fibrin clearing capacity in… (more)

Subjects/Keywords: Adhesion formation; experimental model; cell culture; mesothelial cells; peritoneum; fibrinolytic system; transforming growth factor beta; hyaluronan; proliferation

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

APA (6th Edition):

Falk, P. (2008). Experimental Models of the Human Peritoneal Environment: Effects of TGF-beta and Hyaluronan. (Thesis). University of Gothenburg / Göteborgs Universitet. Retrieved from http://hdl.handle.net/2077/9903

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):

Falk, Peter. “Experimental Models of the Human Peritoneal Environment: Effects of TGF-beta and Hyaluronan.” 2008. Thesis, University of Gothenburg / Göteborgs Universitet. Accessed April 14, 2021. http://hdl.handle.net/2077/9903.

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

MLA Handbook (7th Edition):

Falk, Peter. “Experimental Models of the Human Peritoneal Environment: Effects of TGF-beta and Hyaluronan.” 2008. Web. 14 Apr 2021.

Vancouver:

Falk P. Experimental Models of the Human Peritoneal Environment: Effects of TGF-beta and Hyaluronan. [Internet] [Thesis]. University of Gothenburg / Göteborgs Universitet; 2008. [cited 2021 Apr 14]. Available from: http://hdl.handle.net/2077/9903.

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

Council of Science Editors:

Falk P. Experimental Models of the Human Peritoneal Environment: Effects of TGF-beta and Hyaluronan. [Thesis]. University of Gothenburg / Göteborgs Universitet; 2008. Available from: http://hdl.handle.net/2077/9903

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

29. Brown, Lecia Ashanna Moya. The Potential Role of Antiretroviral Efavirenz in HIV Associated Neurocognitive Disorders.

Degree: 2017, University of South Florida

 The prevalence of milder forms of HIV-associated neurocognitive disorders (HAND) is rising despite combination antiretroviral therapy (cART). Efavirenz (EFV) is among the most commonly used… (more)

Subjects/Keywords: HIV associated neurocognitive disorders; efavirenz; beta amyloid; neural stem cell proliferation; Neurosciences

…pharmacological or cell-based therapy aimed at opposing EFVmediated reductions in NSC proliferation may… …reduce neural stem cell (NSC) proliferation [80]. Further, high… …the negative regulation of stem cell proliferation. Studies showed that the inhibition of… …EFV Reduces Proliferation of NSCs… …82 Figure 4.3: EFV Increases NSC Cytotoxicity and Cell Death… 

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

APA (6th Edition):

Brown, L. A. M. (2017). The Potential Role of Antiretroviral Efavirenz in HIV Associated Neurocognitive Disorders. (Thesis). University of South Florida. Retrieved from https://scholarcommons.usf.edu/etd/6685

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):

Brown, Lecia Ashanna Moya. “The Potential Role of Antiretroviral Efavirenz in HIV Associated Neurocognitive Disorders.” 2017. Thesis, University of South Florida. Accessed April 14, 2021. https://scholarcommons.usf.edu/etd/6685.

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

MLA Handbook (7th Edition):

Brown, Lecia Ashanna Moya. “The Potential Role of Antiretroviral Efavirenz in HIV Associated Neurocognitive Disorders.” 2017. Web. 14 Apr 2021.

Vancouver:

Brown LAM. The Potential Role of Antiretroviral Efavirenz in HIV Associated Neurocognitive Disorders. [Internet] [Thesis]. University of South Florida; 2017. [cited 2021 Apr 14]. Available from: https://scholarcommons.usf.edu/etd/6685.

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

Council of Science Editors:

Brown LAM. The Potential Role of Antiretroviral Efavirenz in HIV Associated Neurocognitive Disorders. [Thesis]. University of South Florida; 2017. Available from: https://scholarcommons.usf.edu/etd/6685

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

30. Σταυρουλάκη, Μελανθία. Μοριακός μηχανισμός απευαισθητοποίησης μελανοκυττάρων στην κυτταροστατική δράση του αυξητικού παράγοντα μετασχηματισμού β (Transforming Growth Factor β, TGF-β) κατά την καρκινογένεση: στόχος φαρμακολογικής παρέμβασης στη θεραπεία του μελανώματος.

Degree: 2007, University of Crete (UOC); Πανεπιστήμιο Κρήτης

Carcinogenesis is likely to result from the production of autocrine growth factors, as well as from loss of response to polypeptide growth inhibitors. TGF-β inhibits… (more)

Subjects/Keywords: Μελανοκύτταρα; Μελάνωμα; Εξαλλαγή; Μετασχηματίζων αυξητικός παράγοντας β; Πρωτείνες Smad; Πρωτεϊνική κινάση C; Καρκινογόνα; Κυτταρικός πολλαπλασιασμός; Melanocytes; Melanoma; Transformation; Transforming Growth Factor β; Smad proteins; Protein kinase C; Carcinogens; Cell proliferation

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

APA (6th Edition):

Σταυρουλάκη, . . (2007). Μοριακός μηχανισμός απευαισθητοποίησης μελανοκυττάρων στην κυτταροστατική δράση του αυξητικού παράγοντα μετασχηματισμού β (Transforming Growth Factor β, TGF-β) κατά την καρκινογένεση: στόχος φαρμακολογικής παρέμβασης στη θεραπεία του μελανώματος. (Thesis). University of Crete (UOC); Πανεπιστήμιο Κρήτης. Retrieved from http://hdl.handle.net/10442/hedi/16272

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):

Σταυρουλάκη, Μελανθία. “Μοριακός μηχανισμός απευαισθητοποίησης μελανοκυττάρων στην κυτταροστατική δράση του αυξητικού παράγοντα μετασχηματισμού β (Transforming Growth Factor β, TGF-β) κατά την καρκινογένεση: στόχος φαρμακολογικής παρέμβασης στη θεραπεία του μελανώματος.” 2007. Thesis, University of Crete (UOC); Πανεπιστήμιο Κρήτης. Accessed April 14, 2021. http://hdl.handle.net/10442/hedi/16272.

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

MLA Handbook (7th Edition):

Σταυρουλάκη, Μελανθία. “Μοριακός μηχανισμός απευαισθητοποίησης μελανοκυττάρων στην κυτταροστατική δράση του αυξητικού παράγοντα μετασχηματισμού β (Transforming Growth Factor β, TGF-β) κατά την καρκινογένεση: στόχος φαρμακολογικής παρέμβασης στη θεραπεία του μελανώματος.” 2007. Web. 14 Apr 2021.

Vancouver:

Σταυρουλάκη . Μοριακός μηχανισμός απευαισθητοποίησης μελανοκυττάρων στην κυτταροστατική δράση του αυξητικού παράγοντα μετασχηματισμού β (Transforming Growth Factor β, TGF-β) κατά την καρκινογένεση: στόχος φαρμακολογικής παρέμβασης στη θεραπεία του μελανώματος. [Internet] [Thesis]. University of Crete (UOC); Πανεπιστήμιο Κρήτης; 2007. [cited 2021 Apr 14]. Available from: http://hdl.handle.net/10442/hedi/16272.

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

Council of Science Editors:

Σταυρουλάκη . Μοριακός μηχανισμός απευαισθητοποίησης μελανοκυττάρων στην κυτταροστατική δράση του αυξητικού παράγοντα μετασχηματισμού β (Transforming Growth Factor β, TGF-β) κατά την καρκινογένεση: στόχος φαρμακολογικής παρέμβασης στη θεραπεία του μελανώματος. [Thesis]. University of Crete (UOC); Πανεπιστήμιο Κρήτης; 2007. Available from: http://hdl.handle.net/10442/hedi/16272

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

[1] [2]

.