subject:(AMPK)

Johannes Gutenberg Universität Mainz

1. Schuhmacher, Swenja. Einfluss der AMPK-Aktivität auf Endothelfunktion, oxidativen Stress und vaskuläre Inflammation.

Degree: 2010, Johannes Gutenberg Universität Mainz

URL: http://ubm.opus.hbz-nrw.de/volltexte/2010/2540/

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Die AMPK ist ein ubiquitär exprimiertes, heterotrimeres Enzym, das bei Energiemangel das Überleben der Zelle sichert. Um diese Funktion ausüben zu können fungiert die AMPK… (more)

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Die AMPK ist ein ubiquitär exprimiertes, heterotrimeres Enzym, das bei Energiemangel das Überleben der Zelle sichert. Um diese Funktion ausüben zu können fungiert die AMPK als sogenannter „Energie-Sensor“, der durch steigende AMP Mengen aktiviert wird. In diesem Zustand werden ATP verbrauchende Reaktionen inhibiert und gleichzeitig ATP generierende Vorgänge induziert. Im vaskulären System konnte gezeigt werden, dass die endotheliale NOSynthase durch die AMPK aktiviert, die Angiogenese stimuliert, die Endothelzellapoptose und das Wachstum von Gefäßmuskelzellen inhibiert wird. All diese Prozesse sind fundamental in der Entwicklung von kardiovaskulären Krankheiten, was auf eine protektive Funktion der AMPK im vaskulären System hindeutet. In der vorliegenden Arbeit sollten die Effekte der in vivo Modulation der AMPK Aktivität auf Endothelfunktion, oxidativen Stress und Inflammation untersucht werden. Dazu wurden zwei unterschiedliche Mausmodelle genutzt: Einerseits wurde die AMPK Aktivität durch den pharmakologischen AMPK-Aktivator AICAR stimuliert und andererseits die vaskulär vorherrschende AMPK-Isoform durch knock out ausgeschaltet. Zur Induktion von oxidativem Stress wurde ein bereits charakterisiertes Angiotensin II-Modell angewandt. Zur Untersuchung gehörten neben den Superoxid-Messungen auch die Bestimmung der Stickstoffmonoxid-Mengen in Serum und Aortengewebe, die Relaxationsmessungen in isometrischen Tonusstudien sowie HPLC-basierte Assays. Es konnte gezeigt werden, dass durch die Aktivierung der AMPK mittels AICAR die Angiotensin II induzierte Endotheldysfunktion, der oxidative Stress und auch die vaskuläre Inflammation verbessert werden konnte. Weiterhin zeigte sich dass der knock out der vaskulären Isoform (α1) im Angiotensin II Modell eine signifikant verstärkte Endotheldysfunktion, oxidativen Stress und Inflammation nach sich zog. Anhand der erhobenen Daten konnte die NADPH-Oxidase als Hauptquelle des Angiotensin II induzierten oxidativen Stresses identifiziert werden, wobei sich diese Quelle als AMPK sensitiv erwies. Durch die Aktivierung konnte die Aktivität der NADPH-Oxidase verringert und durch die α1AMPK Defizienz signifikant erhöht werden. Auch die mitochondriale Superoxidproduktion konnte durch die Modulation der AMPK Aktivität beeinflusst werden. Die vaskuläre Inflammation, die anhand der Surrogaten VCAM-1, COX-2 und iNOS untersucht wurde, konnte durch Aktivierung der AMPK verringert werden, der knock out der α1AMPK führte so einer sehr starken Expressionssteigerung der induzierbaren NO-Synthase, was in einem starken Anstieg der NO-Produktion und somit der Peroxynitritbildung resultierte.Die dargestellten Daten deuten stark auf eine protektive Funktion der AMPK im vaskulären System hin und sollte als therapeutisches Ziel, nicht nur in Bezug auf diabetische Patienten, in Betracht gezogen werden.

The AMP-activated protein kinase (AMPK) is an ubiquitous expressed heterotrimeric enzyme in mammalian cells which allows cellular survival under conditions of decreased energy supply. As a cellular fuel…

Subjects/Keywords: AMPK; AMPK; Natural sciences and mathematics

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

APA (6^th Edition):

Schuhmacher, S. (2010). Einfluss der AMPK-Aktivität auf Endothelfunktion, oxidativen Stress und vaskuläre Inflammation. (Doctoral Dissertation). Johannes Gutenberg Universität Mainz. Retrieved from http://ubm.opus.hbz-nrw.de/volltexte/2010/2540/

Chicago Manual of Style (16^th Edition):

Schuhmacher, Swenja. “Einfluss der AMPK-Aktivität auf Endothelfunktion, oxidativen Stress und vaskuläre Inflammation.” 2010. Doctoral Dissertation, Johannes Gutenberg Universität Mainz. Accessed March 01, 2021. http://ubm.opus.hbz-nrw.de/volltexte/2010/2540/.

MLA Handbook (7^th Edition):

Schuhmacher, Swenja. “Einfluss der AMPK-Aktivität auf Endothelfunktion, oxidativen Stress und vaskuläre Inflammation.” 2010. Web. 01 Mar 2021.

Vancouver:

Schuhmacher S. Einfluss der AMPK-Aktivität auf Endothelfunktion, oxidativen Stress und vaskuläre Inflammation. [Internet] [Doctoral dissertation]. Johannes Gutenberg Universität Mainz; 2010. [cited 2021 Mar 01]. Available from: http://ubm.opus.hbz-nrw.de/volltexte/2010/2540/.

Council of Science Editors:

Schuhmacher S. Einfluss der AMPK-Aktivität auf Endothelfunktion, oxidativen Stress und vaskuläre Inflammation. [Doctoral Dissertation]. Johannes Gutenberg Universität Mainz; 2010. Available from: http://ubm.opus.hbz-nrw.de/volltexte/2010/2540/

Boston University

2. Allen, Katherine. The effects of troglitazone and PMA on AMPK in HepG2 cells.

Degree: MS, Medical Sciences, 2016, Boston University

URL: http://hdl.handle.net/2144/16783

► Type 2 diabetes, as well as other metabolic diseases, is an increasing global health concern and many of the mechanisms of both the disease and… (more)

▼ Type 2 diabetes, as well as other metabolic diseases, is an increasing global health concern and many of the mechanisms of both the disease and its current drug treatments have not been fully described. It has been shown that the anti-diabetic class of drugs, the thiazolidinediones, work via both a known PPARγ-dependent, and a lesser known PPARγ-independent mechanism of action. This PPARγ-independent mechanism likely involves the metabolic regulatory molecule AMPK, which has a newly elucidated inhibitory site of phosphorylation at Ser485/Ser491. In this study we sought to determine if the thiazolidinedione troglitazone affects AMPK in HepG2 liver cells via phosphorylation at both the known Thr172 site as well as the letter understood Ser485 site. We also looked for potential upstream kinases of the Ser485 site by comparing our results to recently proposed mechanisms of phosphorylation here. HepG2 cells were cultured in the lab and treated with troglitazone to determine time- and dose- dependent effects on AMPK. We also treated cultured HepG2 cells with PMA as well as troglitazone and PMA in order to compare mechanisms of action of troglitazone on AMPK. Results were analyzed using common western blot techniques and statistical analysis. Our data found that troglitazone increased AMPK activity by increasing phosphorylation at Thr172 in a time- and dose- dependent manner. The inhibitory site Ser485 was also increasingly phosphorylated with troglitazone treatments, although the net result of troglitazone treatment remained AMPK activation. The recently elucidated results from our laboratory showing the mechanism of p-AMPK Ser485 phosphorylation via PKD after PMA treatment also occurred in HepG2 cells, although this did not appear to be the mechanism by which troglitazone phosphorylated AMPK at Ser485. These data support the current research that there is an AMPK mediated PPARγ-independent mechanism of troglitazone treatment for type 2 diabetes and other metabolic diseases. The results do however bring into question the full effects of the drug on AMPK at a molecular level and leaves room for new research in this area, specifically the exact mechanism by which troglitazone phosphorylates AMPK at Ser485. Our data also brings up new questions as to the simultaneous phosphorylation of AMPK at both Thr172 and Ser485 and what this means for the activity of the molecule as a whole, a current area of critical research. Lastly our data support the newly elucidated mechanism of AMPK phosphorylation at Ser485 via PKD1, an exciting and novel discovery and potential target for therapeutic intervention.

Subjects/Keywords: Endocrinology; AMPK; Troglitazone

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APA (6^th Edition):

Allen, K. (2016). The effects of troglitazone and PMA on AMPK in HepG2 cells. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/16783

Chicago Manual of Style (16^th Edition):

Allen, Katherine. “The effects of troglitazone and PMA on AMPK in HepG2 cells.” 2016. Masters Thesis, Boston University. Accessed March 01, 2021. http://hdl.handle.net/2144/16783.

MLA Handbook (7^th Edition):

Allen, Katherine. “The effects of troglitazone and PMA on AMPK in HepG2 cells.” 2016. Web. 01 Mar 2021.

Vancouver:

Allen K. The effects of troglitazone and PMA on AMPK in HepG2 cells. [Internet] [Masters thesis]. Boston University; 2016. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/2144/16783.

Council of Science Editors:

Allen K. The effects of troglitazone and PMA on AMPK in HepG2 cells. [Masters Thesis]. Boston University; 2016. Available from: http://hdl.handle.net/2144/16783

3. 정, 재원. Roles of AMPK in Drosophila circadian clock.

Degree: 2015, Ajou University

URL: http://repository.ajou.ac.kr/handle/201003/11829 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000019513

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국문요약 ⅰ 차례 ⅳ 그림 차례 ⅵ 표 차례 ⅶ Ⅰ. 서론 1 Ⅱ. 재료 및 방법 5 A. Schneider 2 (S2) 세포에서 발현시키기 위한… (more)

Subjects/Keywords: circadian clock; AMPK

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APA (6^th Edition):

정, �. (2015). Roles of AMPK in Drosophila circadian clock. (Thesis). Ajou University. Retrieved from http://repository.ajou.ac.kr/handle/201003/11829 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000019513

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

Chicago Manual of Style (16^th Edition):

정, 재원. “Roles of AMPK in Drosophila circadian clock.” 2015. Thesis, Ajou University. Accessed March 01, 2021. http://repository.ajou.ac.kr/handle/201003/11829 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000019513.

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

MLA Handbook (7^th Edition):

정, 재원. “Roles of AMPK in Drosophila circadian clock.” 2015. Web. 01 Mar 2021.

Vancouver:

정 �. Roles of AMPK in Drosophila circadian clock. [Internet] [Thesis]. Ajou University; 2015. [cited 2021 Mar 01]. Available from: http://repository.ajou.ac.kr/handle/201003/11829 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000019513.

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

Council of Science Editors:

정 �. Roles of AMPK in Drosophila circadian clock. [Thesis]. Ajou University; 2015. Available from: http://repository.ajou.ac.kr/handle/201003/11829 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000019513

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

McMaster University

4. Day, Emily Anne. Mechanisms By Which Glucose Lowering Therapies Reduce Obesity And Atherosclerosis.

Degree: PhD, 2020, McMaster University

URL: http://hdl.handle.net/11375/25312

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The incidence of obesity, type 2 diabetes and cardiovascular disease (CVD) is increasing at alarming rates worldwide. Obesity is associated with a chronic nutrient surplus… (more)

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The incidence of obesity, type 2 diabetes and cardiovascular disease (CVD) is increasing at alarming rates worldwide. Obesity is associated with a chronic nutrient surplus that contributes to chronic low-grade inflammation, ectopic lipid deposition and insulin resistance. Insulin resistance is an important factor contributing to the development of both type 2 diabetes and CVD. Therefore, therapies that can address multiple aspects of cardio-metabolic diseases could have significant clinical utility to reduce morbidity and mortality associated with these conditions. Several distinct glucose lowering therapies have been developed, targeting unique molecular targets. Interestingly, three district glucose lowering therapies, metformin, canagliflozin and salsalate have been shown to potently activate the central energy regulating enzyme, AMP activated protein kinase (AMPK). Activation of AMPK has been shown to be important for regulating fatty acid and cholesterol synthesis, fatty acid oxidation, glucose homeostasis, inflammation and whole-body energy expenditure. Therefore, the objective of this thesis was to examine the effects of metformin, canagliflozin and salsalate, on obesity, atherosclerosis, hepatic lipid metabolism, and macrophage inflammatory signalling and to delineate the mechanism(s) by which these changes occur. In this thesis we show that metformin reduces obesity through a circulating hormone GDF15, and that AMPK is not required for metformin induced GDF15 secretion. Additionally, we show that canagliflozin reduces hepatic cholesterol synthesis and macrophage IL1-1β secretion through mechanisms requiring AMPKβ1. Lastly, we show that salsalate reduces atherosclerosis in a manner dependent on macrophage AMPK β1 and this is associated with reduced macrophage proliferation in vitro and in vivo. These insights into the mechanisms by which these glucose lowering therapies elicit beneficial effects on obesity and atherosclerosis further our understanding of the potential use of these agents for treatments beyond improved glycemic control. Furthermore, this evidence can direct future drug development or drug combinations to more effectively treat multiple aspects of these common chronic diseases that affect over a billion people worldwide.

Thesis

Doctor of Philosophy (Medical Science)

Advisors/Committee Members: Steinberg, Gregory, R, Health Sciences.

Subjects/Keywords: Diabetes; Obesity; Atherosclerosis; AMPK

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

APA (6^th Edition):

Day, E. A. (2020). Mechanisms By Which Glucose Lowering Therapies Reduce Obesity And Atherosclerosis. (Doctoral Dissertation). McMaster University. Retrieved from http://hdl.handle.net/11375/25312

Chicago Manual of Style (16^th Edition):

Day, Emily Anne. “Mechanisms By Which Glucose Lowering Therapies Reduce Obesity And Atherosclerosis.” 2020. Doctoral Dissertation, McMaster University. Accessed March 01, 2021. http://hdl.handle.net/11375/25312.

MLA Handbook (7^th Edition):

Day, Emily Anne. “Mechanisms By Which Glucose Lowering Therapies Reduce Obesity And Atherosclerosis.” 2020. Web. 01 Mar 2021.

Vancouver:

Day EA. Mechanisms By Which Glucose Lowering Therapies Reduce Obesity And Atherosclerosis. [Internet] [Doctoral dissertation]. McMaster University; 2020. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/11375/25312.

Council of Science Editors:

Day EA. Mechanisms By Which Glucose Lowering Therapies Reduce Obesity And Atherosclerosis. [Doctoral Dissertation]. McMaster University; 2020. Available from: http://hdl.handle.net/11375/25312

Texas A&M University

5. Jing, Ji. ATM and AMPK Regulate Peroxisome Dynamics via PEX5 Phosphorylation in Response to Stress.

Degree: PhD, Biomedical Sciences, 2018, Texas A&M University

URL: http://hdl.handle.net/1969.1/173559

► Peroxisomes are single membrane-bound and autonomously replicating subcellular organelles. While their function as metabolic organelles is well known, their place in the world of cell… (more)

▼ Peroxisomes are single membrane-bound and autonomously replicating subcellular organelles. While their function as metabolic organelles is well known, their place in the world of cell signaling is only just beginning to emerge. Peroxisomes are able to adjust their number in response to changing environmental and/or physiological conditions. It is crucial to maintain peroxisome homeostasis for normal cellular functions. High risk pathologies are associated with too few peroxisomes, such as peroxisome biogenesis disorders (PBDs), and too many peroxisomes, such as disorders that increase cellular ROS production to promote the development of disease, including cancer. Early studies have shown that pexophagy (selective autophagy of peroxisomes) is responsible for the decrease in superfluous or damaged peroxisomes, yet the mechanisms of initiation of pexophagy are not well defined, especially in mammalian cells. In Chapter II of this dissertation, we report a key role for the ataxia-telangiectasia mutated (ATM) kinase at the peroxisomes as a sensor of ROS that regulates pexophagy. ATM is recognized and localized to the peroxisome by PEX5. In response to ROS, ATM signaling activates ULK1 and suppresses mTORC1 to induce pexophagy. Concomitant with activation of ULK1, ATM phosphorylates PEX5 at Serine 141. This modification then promotes PEX5 mono-ubiquitination at Lysine 209. Mono-ubiquitinated PEX5 is iii sufficient to target peroxisomes to the autophagosome via ubiquitin adaptor protein p62, leading to the initiation of pexophagy. Peroxisomes do not contain DNA, hence all their proteins are encoded inside the nucleus, synthesized by free polyribosomes in the cytoplasm and delivered to peroxisome with the help of import receptors. It is known that PEX5 recognizes the peroxisome targeting sequence 1 (PTS1) of peroxisomal proteins and delivers them to peroxisome. However, how cells control this delivery has remained a mystery. In Chapter III of this dissertation, we found that AMP-activated protein kinase (AMPK) phosphorylates PEX5 at Ser279, which correlates with the import of peroxisomal proteins in response to low energy. Thus, we have uncovered a previously unappreciated link between the peroxisome and the ATM and AMPK signaling pathways, which paves the way for a deeper understanding of peroxisome dynamics and its role in cellular metabolism. Advisors/Committee Members: Zhou, Yubin (advisor), Walker, Cheryl Lyn (advisor), Wang, Fen (committee member), Jonasch, Eric (committee member).

Subjects/Keywords: Peroxisome dynamics; ATM; AMPK

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

APA (6^th Edition):

Jing, J. (2018). ATM and AMPK Regulate Peroxisome Dynamics via PEX5 Phosphorylation in Response to Stress. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/173559

Chicago Manual of Style (16^th Edition):

Jing, Ji. “ATM and AMPK Regulate Peroxisome Dynamics via PEX5 Phosphorylation in Response to Stress.” 2018. Doctoral Dissertation, Texas A&M University. Accessed March 01, 2021. http://hdl.handle.net/1969.1/173559.

MLA Handbook (7^th Edition):

Jing, Ji. “ATM and AMPK Regulate Peroxisome Dynamics via PEX5 Phosphorylation in Response to Stress.” 2018. Web. 01 Mar 2021.

Vancouver:

Jing J. ATM and AMPK Regulate Peroxisome Dynamics via PEX5 Phosphorylation in Response to Stress. [Internet] [Doctoral dissertation]. Texas A&M University; 2018. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/1969.1/173559.

Council of Science Editors:

Jing J. ATM and AMPK Regulate Peroxisome Dynamics via PEX5 Phosphorylation in Response to Stress. [Doctoral Dissertation]. Texas A&M University; 2018. Available from: http://hdl.handle.net/1969.1/173559

University of Dundee

6. Auciello, Francesca Romana. Canonical and non-canonical regulation of AMP-activated protein kinase.

Degree: PhD, 2015, University of Dundee

URL: https://discovery.dundee.ac.uk/en/studentTheses/2720a2b7-3f1e-445c-b008-c5c235f35395 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.679087

► The AMP-activated protein kinase (AMPK) is a sensor of cellular energy stress that, once activated, promotes ATP-producing process while it switches off ATP-consuming pathways, in… (more)

Subjects/Keywords: 616; AMPK; Oxidative stress

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

APA (6^th Edition):

Auciello, F. R. (2015). Canonical and non-canonical regulation of AMP-activated protein kinase. (Doctoral Dissertation). University of Dundee. Retrieved from https://discovery.dundee.ac.uk/en/studentTheses/2720a2b7-3f1e-445c-b008-c5c235f35395 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.679087

Chicago Manual of Style (16^th Edition):

Auciello, Francesca Romana. “Canonical and non-canonical regulation of AMP-activated protein kinase.” 2015. Doctoral Dissertation, University of Dundee. Accessed March 01, 2021. https://discovery.dundee.ac.uk/en/studentTheses/2720a2b7-3f1e-445c-b008-c5c235f35395 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.679087.

MLA Handbook (7^th Edition):

Auciello, Francesca Romana. “Canonical and non-canonical regulation of AMP-activated protein kinase.” 2015. Web. 01 Mar 2021.

Vancouver:

Auciello FR. Canonical and non-canonical regulation of AMP-activated protein kinase. [Internet] [Doctoral dissertation]. University of Dundee; 2015. [cited 2021 Mar 01]. Available from: https://discovery.dundee.ac.uk/en/studentTheses/2720a2b7-3f1e-445c-b008-c5c235f35395 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.679087.

Council of Science Editors:

Auciello FR. Canonical and non-canonical regulation of AMP-activated protein kinase. [Doctoral Dissertation]. University of Dundee; 2015. Available from: https://discovery.dundee.ac.uk/en/studentTheses/2720a2b7-3f1e-445c-b008-c5c235f35395 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.679087

IUPUI

7. Steele, Hannah E. Mechanotransduction of subcellular AMPK and its role in breast cancer cell migration.

Degree: 2018, IUPUI

URL: http://hdl.handle.net/1805/15928

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Indiana University-Purdue University Indianapolis (IUPUI)

The biophysical microenvironment of the tumor site has significant impact on breast cancer progression and metastasis. The importance of altered… (more)

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Indiana University-Purdue University Indianapolis (IUPUI)

The biophysical microenvironment of the tumor site has significant impact on breast cancer progression and metastasis. The importance of altered mechanotransduction in cancerous tissue through the integrin-mediated signaling axis has been documented, yet its role in the regulation of cellular metabolism and the potential link between cellular energy and cell migration remain poorly understood. In this study, we investigated the role of mechanotransduction (via Src and FAK) in AMP-activated protein kinase (AMPK) activation in breast cancer cells in response to interstitial fluid flow. Additionally, we explored the involvement of AMPK in breast cancer cell migration. An in-vitro three-dimensional (3D) cell culture model utilizing collagen-Matrigel matrices was used. Interstitial fluid flow was applied to the 3D cell-matrix construct inside a flow chamber. The sub-cellular signaling activity of Src, FAK, and AMPK was visualized in real-time using fluorescent resonance energy transfer (FRET). We observed that breast cancer cells (MDA-MB-231) are more sensitive to interstitial fluid flow than normal epithelial cells (MCF-10A) in the regulation of FAK and Src. AMPK was activated in the mitochondria of MDA-MB-231 cells by interstitial fluid flow, but not in other subcellular domains (i.e., cytosol, plasma membrane, and nucleus). Subcellular AMPK in MCF-10A cells did not respond to interstitial fluid flow. The inhibition of FAK or Src abolished flow-induced AMPK activation in the mitochondria of MDA-MB-231 cells. We also observed that global AMPK activation reduced MDA-MB-231 cell migration. Interestingly, specific AMPK inhibition in the mitochondria reduced cell migration and blocked interstitial fluid flow-induced cell migration. Our results suggest the linkage of FAK/Src and mitochondria-specific AMPK in mechanotransduction and the dual role of AMPK in breast cancer cell migration depending on its subcellular activation. Therefore, subcellular AMPK activation may play an important and distinct role in cancer invasion and progression.

Advisors/Committee Members: Na, Sungsoo.

Subjects/Keywords: Mechanotransduction; AMPK; Breast Cancer; Migration

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

APA (6^th Edition):

Steele, H. E. (2018). Mechanotransduction of subcellular AMPK and its role in breast cancer cell migration. (Thesis). IUPUI. Retrieved from http://hdl.handle.net/1805/15928

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

Chicago Manual of Style (16^th Edition):

Steele, Hannah E. “Mechanotransduction of subcellular AMPK and its role in breast cancer cell migration.” 2018. Thesis, IUPUI. Accessed March 01, 2021. http://hdl.handle.net/1805/15928.

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

MLA Handbook (7^th Edition):

Steele, Hannah E. “Mechanotransduction of subcellular AMPK and its role in breast cancer cell migration.” 2018. Web. 01 Mar 2021.

Vancouver:

Steele HE. Mechanotransduction of subcellular AMPK and its role in breast cancer cell migration. [Internet] [Thesis]. IUPUI; 2018. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/1805/15928.

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

Council of Science Editors:

Steele HE. Mechanotransduction of subcellular AMPK and its role in breast cancer cell migration. [Thesis]. IUPUI; 2018. Available from: http://hdl.handle.net/1805/15928

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

University of Southern California

8. Ybanez, Maria Cecilia D. Protein kinase C (PKC) participates in acetaminophen hepatotoxicity through JNK dependent and independent pathways.

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

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/247992/rec/5301

► Our previous studies have shown that acetaminophen (APAP)-induced hepatocyte necrosis is mediated by JNK. In the present study we show that protein kinase C (PKC)… (more)

Subjects/Keywords: acetaminophen (APAP); AMPK; p70S6K; necrosis

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

APA (6^th Edition):

Ybanez, M. C. D. (2013). Protein kinase C (PKC) participates in acetaminophen hepatotoxicity through JNK dependent and independent pathways. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/247992/rec/5301

Chicago Manual of Style (16^th Edition):

Ybanez, Maria Cecilia D. “Protein kinase C (PKC) participates in acetaminophen hepatotoxicity through JNK dependent and independent pathways.” 2013. Masters Thesis, University of Southern California. Accessed March 01, 2021. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/247992/rec/5301.

MLA Handbook (7^th Edition):

Ybanez, Maria Cecilia D. “Protein kinase C (PKC) participates in acetaminophen hepatotoxicity through JNK dependent and independent pathways.” 2013. Web. 01 Mar 2021.

Vancouver:

Ybanez MCD. Protein kinase C (PKC) participates in acetaminophen hepatotoxicity through JNK dependent and independent pathways. [Internet] [Masters thesis]. University of Southern California; 2013. [cited 2021 Mar 01]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/247992/rec/5301.

Council of Science Editors:

Ybanez MCD. Protein kinase C (PKC) participates in acetaminophen hepatotoxicity through JNK dependent and independent pathways. [Masters Thesis]. University of Southern California; 2013. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/247992/rec/5301

9. Hurtado de Llera, Ana. Expresión y función de la proteína quinasa activada por AMP, AMPK, en la célula germinal masculina de cerdo .

Degree: 2014, Universidad de Extremadura

URL: http://hdl.handle.net/10662/1357

► El espermatozoide es una célula germinal altamente especializada que debe experimentar unos procesos funcionales característicos para lograr su función primordial: la fecundación del ovocito. Estos… (more)

Subjects/Keywords: Quinasa; AMPK; Espermatozoide; Kinase; Spermatozoa

10 more images…

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APA (6^th Edition):

Hurtado de Llera, A. (2014). Expresión y función de la proteína quinasa activada por AMP, AMPK, en la célula germinal masculina de cerdo . (Thesis). Universidad de Extremadura. Retrieved from http://hdl.handle.net/10662/1357

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

Chicago Manual of Style (16^th Edition):

Hurtado de Llera, Ana. “Expresión y función de la proteína quinasa activada por AMP, AMPK, en la célula germinal masculina de cerdo .” 2014. Thesis, Universidad de Extremadura. Accessed March 01, 2021. http://hdl.handle.net/10662/1357.

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

MLA Handbook (7^th Edition):

Hurtado de Llera, Ana. “Expresión y función de la proteína quinasa activada por AMP, AMPK, en la célula germinal masculina de cerdo .” 2014. Web. 01 Mar 2021.

Vancouver:

Hurtado de Llera A. Expresión y función de la proteína quinasa activada por AMP, AMPK, en la célula germinal masculina de cerdo . [Internet] [Thesis]. Universidad de Extremadura; 2014. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/10662/1357.

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

Council of Science Editors:

Hurtado de Llera A. Expresión y función de la proteína quinasa activada por AMP, AMPK, en la célula germinal masculina de cerdo . [Thesis]. Universidad de Extremadura; 2014. Available from: http://hdl.handle.net/10662/1357

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

Queens University

10. Snider, Trevor. Evaluating the Role of Peroxisome Proliferator-Activated Receptor Gama Coactivator-1 Alpha in Mitochondrial Biogenesis in Goldfish .

Degree: Biology, 2013, Queens University

URL: http://hdl.handle.net/1974/8254

► The production of ATP is of the utmost importance to cell survival. To maintain energy homeostasis, cells regulate mitochondrial content through the control of degradative… (more)

▼ The production of ATP is of the utmost importance to cell survival. To maintain energy homeostasis, cells regulate mitochondrial content through the control of degradative and synthetic processes. Mitochondrial biogenesis is primarily controlled through a small number of transcriptional regulators, primarily nuclear respiratory factor-1 (NRF-1), NRF-2, and peroxisome proliferator-activated receptors (PPARs). DNA-binding proteins regulate genes encoding the machinery of oxidative phosphorylation. In addition to these DNA-binding proteins, the coactivator PPAR gamma coactivator-1 alpha (PGC-1α) is central to control of mitochondrial genes, so much so that it has been dubbed a “master controller” of energy homeostasis in mammalian muscle tissues. Though well studied in mammals, previous studies suggest that this NRF-1-PGC1α axis may be disrupted in fish. The response to treatments such as temperature and diet cause reciprocal effects on NRF-1 and PGC-1α. A serine-rich insertion into the NRF-1 binding domain of PGC-1α most likely disrupts this interaction. In this study I looked at the ability for the goldfish PGC-1α gene to interact with the PGC-1α binding domain of NRF-1. I have found that goldfish PGC-1α does not physically bind NRF-1, which would suggest that the PGC-1α-NRF-1 axis in fish is disrupted. To further explore the role of PGC-1α in fish we looked at the role of AMP-activated kinase (AMPK) to phosphorylate goldfish, zebrafish, and human PGC-1α. The results from this analysis show that AMPK in a zebrafish embryonic cell line (ZEB2J) have their AMPK activated by the AMPK activator AICAR. This response was shown to be both dose and time dependent. Transcript data was generated looking at typical AMPK responsive targets in the mammalian system. The target of ramapamycin (TOR) gene responded with a decrease as is expected in mammals. Hexokinase 2 (HK2), PGC-1α, and NRF-1 all decreased which is opposite of the typical mammalian response. COX7C a downstream target of the PGC-1α-NRF-1 axis did not respond to treatment. Indicating a disruption in the AMPK- PGC-1α-NRF-1 pathway.

Subjects/Keywords: PGC1 ; AMPK ; Animal physiology

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

APA (6^th Edition):

Snider, T. (2013). Evaluating the Role of Peroxisome Proliferator-Activated Receptor Gama Coactivator-1 Alpha in Mitochondrial Biogenesis in Goldfish . (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/8254

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

Chicago Manual of Style (16^th Edition):

Snider, Trevor. “Evaluating the Role of Peroxisome Proliferator-Activated Receptor Gama Coactivator-1 Alpha in Mitochondrial Biogenesis in Goldfish .” 2013. Thesis, Queens University. Accessed March 01, 2021. http://hdl.handle.net/1974/8254.

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

MLA Handbook (7^th Edition):

Snider, Trevor. “Evaluating the Role of Peroxisome Proliferator-Activated Receptor Gama Coactivator-1 Alpha in Mitochondrial Biogenesis in Goldfish .” 2013. Web. 01 Mar 2021.

Vancouver:

Snider T. Evaluating the Role of Peroxisome Proliferator-Activated Receptor Gama Coactivator-1 Alpha in Mitochondrial Biogenesis in Goldfish . [Internet] [Thesis]. Queens University; 2013. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/1974/8254.

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

Council of Science Editors:

Snider T. Evaluating the Role of Peroxisome Proliferator-Activated Receptor Gama Coactivator-1 Alpha in Mitochondrial Biogenesis in Goldfish . [Thesis]. Queens University; 2013. Available from: http://hdl.handle.net/1974/8254

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

University of British Columbia

11. Puthanveetil, Prasanth Nair. Glucocorticoid and its effect on cardiac glucose utilization.

Degree: MS- MSc, Pharmaceutical Sciences, 2008, University of British Columbia

URL: http://hdl.handle.net/2429/5038

► Glycogen is an immediate source of glucose for cardiac tissue to maintain its metabolic homeostasis. However, its excess brings about cardiac structural and physiological impairments.… (more)

Subjects/Keywords: AMPK; Glycogen

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

APA (6^th Edition):

Puthanveetil, P. N. (2008). Glucocorticoid and its effect on cardiac glucose utilization. (Masters Thesis). University of British Columbia. Retrieved from http://hdl.handle.net/2429/5038

Chicago Manual of Style (16^th Edition):

Puthanveetil, Prasanth Nair. “Glucocorticoid and its effect on cardiac glucose utilization.” 2008. Masters Thesis, University of British Columbia. Accessed March 01, 2021. http://hdl.handle.net/2429/5038.

MLA Handbook (7^th Edition):

Puthanveetil, Prasanth Nair. “Glucocorticoid and its effect on cardiac glucose utilization.” 2008. Web. 01 Mar 2021.

Vancouver:

Puthanveetil PN. Glucocorticoid and its effect on cardiac glucose utilization. [Internet] [Masters thesis]. University of British Columbia; 2008. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/2429/5038.

Council of Science Editors:

Puthanveetil PN. Glucocorticoid and its effect on cardiac glucose utilization. [Masters Thesis]. University of British Columbia; 2008. Available from: http://hdl.handle.net/2429/5038

12. Mohsen Mroueh, Fatima. Diabète et cancer colorectal : épidémiologie et physiopathologie : Diabetes and colorectal cancer : epidemiological and physiopathological studies.

Degree: Docteur es, Aspects moléculaires et cellulaires de la biologie, 2017, Université de Strasbourg

URL: http://www.theses.fr/2017STRAJ117

►

Le diabète est une dérégulation systémique chronique caractérisée par des perturbations métaboliques permanentes à l’origine de nombreuses complications, y compris le cancer. Le diabète augmente… (more)

▼

Le diabète est une dérégulation systémique chronique caractérisée par des perturbations métaboliques permanentes à l’origine de nombreuses complications, y compris le cancer. Le diabète augmente le risque du cancer colorectal (CRC) de 1,2 à 1,5 fois. Cependant, les voies moléculaires et cellulaires en jeu ne sont pas assez élucidées. Nos résultats témoignent d’une dérégulation de la voie AMPK/mTORC1 dans le diabète et le CRC avec une surexpression de la NADPH oxydase Nox4, augmentant ainsi la production de ROS. Ceci provoque un stress oxydatif qui s’élève en cas de diabète et contribue à la progression du CRC. De plus, nos résultats montrent que ce stress induit une altération de la voie de signalisation AMPK/mTORC1, aboutissant à une agressivité accrue du comportement des cellules cancéreuses du côlon et de la formation de polypes. Notre projet permet, d’une part, d’identifier de nouveaux mécanismes moléculaires impliqués dans la progression du CRC induite par le diabète et d’autre part, de développer des stratégies thérapeutiques efficaces pour inverser la progression du CRC chez les patients diabétiques.

Diabetes is a chronic systemic malfunction characterized by persistent metabolic disturbances that culminate in a high rate of complications to which cancer was recently annexed. In fact, diabetes inflates colorectal cancer (CRC) risk by 1.2-1.5 folds. However, the cellular and molecular pathways involved are not well understood. Our results show that AMPK/mTORC1 pathway is deregulated in both diabetes and CRC. This was paralleled by an elevation in the expression of the NADPH oxidase Nox4 leading to an increase in ROS production. Furthermore, our results show that oxidative stress, secondary to alteration in the level and activity of Nox4 is augmented in diabetes and contributes to the progression of CRC. The resulting oxidative stress further led to an alteration in the signaling of the AMPK/mTORC1 pathways culminating in an exacerbated aggressiveness in cancer cell behavior and colon polyp formation. Our project allows the identification of novel molecular mechanisms involved in diabetes-induced CRC progression and development of effective therapeutic strategies to reverse the progression of CRC in diabetic patients.

Advisors/Committee Members: Sauleau, Erik-André (thesis director), Eid, Assaad (thesis director).

Subjects/Keywords: Diabète; CRC; ROS; AMPK; Diabetes; CRC; ROS; AMPK; 572.8; 616.99; 616.4

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

APA (6^th Edition):

Mohsen Mroueh, F. (2017). Diabète et cancer colorectal : épidémiologie et physiopathologie : Diabetes and colorectal cancer : epidemiological and physiopathological studies. (Doctoral Dissertation). Université de Strasbourg. Retrieved from http://www.theses.fr/2017STRAJ117

Chicago Manual of Style (16^th Edition):

Mohsen Mroueh, Fatima. “Diabète et cancer colorectal : épidémiologie et physiopathologie : Diabetes and colorectal cancer : epidemiological and physiopathological studies.” 2017. Doctoral Dissertation, Université de Strasbourg. Accessed March 01, 2021. http://www.theses.fr/2017STRAJ117.

MLA Handbook (7^th Edition):

Mohsen Mroueh, Fatima. “Diabète et cancer colorectal : épidémiologie et physiopathologie : Diabetes and colorectal cancer : epidemiological and physiopathological studies.” 2017. Web. 01 Mar 2021.

Vancouver:

Mohsen Mroueh F. Diabète et cancer colorectal : épidémiologie et physiopathologie : Diabetes and colorectal cancer : epidemiological and physiopathological studies. [Internet] [Doctoral dissertation]. Université de Strasbourg; 2017. [cited 2021 Mar 01]. Available from: http://www.theses.fr/2017STRAJ117.

Council of Science Editors:

Mohsen Mroueh F. Diabète et cancer colorectal : épidémiologie et physiopathologie : Diabetes and colorectal cancer : epidemiological and physiopathological studies. [Doctoral Dissertation]. Université de Strasbourg; 2017. Available from: http://www.theses.fr/2017STRAJ117

13. Desgeorges, Thibaut. Crosstalk of Glucocorticoid Receptor and AMP-activated protein kinase in macrophages during skeletal muscle regeneration : Interactions entre le Récepteur aux glucocorticoïdes et l'AMP-activated protein kinase dans les macrophages au cours de la régénération du muscle strié squelettique.

Degree: Docteur es, Biologie cellulaire, 2019, Lyon

URL: http://www.theses.fr/2019LYSE1058

►

Le muscle strié squelettique régénère ad integrum après une lésion aigüe stérile grâce aux cellules satellites qui sont les cellules souches du muscle strié squelettique.… (more)

▼

Le muscle strié squelettique régénère ad integrum après une lésion aigüe stérile grâce aux cellules satellites qui sont les cellules souches du muscle strié squelettique. L'inflammation, et notamment les macrophages, joue un rôle important durant ce processus. En effet, après une lésion, les monocytes sanguins infiltrent le tissu et deviennent des macrophages avec un phénotype pro-inflammatoire associé à la lésion. Ces macrophages phagocytent les débris cellulaires et promeuvent la prolifération des cellules souches musculaires. Ensuite, les macrophages changent leur phénotype vers un phénotype anti-inflammatoire associé à la restauration du tissu. Ils promeuvent la différenciation, puis la fusion des cellules souches musculaires et la croissance des myofibres. Cette séquence de phénotypes inflammatoires est essentielle pour une régénération musculaire efficace. Le laboratoire a montré que ce changement de phénotype est dépendant d'un senseur énergétique majeur de la cellule qui contrôle le métabolisme cellulaire, l'AMP kinase (AMPK)al. Par ailleurs, les glucocorticoïdes sont utilisés depuis des décennies pour leurs effets anti-inflammatoires sur l'inflammation. Leur action est médiée par le Récepteur aux Glucocorticoïdes qui induit ou réprime l'expression de gènes par interaction directe ou indirecte à l'ADN. Comme l'AMPKal et les glucocorticoïdes induisent des effets anti-inflammatoires similaires sur les macrophages, nous avons posé l'hypothèse que ces 2 voies de signalisation pourraient être interconnectées dans les macrophages afin de permettre leur changement de phénotype et la régénération musculaire. Les données issues d'un modèle in vitro de lésion musculaire utilisant des macrophages dérivés de la moelle osseuse de souris ont montré que : i) les glucocorticoïdes induisaient la phosphorylation de l'AMPKal ; ii) l'AMPKal était requise pour l'acquisition fonctionnelle du statut anti-inflammatoire des macrophages induit par les glucocorticoïdes puisque des macrophages déficients pour l'AMPKal ne modifiaient pas leur phénotype et ne stimulaient pas la myogenèse. Les expériences in vivo utilisant des souris LysMCre/+;AMPKalfl/fl dans lesquelles l'AMPKal est invalidée uniquement dans les cellules myéloïdes ont montré que l'AMPKal dans les macrophages régulait les effets bénéfiques des glucocorticoïdes au cours de la régénération du muscle strié squelettique. En effet, en absence d'AMPKal dans les macrophages, les glucocorticoïdes induisaient un retard de régénération et une modification de la maturation des fibres attestée par une modification de l'expression des isoformes des chaînes lourdes de myosines. En conclusion, ces données montrent que l'AMPKal est requise pour le changement de phénotype des macrophages induit par les glucocorticoïdes et une régénération musculaire efficace

Skeletal muscle regenerates ad integrum after a sterile acute injury thanks to satellite cells (muscle stem cells). Inflammation, and notably macrophages, plays important roles during this process. Just after injury, monocytes…

Advisors/Committee Members: Chazaud, Bénédicte (thesis director), Mounier, Rémi (thesis director).

Subjects/Keywords: Muscle; Régénération; Macrophages; AMPK; Glucocorticoïdes; Muscle; Regeneration; Macrophages; AMPK; Glucocorticoids; 570

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❌

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

APA (6^th Edition):

Desgeorges, T. (2019). Crosstalk of Glucocorticoid Receptor and AMP-activated protein kinase in macrophages during skeletal muscle regeneration : Interactions entre le Récepteur aux glucocorticoïdes et l'AMP-activated protein kinase dans les macrophages au cours de la régénération du muscle strié squelettique. (Doctoral Dissertation). Lyon. Retrieved from http://www.theses.fr/2019LYSE1058

Chicago Manual of Style (16^th Edition):

Desgeorges, Thibaut. “Crosstalk of Glucocorticoid Receptor and AMP-activated protein kinase in macrophages during skeletal muscle regeneration : Interactions entre le Récepteur aux glucocorticoïdes et l'AMP-activated protein kinase dans les macrophages au cours de la régénération du muscle strié squelettique.” 2019. Doctoral Dissertation, Lyon. Accessed March 01, 2021. http://www.theses.fr/2019LYSE1058.

MLA Handbook (7^th Edition):

Desgeorges, Thibaut. “Crosstalk of Glucocorticoid Receptor and AMP-activated protein kinase in macrophages during skeletal muscle regeneration : Interactions entre le Récepteur aux glucocorticoïdes et l'AMP-activated protein kinase dans les macrophages au cours de la régénération du muscle strié squelettique.” 2019. Web. 01 Mar 2021.

Vancouver:

Desgeorges T. Crosstalk of Glucocorticoid Receptor and AMP-activated protein kinase in macrophages during skeletal muscle regeneration : Interactions entre le Récepteur aux glucocorticoïdes et l'AMP-activated protein kinase dans les macrophages au cours de la régénération du muscle strié squelettique. [Internet] [Doctoral dissertation]. Lyon; 2019. [cited 2021 Mar 01]. Available from: http://www.theses.fr/2019LYSE1058.

Council of Science Editors:

Desgeorges T. Crosstalk of Glucocorticoid Receptor and AMP-activated protein kinase in macrophages during skeletal muscle regeneration : Interactions entre le Récepteur aux glucocorticoïdes et l'AMP-activated protein kinase dans les macrophages au cours de la régénération du muscle strié squelettique. [Doctoral Dissertation]. Lyon; 2019. Available from: http://www.theses.fr/2019LYSE1058

14. Gsaier, Linda. Rôle du métabolisme sur le devenir des cellules souches musculaires et l'homéostasie du muscle squelettique : Role of cell-autonomous regulation of metabolism on muscle stem cell fate and skeletal muscle homeostasis.

Degree: Docteur es, Biologie cellulaire, 2018, Lyon

URL: http://www.theses.fr/2018LYSE1208

►

Durant la régénération du muscle suite à une lésion, les cellules souches musculaires, aussi appelées les cellules satellites, quittent leur état de quiescence et s’activent.… (more)

▼

Durant la régénération du muscle suite à une lésion, les cellules souches musculaires, aussi appelées les cellules satellites, quittent leur état de quiescence et s’activent. Elles pourront soit emprunter la voie de la myogenèse afin de former de nouvelles fibres musculaires, soit retourner à leur état de quiescence pour reformer la réserve de cellules souches mobilisable en cas de lésion ultérieure. La régulation du devenir de la cellule souche est modulée par de nombreuses voies de signalisation telles que la voie Wnt, la voie Notch ou la voie des TGFb. Cependant, rares sont les données concernant l’implication du métabolisme sur le devenir de la cellule souche. Pourtant il a été démontré que l’activation des cellules satellites est étroitement liée avec le métabolisme cellulaire, dont l’un des principaux acteurs est la protéine kinase AMPK. Ce complexe hétérotrimérique, composé de trois sous-unités a, b et g est responsable de l’équilibre entre consommation énergétique et production d’énergie au sein de la cellule. Grâce à la modulation de mTORC1, il a également été prouvé que l’AMPKa1 était responsable de la croissance cellulaire et de la prolifération des précurseurs myogéniques. A l’aide de différents modèles murins, de lignées primaires et de cellules satellites en sortie de tri, nous avons déterminé le rôle que pouvait jouer chacun des isoformes, AMPKa1 et AMPKa2 au sein de la cellule souche, sur le déroulement de la myogenèse adulte post- lésionnelle ainsi que sur l’homéostasie du muscle régénéré. Dans un premier temps nous avons démontré que la voie de signalisation AMPKa1-LDH permettait de réguler l’autorenouvellement des cellules satellites grâce au contrôle du métabolisme. En effet, au moment de l’entrée de la cellule dans la voie de la différenciation, la voie de l’AMPKa1 induit une diminution de l’activité de la LDH, permettant aux cellules d’adopter un métabolisme de phosphorylation oxydative répondant à leurs besoins énergétiques. Dans un second temps, nous avons démontré que l’isoforme AMPKa2, exprimé uniquement après l’entrée de la cellule dans la voie de la myogenèse, était responsable d’une modulation de la régénération musculaire et que son absence induisait un défaut de différenciation et un retard de maturation des fibres néoformées. Nos travaux nous ont ainsi permis de confirmer la place centrale de la protéine kinase AMPK dans la modulation via le métabolisme du devenir de la cellule souche musculaire dans un contexte de régénération du tissu musculaire squelettique dans un modèle murin

During muscle regeneration following injury, muscle stem cells, also called satellite cells,leave their quiescent state and activate. MuSCs are capable of both differentiating torepair muscle tissue after an injury and self-renewing to replenish the pool of stem cells.The regulation of their fate is modulated by several signaling pathways such as Wnt,Notch or TGFb pathway. However, there are few data concerning the involvement ofmetabolism in the fate of satellite cells. Yet it has been shown that the…

Advisors/Committee Members: Mounier, Rémi (thesis director).

Subjects/Keywords: Muscle; Régénération; Métabolisme; Myogenèse; AMPK; Muscle; Regeneration; Metabolism; Myogenesis; AMPK; 570

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

APA (6^th Edition):

Gsaier, L. (2018). Rôle du métabolisme sur le devenir des cellules souches musculaires et l'homéostasie du muscle squelettique : Role of cell-autonomous regulation of metabolism on muscle stem cell fate and skeletal muscle homeostasis. (Doctoral Dissertation). Lyon. Retrieved from http://www.theses.fr/2018LYSE1208

Chicago Manual of Style (16^th Edition):

Gsaier, Linda. “Rôle du métabolisme sur le devenir des cellules souches musculaires et l'homéostasie du muscle squelettique : Role of cell-autonomous regulation of metabolism on muscle stem cell fate and skeletal muscle homeostasis.” 2018. Doctoral Dissertation, Lyon. Accessed March 01, 2021. http://www.theses.fr/2018LYSE1208.

MLA Handbook (7^th Edition):

Gsaier, Linda. “Rôle du métabolisme sur le devenir des cellules souches musculaires et l'homéostasie du muscle squelettique : Role of cell-autonomous regulation of metabolism on muscle stem cell fate and skeletal muscle homeostasis.” 2018. Web. 01 Mar 2021.

Vancouver:

Gsaier L. Rôle du métabolisme sur le devenir des cellules souches musculaires et l'homéostasie du muscle squelettique : Role of cell-autonomous regulation of metabolism on muscle stem cell fate and skeletal muscle homeostasis. [Internet] [Doctoral dissertation]. Lyon; 2018. [cited 2021 Mar 01]. Available from: http://www.theses.fr/2018LYSE1208.

Council of Science Editors:

Gsaier L. Rôle du métabolisme sur le devenir des cellules souches musculaires et l'homéostasie du muscle squelettique : Role of cell-autonomous regulation of metabolism on muscle stem cell fate and skeletal muscle homeostasis. [Doctoral Dissertation]. Lyon; 2018. Available from: http://www.theses.fr/2018LYSE1208

NSYSU

15. Chen, Shin-yi. The role of LKB1 in the regulation of energetic checkpoints and DNA damage in the lung cancer.

Degree: Master, Institute of Biomedical Sciences, 2011, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0809111-135626

► STK11/LKB1, a serine/threonine protein kinase, is a key upstream kinase of adenine monophosphate-activated protein kinase (AMPK), a necessary kinase in the control of metabolism for… (more)

▼ STK11/LKB1, a serine/threonine protein kinase, is a key upstream kinase of adenine monophosphate-activated protein kinase (AMPK), a necessary kinase in the control of metabolism for maintaining energy homeostasis. Although it has become clear that LKB1 is mutated in a significant number of PeutzâJeghers syndrome (PJS) and sporadic cancers, most frequently in adenocarcinoma of the lung, little is known about how the LKB1 signaling regulates the metabolic process and energy production underlying hypoxia and increased radiosensitivity of lung tumor. Here, we employed lung cancer cells as a model system to dissect the functional roles of LKB1 signaling in human lung adenocarcinoma. We found that LKB1 inhibits lung cancer cell migration, transformation and chemo-resistance in vitro after we restored LKB1 expression in LKB1 null A549 and H460 lung cancer cells. We also found that LKB1 prevents UV-induced DNA damage in human lung cancer cell lines by comet assay and activated UV-induced apopotsis by MTT assays. Furthermore, we designed a systems biology approach to provide a comprehensive protein-protein interaction analysis in order to elucidate the LKB1 tumor suppressor network in vivo. We employed Immunoprecipitation-HPLC- Mass Spectrometry (IP-LC-MS) to identify the novel proteins interacting with LKB1 under different cellular stress conditions. We have identified that LKB1 is involved in CFTR synthesis pathway underlying normoxia condition and participates in the glycolysis and gluconeogenesis pathways underlying hypoxia condition. Together, our findings indicated that LKB1 is involved in the regulation of cell migration, energy metabolism and DNA repair in lung cancer cells, and should provides insights to further exploit the concept of deranged cancer bioenergetics and aberrant growth signals to achieve more effective and selective strategies for lung cancer patients. Advisors/Committee Members: Hong-wun Huang (chair), Kuang-Hung Cheng (committee member), Chang-Chun Hsiao (chair).

Subjects/Keywords: Wnt pathway; LKB1; AMPK; PJS; hypoxia

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

APA (6^th Edition):

Chen, S. (2011). The role of LKB1 in the regulation of energetic checkpoints and DNA damage in the lung cancer. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0809111-135626

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

Chicago Manual of Style (16^th Edition):

Chen, Shin-yi. “The role of LKB1 in the regulation of energetic checkpoints and DNA damage in the lung cancer.” 2011. Thesis, NSYSU. Accessed March 01, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0809111-135626.

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

MLA Handbook (7^th Edition):

Chen, Shin-yi. “The role of LKB1 in the regulation of energetic checkpoints and DNA damage in the lung cancer.” 2011. Web. 01 Mar 2021.

Vancouver:

Chen S. The role of LKB1 in the regulation of energetic checkpoints and DNA damage in the lung cancer. [Internet] [Thesis]. NSYSU; 2011. [cited 2021 Mar 01]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0809111-135626.

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

Council of Science Editors:

Chen S. The role of LKB1 in the regulation of energetic checkpoints and DNA damage in the lung cancer. [Thesis]. NSYSU; 2011. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0809111-135626

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

University of California – San Diego

16. Lombardo, Portia Sachi. Phosphorylation of Parkin by the autophagy initiating kinase ULK1 regulates mitochondrial homeostasis.

Degree: Biology, 2017, University of California – San Diego

URL: http://www.escholarship.org/uc/item/515006px

► Our laboratory recently identified the autophagy initiating kinase ULK1 as a novel AMPK substrate, which directly connects the highly conserved AMPK-mediated energy sensing pathway to… (more)

Subjects/Keywords: Molecular biology; AMPK; mitophagy; Parkin; ULK1

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

APA (6^th Edition):

Lombardo, P. S. (2017). Phosphorylation of Parkin by the autophagy initiating kinase ULK1 regulates mitochondrial homeostasis. (Thesis). University of California – San Diego. Retrieved from http://www.escholarship.org/uc/item/515006px

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

Chicago Manual of Style (16^th Edition):

Lombardo, Portia Sachi. “Phosphorylation of Parkin by the autophagy initiating kinase ULK1 regulates mitochondrial homeostasis.” 2017. Thesis, University of California – San Diego. Accessed March 01, 2021. http://www.escholarship.org/uc/item/515006px.

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

MLA Handbook (7^th Edition):

Lombardo, Portia Sachi. “Phosphorylation of Parkin by the autophagy initiating kinase ULK1 regulates mitochondrial homeostasis.” 2017. Web. 01 Mar 2021.

Vancouver:

Lombardo PS. Phosphorylation of Parkin by the autophagy initiating kinase ULK1 regulates mitochondrial homeostasis. [Internet] [Thesis]. University of California – San Diego; 2017. [cited 2021 Mar 01]. Available from: http://www.escholarship.org/uc/item/515006px.

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

Council of Science Editors:

Lombardo PS. Phosphorylation of Parkin by the autophagy initiating kinase ULK1 regulates mitochondrial homeostasis. [Thesis]. University of California – San Diego; 2017. Available from: http://www.escholarship.org/uc/item/515006px

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

University of California – Riverside

17. Marin, Traci. AMPK Targets Involved in Energy Homeostasis and Epigenetic Regulation of Mitochondrial Function-related Genes.

Degree: Biochemistry and Molecular Biology, 2013, University of California – Riverside

URL: http://www.escholarship.org/uc/item/5z46r2s4

► Mitochondria serve to regulate energy and redox homeostasis, ultimately determining cell fate. While mitochondrial dysfunction is characteristic of many metabolic, cardiovascular and neurodegenerative diseases, AMP-activated… (more)

Subjects/Keywords: Biochemistry; AMPK; chromatin; DNMT1; epigenetic; Mitochondria; transcription

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APA (6^th Edition):

Marin, T. (2013). AMPK Targets Involved in Energy Homeostasis and Epigenetic Regulation of Mitochondrial Function-related Genes. (Thesis). University of California – Riverside. Retrieved from http://www.escholarship.org/uc/item/5z46r2s4

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

Chicago Manual of Style (16^th Edition):

Marin, Traci. “AMPK Targets Involved in Energy Homeostasis and Epigenetic Regulation of Mitochondrial Function-related Genes.” 2013. Thesis, University of California – Riverside. Accessed March 01, 2021. http://www.escholarship.org/uc/item/5z46r2s4.

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

MLA Handbook (7^th Edition):

Marin, Traci. “AMPK Targets Involved in Energy Homeostasis and Epigenetic Regulation of Mitochondrial Function-related Genes.” 2013. Web. 01 Mar 2021.

Vancouver:

Marin T. AMPK Targets Involved in Energy Homeostasis and Epigenetic Regulation of Mitochondrial Function-related Genes. [Internet] [Thesis]. University of California – Riverside; 2013. [cited 2021 Mar 01]. Available from: http://www.escholarship.org/uc/item/5z46r2s4.

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

Council of Science Editors:

Marin T. AMPK Targets Involved in Energy Homeostasis and Epigenetic Regulation of Mitochondrial Function-related Genes. [Thesis]. University of California – Riverside; 2013. Available from: http://www.escholarship.org/uc/item/5z46r2s4

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

University of Toronto

18. Ehsan, Mehroz. Role of Adiponectin in Monocytic Microparticle-Induced Endothelial Dysfunction.

Degree: 2015, University of Toronto

URL: http://hdl.handle.net/1807/71230

►

Monocyte-derived microparticles (MPs) have been suggested to link cardiovascular risk factors to vascular injury. We hypothesized that adiponectin, an anti-inflammatory and vasculoprotective adipokine, limits the… (more)

Subjects/Keywords: Adiponectin; AMPK; inflammation; Microparticles; microvesicles; 0564

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APA (6^th Edition):

Ehsan, M. (2015). Role of Adiponectin in Monocytic Microparticle-Induced Endothelial Dysfunction. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/71230

Chicago Manual of Style (16^th Edition):

Ehsan, Mehroz. “Role of Adiponectin in Monocytic Microparticle-Induced Endothelial Dysfunction.” 2015. Masters Thesis, University of Toronto. Accessed March 01, 2021. http://hdl.handle.net/1807/71230.

MLA Handbook (7^th Edition):

Ehsan, Mehroz. “Role of Adiponectin in Monocytic Microparticle-Induced Endothelial Dysfunction.” 2015. Web. 01 Mar 2021.

Vancouver:

Ehsan M. Role of Adiponectin in Monocytic Microparticle-Induced Endothelial Dysfunction. [Internet] [Masters thesis]. University of Toronto; 2015. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/1807/71230.

Council of Science Editors:

Ehsan M. Role of Adiponectin in Monocytic Microparticle-Induced Endothelial Dysfunction. [Masters Thesis]. University of Toronto; 2015. Available from: http://hdl.handle.net/1807/71230

19. 정, 종갑. Protective effect of TM-25659, known as TAZ activator, on high-fat diet-induced insulin resistance in C57BL/6J mice.

Degree: 2016, Ajou University

URL: http://repository.ajou.ac.kr/handle/201003/13021 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000021474

►

PART 1. TM-25659-induced activation of FGF21 level decreases insulin resistance and inflammation in skeletal muscle via GCN2 pathways 1 Ⅰ. INTRODUCTION 2 Ⅱ. MATERIALS AND… (more)

▼

PART 1. TM-25659-induced activation of FGF21 level decreases insulin resistance and inflammation in skeletal muscle via GCN2 pathways 1 Ⅰ. INTRODUCTION 2 Ⅱ. MATERIALS AND METHODS 8 A. MATERIALS 9 B. METHODS 10 1. Preparation of PA 10 2. Cell culture 10 3. Immunoblot analysis 11 4. RNA isolation and quantitative real-time polymerase chain reaction (PCR) 12 5. siRNAs 13 6. Uptake of 2-N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl) amino-2-deoxyglucose (2-NBDG) 14 7. Animal experiments 14 8. FGF21 secretion 15 9. IL-1β assay 15 10. Statistical analysis 15 Ⅲ. RESULTS 16 A. TM-25659 restored PA-induced insulin resistance and inflammation in skeletal muscle cells 17 B. TM-25659 increased FGF21 levels by GCN2 pathways in skeletal muscle cells 22 C. Effects of TM-25659 reduced insulin resistance and inflammation in skeletal muscle cells treated with or without FGF21 siRNA 27 D. TM-25659 prevented HF-diet induced obesity 31 E. TM-25659 restored the insulin signaling pathways in DIO mice skeletal muscle 33 F. TM-25659 lowered the muscle pro-inflammatory cytokine levels in DIO mice 35 G. TM-25659 regulates expression of both FGF21 mRNA and protein in DIO mice skeletal muscles 37 Ⅳ. DISCUSSION 38 Ⅴ. CONCLUSION 42 PART 2. Protective effects of TM-25659 on high-fat diet-induced insulin resistance in liver via AMPK pathways 44 Ⅰ. INTRODUCTION 45 Ⅱ. MATERIALS AND METHODS 52 A. MATERIALS 53 B. METHODS 54 1. Preparation of PA 54 2. Cell culture 54 3. Immunoblot analysis 54 4. RNA isolation and quantitative real-time polymerase chain reaction (PCR) 55 5. Animal experiments 56 6. Insulin tolerance tests 57 7. Glucose tolerance tests 57 8. Statistical analysis 57 Ⅲ. RESULTS 58 A. TM-25659 restored PA-induced reduction of insulin signaling pathway and induction of in flammation in HepG2 cells 59 B. TM-25659 increased AMPK and ACC phosphorylation in HepG2 cells 62 C. TM-25659 reduced PA-induced reduction of insulin signaling pathway in HepG2 cells 65 D. TM-25659 reduced PA-induced reduction of inflammation in HepG2 cells 67 E. TM-25659 improved glucose homeostasis and insulin sensitivity in DIO mice 69 F. TM-25659 restored the insulin signaling pathways in DIO mice liver 71 G. TM-25659 lowered the serum and liver pro-inflammatory cytokine levels in DIO mice 73 H. TM-25659 activated AMPK pathways in DIO mice liver 77 I. TM-25659 repressed serum lipid levels in HF-diet fed mice 79 J. TM-25659 prevented HF-diet induced hepatic steatosis 81 K. TM-25659 reduced expression of lipogenic genes but increased expression of fatty acid oxidation genes in HF diet-fed mice 83 Ⅳ. DISCUSSION 85 Ⅴ. CONCLUSION 88 REFERENCES 90 국문요약 108

Doctor

Advisors/Committee Members: 대학원 의생명과학과, 201225058, 정, 종갑.

Subjects/Keywords: TAZ; TM-25659; insulin resistance; FGF21; AMPK

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APA (6^th Edition):

정, �. (2016). Protective effect of TM-25659, known as TAZ activator, on high-fat diet-induced insulin resistance in C57BL/6J mice. (Thesis). Ajou University. Retrieved from http://repository.ajou.ac.kr/handle/201003/13021 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000021474

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

Chicago Manual of Style (16^th Edition):

정, 종갑. “Protective effect of TM-25659, known as TAZ activator, on high-fat diet-induced insulin resistance in C57BL/6J mice.” 2016. Thesis, Ajou University. Accessed March 01, 2021. http://repository.ajou.ac.kr/handle/201003/13021 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000021474.

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

MLA Handbook (7^th Edition):

정, 종갑. “Protective effect of TM-25659, known as TAZ activator, on high-fat diet-induced insulin resistance in C57BL/6J mice.” 2016. Web. 01 Mar 2021.

Vancouver:

정 �. Protective effect of TM-25659, known as TAZ activator, on high-fat diet-induced insulin resistance in C57BL/6J mice. [Internet] [Thesis]. Ajou University; 2016. [cited 2021 Mar 01]. Available from: http://repository.ajou.ac.kr/handle/201003/13021 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000021474.

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

Council of Science Editors:

정 �. Protective effect of TM-25659, known as TAZ activator, on high-fat diet-induced insulin resistance in C57BL/6J mice. [Thesis]. Ajou University; 2016. Available from: http://repository.ajou.ac.kr/handle/201003/13021 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000021474

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

University of North Texas

20. LaRue, Bobby Lee, Jr. Genetic and Environmental Factors that Mediate Survival of Prolonged Oxygen Deprivation in the Nematode Caenorhabditis Elegans.

Degree: 2010, University of North Texas

URL: https://digital.library.unt.edu/ark:/67531/metadc103350/

► Ischemic events of even a very short duration are not tolerated Ill in humans. The human cost of ischemia, when looked at as combined cardiovascular… (more)

Subjects/Keywords: Oxygen; ischemia; AMPK

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APA (6^th Edition):

LaRue, Bobby Lee, J. (2010). Genetic and Environmental Factors that Mediate Survival of Prolonged Oxygen Deprivation in the Nematode Caenorhabditis Elegans. (Thesis). University of North Texas. Retrieved from https://digital.library.unt.edu/ark:/67531/metadc103350/

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

Chicago Manual of Style (16^th Edition):

LaRue, Bobby Lee, Jr. “Genetic and Environmental Factors that Mediate Survival of Prolonged Oxygen Deprivation in the Nematode Caenorhabditis Elegans.” 2010. Thesis, University of North Texas. Accessed March 01, 2021. https://digital.library.unt.edu/ark:/67531/metadc103350/.

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

MLA Handbook (7^th Edition):

LaRue, Bobby Lee, Jr. “Genetic and Environmental Factors that Mediate Survival of Prolonged Oxygen Deprivation in the Nematode Caenorhabditis Elegans.” 2010. Web. 01 Mar 2021.

Vancouver:

LaRue, Bobby Lee J. Genetic and Environmental Factors that Mediate Survival of Prolonged Oxygen Deprivation in the Nematode Caenorhabditis Elegans. [Internet] [Thesis]. University of North Texas; 2010. [cited 2021 Mar 01]. Available from: https://digital.library.unt.edu/ark:/67531/metadc103350/.

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

Council of Science Editors:

LaRue, Bobby Lee J. Genetic and Environmental Factors that Mediate Survival of Prolonged Oxygen Deprivation in the Nematode Caenorhabditis Elegans. [Thesis]. University of North Texas; 2010. Available from: https://digital.library.unt.edu/ark:/67531/metadc103350/

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

Colorado State University

21. Mudron, Megan Reese. Molecular regulation of growth and molting in decapod crustaceans.

Degree: MS(M.S.), Biology, 2014, Colorado State University

URL: http://hdl.handle.net/10217/84008

► The green shore crab, Carcinus maenas, is a highly invasive species that inhabits coastal temperate zones worldwide. The reaction of C. maenas to acute temperature… (more)

▼ The green shore crab, Carcinus maenas, is a highly invasive species that inhabits coastal temperate zones worldwide. The reaction of C. maenas to acute temperature change was determined in six tissues (heart, gill, thoracic ganglion, eyestalk ganglion, Y-organ, and claw muscle) using genetic markers for temperature-induced metabolic stress, including HSP70, AMPKγ, mTOR, and Rheb. Animals were exposed to temperatures between 5° and 30°C for 1 or 2 h. mRNA levels in six tissues were quantified by quantitative RT-PCR (qPCR). The results indicate that C. maenas tolerated a wide temperature range, requiring 2-h exposures at 5 °C and 30 °C to affect tissue-specific changes in gene expression. Cm-HSP70 expression was robustly increased at 30 °C in all tissues. Ecdysteroids produced from the molting gland (Y-organ or YO) induce molting in decapod crustaceans. Reduction in molt-inhibiting hormone (MIH) activates the YO and animals enter premolt. At mid-premolt, YOs transition to the committed state, during which ecdysteroid production increases further. In blackback land crab (Gecarcinus lateralis), a tropical decapod species, SB1431542, an inhibitor of Activin receptors, decreases hemolymph ecdysteroid titers in premolt animals, suggesting that an Activin-like transforming-growth factor (TGF-β) is produced by the activated YO and drives the transition of the YO to the committed state. Myostatin (Gl-Mstn) is an Activin-like factor that is highly expressed in skeletal muscle. Rapamycin lowers hemolymph ecdysteroid titers by inhibiting mTOR, which controls global translation of mRNA into protein. Endpoint RT-PCR established that Gl-Mstn was expressed in the YO, not just muscle tissue. YOs were harvested from intact (intermolt) animals and from animals at 1, 3, 5, 7, and 14 days post-ESA. Quantitative PCR was used to quantify the effects of molt induction by eyestalk ablation (ESA) on gene expression. Expression of mTOR components peaked at 3 days post-ESA, which is consistent with the increased activity required for activation of the YO. Gl-Mstn expression also peaked at 3 days post-ESA, which is before the transition to the committed state at 7 days post-ESA. These results indicate that mTOR components are involved in activation of the YO, and Mstn is involved in transitioning the YO to the committed state. Advisors/Committee Members: Mykles, Donald L. (advisor), Garrity, Deborah M. (committee member), Curthoys, Norman P. (committee member).

Subjects/Keywords: AMPK; crustacean; HSP70; molting; mTOR; myostatin

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APA (6^th Edition):

Mudron, M. R. (2014). Molecular regulation of growth and molting in decapod crustaceans. (Masters Thesis). Colorado State University. Retrieved from http://hdl.handle.net/10217/84008

Chicago Manual of Style (16^th Edition):

Mudron, Megan Reese. “Molecular regulation of growth and molting in decapod crustaceans.” 2014. Masters Thesis, Colorado State University. Accessed March 01, 2021. http://hdl.handle.net/10217/84008.

MLA Handbook (7^th Edition):

Mudron, Megan Reese. “Molecular regulation of growth and molting in decapod crustaceans.” 2014. Web. 01 Mar 2021.

Vancouver:

Mudron MR. Molecular regulation of growth and molting in decapod crustaceans. [Internet] [Masters thesis]. Colorado State University; 2014. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/10217/84008.

Council of Science Editors:

Mudron MR. Molecular regulation of growth and molting in decapod crustaceans. [Masters Thesis]. Colorado State University; 2014. Available from: http://hdl.handle.net/10217/84008

University of Ottawa

22. Al-Rewashdy, Hasanen. Determining the Contribution of Utrophin A Versus Other Components of the Slow, Oxidative Phenotype in the Beneficial Adaptations of Dystrophic Muscle Fibers Following AMPK Activation .

Degree: 2014, University of Ottawa

URL: http://hdl.handle.net/10393/31470

► Duchenne Muscular Dystrophy (DMD) results from the absence of a functional dystrophin protein. Among its possible therapeutic options is the upregulation of dystrophin’s autosomal analogue,… (more)

Subjects/Keywords: Utrophin; Duchenne Muscular Dystrophy; Dystrophin; AMPK; AICAR

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APA (6^th Edition):

Al-Rewashdy, H. (2014). Determining the Contribution of Utrophin A Versus Other Components of the Slow, Oxidative Phenotype in the Beneficial Adaptations of Dystrophic Muscle Fibers Following AMPK Activation . (Thesis). University of Ottawa. Retrieved from http://hdl.handle.net/10393/31470

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

Chicago Manual of Style (16^th Edition):

Al-Rewashdy, Hasanen. “Determining the Contribution of Utrophin A Versus Other Components of the Slow, Oxidative Phenotype in the Beneficial Adaptations of Dystrophic Muscle Fibers Following AMPK Activation .” 2014. Thesis, University of Ottawa. Accessed March 01, 2021. http://hdl.handle.net/10393/31470.

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

MLA Handbook (7^th Edition):

Al-Rewashdy, Hasanen. “Determining the Contribution of Utrophin A Versus Other Components of the Slow, Oxidative Phenotype in the Beneficial Adaptations of Dystrophic Muscle Fibers Following AMPK Activation .” 2014. Web. 01 Mar 2021.

Vancouver:

Al-Rewashdy H. Determining the Contribution of Utrophin A Versus Other Components of the Slow, Oxidative Phenotype in the Beneficial Adaptations of Dystrophic Muscle Fibers Following AMPK Activation . [Internet] [Thesis]. University of Ottawa; 2014. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/10393/31470.

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

Council of Science Editors:

Al-Rewashdy H. Determining the Contribution of Utrophin A Versus Other Components of the Slow, Oxidative Phenotype in the Beneficial Adaptations of Dystrophic Muscle Fibers Following AMPK Activation . [Thesis]. University of Ottawa; 2014. Available from: http://hdl.handle.net/10393/31470

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

Université Catholique de Louvain

23. Dufeys, Cécile. Exploring the role of fibroblastic AMPKalpha1 in ventricular remodelling after myocardial infarction : implication of connexin 43 and miR-125b.

Degree: 2019, Université Catholique de Louvain

URL: http://hdl.handle.net/2078.1/216751

►

Myofibroblasts (MFs) are crucial components of the fibrotic remodelling after cardiac injury. In the present work, we investigate whether AMP-activated protein kinase α1 (AMPKα1) from… (more)

Subjects/Keywords: AMPK; Connexin 43; MiR-125b; Cardiac fibrosis

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APA (6^th Edition):

Dufeys, C. (2019). Exploring the role of fibroblastic AMPKalpha1 in ventricular remodelling after myocardial infarction : implication of connexin 43 and miR-125b. (Thesis). Université Catholique de Louvain. Retrieved from http://hdl.handle.net/2078.1/216751

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

Chicago Manual of Style (16^th Edition):

Dufeys, Cécile. “Exploring the role of fibroblastic AMPKalpha1 in ventricular remodelling after myocardial infarction : implication of connexin 43 and miR-125b.” 2019. Thesis, Université Catholique de Louvain. Accessed March 01, 2021. http://hdl.handle.net/2078.1/216751.

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

MLA Handbook (7^th Edition):

Dufeys, Cécile. “Exploring the role of fibroblastic AMPKalpha1 in ventricular remodelling after myocardial infarction : implication of connexin 43 and miR-125b.” 2019. Web. 01 Mar 2021.

Vancouver:

Dufeys C. Exploring the role of fibroblastic AMPKalpha1 in ventricular remodelling after myocardial infarction : implication of connexin 43 and miR-125b. [Internet] [Thesis]. Université Catholique de Louvain; 2019. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/2078.1/216751.

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

Council of Science Editors:

Dufeys C. Exploring the role of fibroblastic AMPKalpha1 in ventricular remodelling after myocardial infarction : implication of connexin 43 and miR-125b. [Thesis]. Université Catholique de Louvain; 2019. Available from: http://hdl.handle.net/2078.1/216751

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

University of Edinburgh

24. Mahmoud, Amira Dia. The LKB1-AMPK signalling pathway drives the hypoxic ventilatory response by regulating brainstem nuclei but not the carotid body.

Degree: PhD, 2015, University of Edinburgh

URL: http://hdl.handle.net/1842/17886

► Ventilatory drive is mediated by respiratory central pattern generators that are located in the brainstem, which are continuously modulated by specialised peripheral and central chemoreceptors… (more)

▼ Ventilatory drive is mediated by respiratory central pattern generators that are located in the brainstem, which are continuously modulated by specialised peripheral and central chemoreceptors to adjust ventilatory patterns according to changes in arterial PO2. These specialised oxygen-sensing chemoreceptors are activated in response to acute reductions in arterial PO2 and ultimately trigger a respiratory response that acts to restore oxygen-levels. However, the molecular mechanism by which mammals are able to regulate their breathing pattern in such a manner during hypoxia remains controversial. Therefore, the studies performed in this thesis aimed to investigate the possibility that this process may be mediated by the liver kinase B 1 (LKB1)/ AMP-activated protein kinase (AMPK) signalling pathway, which is central to cellular adaptations to metabolic stress. This first involved the development of transgenic mice in which Lkb1 or AMPK were deleted. Global knockout of Lkb1 (Sakamoto, 2006) or AMPK activity (Viollet et al., 2009) are embryonic lethal. Thus, the Cre/loxP system was used to develop transgenic mice that had either Lkb1 or both isoforms of the AMPK catalytic α- subunit (α1 and α2) conditionally knocked out in catecholaminergic cells (including therein hypoxia-activated cells of the brainstem and carotid body) by driving Cre expression through a tyrosine-hydroxylase-specific promoter region. The consequent effects on the ventilatory response to hypoxia were then examined using unrestrained whole-body plethysmography. This demonstrated that, in contrast to the hyperventilation evoked in controls, increased ventilation was virtually abolished in the Lkb1 and AMPK α1 and α2 double knockouts during hypoxia. Both knockout mice also exhibited periods of hypoventilation with frequent apnoeas during hypoxia. Additionally, studies on single AMPK α1 and AMPK α2 knockouts identified that the ventilatory dysfunction in AMPK α1 and α2 double knockouts was primarily caused by AMPK α1 deletion. In contrast, the severe ventilatory abnormalities exhibited during hypoxia following the deletion of Lkb1 and AMPK in catecholaminergic cells were mostly reversed upon exposure of mice to hypoxia with hypercapnia. Also, the ventilatory response to hypercapnia alone was without any major effect as a result of Lkb1 deletion or the dual-deletion of AMPK α1 and α2 catalytic subunits in catecholaminergic cells. This thesis therefore demonstrates, for the first time, that the LKB1-AMPK signalling pathway is key to respiratory adaptations during hypoxia, by regulating catecholaminergic oxygen-sensing cells, thus protecting against hypoventilation and apnoeas. The LKB1-AMPK signaling pathway can thereby determine oxygen and energy supply at both a cellular and whole-body level.

Subjects/Keywords: 616.2; hypoxia; Lkb1; AMPK; apnoeas; ventilatory response

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APA (6^th Edition):

Mahmoud, A. D. (2015). The LKB1-AMPK signalling pathway drives the hypoxic ventilatory response by regulating brainstem nuclei but not the carotid body. (Doctoral Dissertation). University of Edinburgh. Retrieved from http://hdl.handle.net/1842/17886

Chicago Manual of Style (16^th Edition):

Mahmoud, Amira Dia. “The LKB1-AMPK signalling pathway drives the hypoxic ventilatory response by regulating brainstem nuclei but not the carotid body.” 2015. Doctoral Dissertation, University of Edinburgh. Accessed March 01, 2021. http://hdl.handle.net/1842/17886.

MLA Handbook (7^th Edition):

Mahmoud, Amira Dia. “The LKB1-AMPK signalling pathway drives the hypoxic ventilatory response by regulating brainstem nuclei but not the carotid body.” 2015. Web. 01 Mar 2021.

Vancouver:

Mahmoud AD. The LKB1-AMPK signalling pathway drives the hypoxic ventilatory response by regulating brainstem nuclei but not the carotid body. [Internet] [Doctoral dissertation]. University of Edinburgh; 2015. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/1842/17886.

Council of Science Editors:

Mahmoud AD. The LKB1-AMPK signalling pathway drives the hypoxic ventilatory response by regulating brainstem nuclei but not the carotid body. [Doctoral Dissertation]. University of Edinburgh; 2015. Available from: http://hdl.handle.net/1842/17886

University of Gothenburg / Göteborgs Universitet

25. Cansby, Emmelie. Regulation of metabolism and inflammation by two protein kinases - AMPK and STK25.

Degree: 2014, University of Gothenburg / Göteborgs Universitet

URL: http://hdl.handle.net/2077/35938

► Type 2 diabetes mellitus (T2DM) is a widespread metabolic disorder that has reached epidemic proportions globally, and is now considered to be one of the… (more)

▼ Type 2 diabetes mellitus (T2DM) is a widespread metabolic disorder that has reached epidemic proportions globally, and is now considered to be one of the main threats to human health. The currently available treatment options in T2DM suffer from inadequate efficacy and durability, as well as liabilities, including hypoglycemia, weight gain, edema and gastrointestinal intolerance. Since the efficacy and patient compliance of existing treatments are in many cases unsatisfactory, there is a pronounced need for novel targets, which could complement current treatment. Evidence accumulated during the last two decades indicates that excessive caloric intake and obesity lead to a chronic low-grade inflammation in metabolic tissues, and increased inflammation may be directly involved in the pathogenesis of T2DM. Therefore, novel pharmacological treatments targeting both the metabolic and inflammatory disruptions seen in T2DM are warranted. AMP-activated protein kinase (AMPK) is a central master switch important for regulating energy homeostasis at cellular as well as whole body level. Recently, evidence for a role of AMPK in regulation of inflammatory balance has emerged. By using AMPK agonists AICAR and metformin in liver cell lines, primary hepatocytes and in mouse model system in vivo, we demonstrate that AMPK activation in liver leads to decreased inflammatory response to the proinflammatory cytokine IL-6. We further show that the anti-inflammatory action of AMPK was mediated via decreased phosphorylation of several downstream components of the canonical IL-6 receptor signalling pathway. Inhibition of the IL-6 signalling cascade in liver by AMPK supports a role of this kinase as a crucial point of convergence of metabolic and inflammatory pathways in hepatocytes. Serine/threonine protein kinase 25 (STK25) is broadly expressed in mouse, rat and human tissues. When activated, this kinase is part of several cell processes, such as development, migration and apoptosis. We, for the first time, show that STK25 also has metabolic effects. By using small interfering RNA for Stk25 in rodent muscle cell line L6, we demonstrate that STK25 is involved in regulation of glucose uptake and lipid oxidation. Furthermore, mice overexpressing STK25, when challenged with a high-fat diet, develop reduced glucose tolerance and insulin sensitivity compared to wild-type siblings. Increased triglyceride deposition in liver and skeletal muscle, and adipocyte hypertrophy, as observed in Stk25 transgenic mice, suggest that the underlying cause of insulin resistance in conditions of excess dietary fuels is a shift in the metabolic balance from lipid oxidation toward lipid storage in peripheral tissues. Furthermore, Stk25 transgenic mice show increased infiltration of inflammatory cells in liver. Taken together, both AMPK and STK25 emerge as interesting targets for future treatment of T2DM, enabling to target the dysregulation of both metabolism and inflammation seen in connection with this disease.

Subjects/Keywords: AMPK; STK25; Metabolism; Type 2 diabetes; Inflammation

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

APA (6^th Edition):

Cansby, E. (2014). Regulation of metabolism and inflammation by two protein kinases - AMPK and STK25. (Thesis). University of Gothenburg / Göteborgs Universitet. Retrieved from http://hdl.handle.net/2077/35938

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

Chicago Manual of Style (16^th Edition):

Cansby, Emmelie. “Regulation of metabolism and inflammation by two protein kinases - AMPK and STK25.” 2014. Thesis, University of Gothenburg / Göteborgs Universitet. Accessed March 01, 2021. http://hdl.handle.net/2077/35938.

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

MLA Handbook (7^th Edition):

Cansby, Emmelie. “Regulation of metabolism and inflammation by two protein kinases - AMPK and STK25.” 2014. Web. 01 Mar 2021.

Vancouver:

Cansby E. Regulation of metabolism and inflammation by two protein kinases - AMPK and STK25. [Internet] [Thesis]. University of Gothenburg / Göteborgs Universitet; 2014. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/2077/35938.

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

Council of Science Editors:

Cansby E. Regulation of metabolism and inflammation by two protein kinases - AMPK and STK25. [Thesis]. University of Gothenburg / Göteborgs Universitet; 2014. Available from: http://hdl.handle.net/2077/35938

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

Virginia Tech

26. Xu, Pingwen. Involvement of AMP-activated protein kinase in differential regulation of appetite between lines of chickens selected for low or high juvenile body weight.

Degree: PhD, Animal and Poultry Sciences, 2011, Virginia Tech

URL: http://hdl.handle.net/10919/37680

► This study was to determine (1) if genetic selection for high (HWS) or low (LWS) body weight in chickens has altered the hypothalamic AMP-activated protein… (more)

▼ This study was to determine (1) if genetic selection for high (HWS) or low (LWS) body weight in chickens has altered the hypothalamic AMP-activated protein kinase (AMPK) system and (2) if this alteration contributes to the dissimilar feeding response to various appetite modulators between HWS and LWS lines. Compared to HWS, LWS chickens had higher levels of AMPK Î± and acetyl-CoA carboxylase (ACC) phosphorylation, which was caused by upregulation of the upstream factor calcium/calmodulin-dependent protein kinase kinase 2 (CAMKK Î²). There was greater mRNA expression of carnitine palmitoyltransferase I (CPT1), leptin receptor (LEPR) and neuropeptide Y (NPY) and less mRNA expression of ACC Î±, fatty acid synthase (FAS), fat mass and obesity associated gene (FTO), pro-opiomelanocortin (POMC) and orexin in LWS than HWS chickens. At 5 days of age, intracerebroventricular (ICV) injection of AICAR, 5-amino- 4-imidazolecarboxamide riboside, caused a quadratic dose-dependent decrease in food intake in LWS but not HWS chicks. Compound C, (6-(4-(2-piperidin-1-yl-ethoxy)- phenyl))-3-pyridin-4-yl-pyrazolo(1,5-a)-pyrimidine, caused a quadratic dose-dependent increase in food intake in HWS but not LWS chicks. The anorexigenic effect of AICAR in LWS chicks and orexigenic effect of Compound C in HWS chicks resulted from either activation or inhibition of other kinase pathways separate from AMPK. There is a lower threshold for the anorexigenic effect of ghrelin in LWS than HWS chicks, which was associated with differential hypothalamic AMPK signaling. ICV injection of ghrelin iii inhibited corticotrophin-releasing hormone (CRH), 20-hydroxysteroid dehydrogenase (20HSD), glucocorticoid receptor (GR), CPT1 and FTO expression in LWS but not HWS chicks. Additionally, the hypothalamic mRNA level of ghrelin was significantly higher in LWS than HWS chicks, which may also contribute to the differential threshold response to ghrelin in these two lines. Obestatin caused a linear dose-dependent increase in food intake in HWS but not LWS chicks. The orexigenic effect of obestatin in HWS chicks was not associated with altered AMPK. Obestatin inhibited LEPR and FTO expression in HWS but not LWS chicks. Thus, selection for body weight may alter the hypothalamic response to ghrelin by the AMPK pathway, CRH pathway, CPT1 and FTO, and to obestatin by LEPR and FTO. Advisors/Committee Members: Denbow, D. Michael (committeechair), Siegel, Paul B. (committee member), Wong, Eric A. (committee member), Denbow, Cynthia J. (committee member), Cline, Mark A. (committee member).

Subjects/Keywords: ghrelin; food intake; chicken; AMPK; obestatin

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

APA (6^th Edition):

Xu, P. (2011). Involvement of AMP-activated protein kinase in differential regulation of appetite between lines of chickens selected for low or high juvenile body weight. (Doctoral Dissertation). Virginia Tech. Retrieved from http://hdl.handle.net/10919/37680

Chicago Manual of Style (16^th Edition):

Xu, Pingwen. “Involvement of AMP-activated protein kinase in differential regulation of appetite between lines of chickens selected for low or high juvenile body weight.” 2011. Doctoral Dissertation, Virginia Tech. Accessed March 01, 2021. http://hdl.handle.net/10919/37680.

MLA Handbook (7^th Edition):

Xu, Pingwen. “Involvement of AMP-activated protein kinase in differential regulation of appetite between lines of chickens selected for low or high juvenile body weight.” 2011. Web. 01 Mar 2021.

Vancouver:

Xu P. Involvement of AMP-activated protein kinase in differential regulation of appetite between lines of chickens selected for low or high juvenile body weight. [Internet] [Doctoral dissertation]. Virginia Tech; 2011. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/10919/37680.

Council of Science Editors:

Xu P. Involvement of AMP-activated protein kinase in differential regulation of appetite between lines of chickens selected for low or high juvenile body weight. [Doctoral Dissertation]. Virginia Tech; 2011. Available from: http://hdl.handle.net/10919/37680

University of Minnesota

27. Yan, Yan. Regulation and Function of the Phosphatase PHLPP2 in Leukemia.

Degree: PhD, Pharmacology, 2017, University of Minnesota

URL: http://hdl.handle.net/11299/191472

► PHLPP2, a member of the PHLPP phosphatase family, which targets oncogenic kinases, has been actively investigated as a tumor suppressor in solid tumors. Little was… (more)

Subjects/Keywords: AMPK; ATRA; leukemia; microRNA; PHLPP2; phosphatase

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

APA (6^th Edition):

Yan, Y. (2017). Regulation and Function of the Phosphatase PHLPP2 in Leukemia. (Doctoral Dissertation). University of Minnesota. Retrieved from http://hdl.handle.net/11299/191472

Chicago Manual of Style (16^th Edition):

Yan, Yan. “Regulation and Function of the Phosphatase PHLPP2 in Leukemia.” 2017. Doctoral Dissertation, University of Minnesota. Accessed March 01, 2021. http://hdl.handle.net/11299/191472.

MLA Handbook (7^th Edition):

Yan, Yan. “Regulation and Function of the Phosphatase PHLPP2 in Leukemia.” 2017. Web. 01 Mar 2021.

Vancouver:

Yan Y. Regulation and Function of the Phosphatase PHLPP2 in Leukemia. [Internet] [Doctoral dissertation]. University of Minnesota; 2017. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/11299/191472.

Council of Science Editors:

Yan Y. Regulation and Function of the Phosphatase PHLPP2 in Leukemia. [Doctoral Dissertation]. University of Minnesota; 2017. Available from: http://hdl.handle.net/11299/191472

University of Melbourne

28. EMANUELLE, SHANE. The regulation of SnRK1 from Arabidopsis thaliana.

Degree: 2013, University of Melbourne

URL: http://hdl.handle.net/11343/38299

► An intrinsic characteristic of all life is the ability to regulate the organism’s internal energy status despite sometimes wildly fluctuating conditions in the external environment.… (more)

▼ An intrinsic characteristic of all life is the ability to regulate the organism’s internal energy status despite sometimes wildly fluctuating conditions in the external environment. SnRK1 (SNF1-related kinase 1) is the plant orthologue of an evolutionarily conserved, energy-sensing, eukaryotic protein kinase family, including SNF1 from yeast and AMPK from mammals, that plays a major role in the regulation of both cellular and systemic energy homeostasis. The family is functional as heterotrimeric holoenzymes comprising catalytic α¬ and regulatory β and γ subunits, each consisting of several functional domains and each of which may exist in multiple isoforms giving rise to various isoenzymes. Plants contain genes encoding isoforms for each of these subunit types, some of which display unique domain architecture not found outside the plant kingdom. Whilst SNF1 and AMPK have been extensively studied, relatively little is known of how the SnRK1 holoenzyme from plants is regulated and how the various subunit isoforms and their respective functional domains contribute to this regulation. This thesis addresses several aspects of SnRK1 regulation by using biochemical, molecular, and genetic techniques. The present work has described SnRK1 from the model plant Arabidopsis thaliana as a heterotrimeric complex in vitro, existing in six isoenzyme combinations, comprising both classical-type SNF1/AMPK subunits and non-typical plant isoforms, these subunit interactions being confirmed in vivo, with the plant-specific βγ determined to be the sole γ-type subunit. SnRK1, like SNF1 and AMPK, is only minimally active as individual catalytic subunits indicating that SnRK1 is functional as a heterotrimer. Whilst phosphorylation of the α-subunit T-loop threonine is critical for activity this residue is resistant to dephosphorylation by phosphoprotein phosphatases signifying a major divergence in mode of regulation in comparison to SNF1 and AMPK. In addition, whilst the β-subunit carbohydrate-binding modules of AMPK bind glycogen, those of SnRK1 unexpectedly do not associate with glycogen, starch, or a vast array of oligosaccharides and plant-derived polysaccharides. Genetic and molecular studies focused on the β2 subunit. Analysis of T-DNA insertion mutations in this gene suggest that β2, whilst not drastically impacting plant phenotype under normal growth condition, does reduce the plant’s extent of growth. When the dark period was extended, however, the β2 mutants appeared to suffer from a starch rationing phenotype, not being able to conserve transient leaf starch as in wild-type plants. Using the GUS reporter system, β2 gene expression was observed strongly in vascular tissue, some floral tissue, and the floral organ abscission zone. Finally, in accordance with SnRK1’s role as a central integrator of metabolism, the β2 protein was observed to be localised mainly to the cytoplasm and nucleus by way of fusion to the yellow fluorescent…

Subjects/Keywords: SnRK1; SNF1; AMPK; enzyme; biochemistry; botany

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

APA (6^th Edition):

EMANUELLE, S. (2013). The regulation of SnRK1 from Arabidopsis thaliana. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/38299

Chicago Manual of Style (16^th Edition):

EMANUELLE, SHANE. “The regulation of SnRK1 from Arabidopsis thaliana.” 2013. Doctoral Dissertation, University of Melbourne. Accessed March 01, 2021. http://hdl.handle.net/11343/38299.

MLA Handbook (7^th Edition):

EMANUELLE, SHANE. “The regulation of SnRK1 from Arabidopsis thaliana.” 2013. Web. 01 Mar 2021.

Vancouver:

EMANUELLE S. The regulation of SnRK1 from Arabidopsis thaliana. [Internet] [Doctoral dissertation]. University of Melbourne; 2013. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/11343/38299.

Council of Science Editors:

EMANUELLE S. The regulation of SnRK1 from Arabidopsis thaliana. [Doctoral Dissertation]. University of Melbourne; 2013. Available from: http://hdl.handle.net/11343/38299

University of Southern California

29. Shim, Hong Seok. Differential effects of starvation in normal and cancer cells: from EGR1-dependent protection to p53-mediated apoptosis.

Degree: PhD, Integrative and Evolutionary Biology, 2016, University of Southern California

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/566322/rec/1987

► Dietary or calorie restriction has been a well‐studied strategy for increasing survival and preventing carcinogenesis in mammals. Short‐term starvation, an extreme form of dietary restriction,… (more)

▼ Dietary or calorie restriction has been a well‐studied strategy for increasing survival and preventing carcinogenesis in mammals. Short‐term starvation, an extreme form of dietary restriction, can augment cancer treatment efficacy and can be effective in delaying cancer progression in the absence of chemotherapy. However, the underlying molecular mechanisms of these dietary interventions remain elusive. ❧ Here I describe REV1, a specialized DNA polymerase involved in DNA repair, as an important signaling node linking nutrient sensing and metabolic control to cell fate in cancer cells. I have identified that REV1 is a novel binding partner of the tumor suppressor p53 and regulates its activity, and that short‐term starvation facilitates the modifications of these proteins. Under starvation, REV1 is modified by SUMO2/3, resulting in consequent relief of REV1’s inhibition of p53 and enhancing p53 activation, pro‐apoptotic genes expression and in turn p53‐mediated apoptosis in breast cancer and melanoma cells. Thus, fasting through its effect on REV1 is a promising non‐toxic strategy to increase p53‐dependent cell death and to enhance the efficacy of cancer therapies. ❧ In addition, my study reveals that AMPK, PKA, and EGR1 are the molecular components of functional signaling pathway that allows cardiomyocytes to sense and react to nutrient availability. AMPK activation and PKA inhibition under glucose restriction and metformin treatment are required to promote the induction of EGR1, an immediately early response gene, and the expression of antioxidant and stress resistance genes in cardiomyocytes. EGR1 has a consequent cardioprotective function following doxorubicin treatment. This study provides that short‐term starvation and metformin have a protective role in doxorubicin‐induced cardiotoxicity through AMPK/PKA-EGR1 pathway. ❧ In conclusion, this thesis provides molecular evidence for short‐term starvation as the promising intervention to exert differential effects in normal and cancer cells, contributing to their protection and death in response to stress, respectively. These data describe REV1 and EGR1 as the important signaling nodes linking nutrient sensing and metabolic control under starvation conditions. Advisors/Committee Members: Longo, Valter D. (Committee Chair), Lee, Amy S. (Committee Member), Tower, John G. (Committee Member).

Subjects/Keywords: starvation; REV1; sumoylation; p53; EGR1; AMPK; PKA

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

APA (6^th Edition):

Shim, H. S. (2016). Differential effects of starvation in normal and cancer cells: from EGR1-dependent protection to p53-mediated apoptosis. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/566322/rec/1987

Chicago Manual of Style (16^th Edition):

Shim, Hong Seok. “Differential effects of starvation in normal and cancer cells: from EGR1-dependent protection to p53-mediated apoptosis.” 2016. Doctoral Dissertation, University of Southern California. Accessed March 01, 2021. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/566322/rec/1987.

MLA Handbook (7^th Edition):

Shim, Hong Seok. “Differential effects of starvation in normal and cancer cells: from EGR1-dependent protection to p53-mediated apoptosis.” 2016. Web. 01 Mar 2021.

Vancouver:

Shim HS. Differential effects of starvation in normal and cancer cells: from EGR1-dependent protection to p53-mediated apoptosis. [Internet] [Doctoral dissertation]. University of Southern California; 2016. [cited 2021 Mar 01]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/566322/rec/1987.

Council of Science Editors:

Shim HS. Differential effects of starvation in normal and cancer cells: from EGR1-dependent protection to p53-mediated apoptosis. [Doctoral Dissertation]. University of Southern California; 2016. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/566322/rec/1987

Univerzitet u Beogradu

30. Pantović, Aleksandar, 1982-, 59207177. Uloga adenozin-monofosfatom aktivirane protein-kinaze i mTOR kompleksa 1 u in vitro citotoksičnom dejstvu nesteroidnih anti-inflamatornih lekova na ćelije glioma.

Degree: Medicinski fakultet, 2020, Univerzitet u Beogradu

URL: https://fedorabg.bg.ac.rs/fedora/get/o:23025/bdef:Content/get

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Medicina - Molekularna medicina / Medicine - Molecular medicine

Gliomi su najčešći primarni tumori centralnog nervnog sistema. Glioblastom je gliom gradusa IV, terapijski rezistentan maligni… (more)

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Medicina - Molekularna medicina / Medicine - Molecular medicine

Gliomi su najčešći primarni tumori centralnog nervnog sistema. Glioblastom je gliom gradusa IV, terapijski rezistentan maligni tumor centralnog nervnog sistema. Nesteroidni anti-inflamatorni lekovi (NSAIL) su strukturno različite grupe molekula sa anti-inflamatornim i analgetskim dejstvom koji ispoljavaju i jak antitumorski efekat kako in vitro tako i in vivo. U ovoj doktorskoj disertaciji ispitivano je citotoksično dejstvo NSAIL na ćelije humane linije glioma U251 i ćelije primarne kulture glioblastoma izolovane iz tkiva obolelih pacijenata. Takođe, istraživali smo ulogu signalnog puta adenozin-monofosfatom aktivirane protein-kinaze (AMPK) i mTOR kompleksa 1 (mTORC1 - engl. mammalian target of rapamycin complex 1) u antigliomskom dejstvu NSAIL. Indometacin je snažnije od ostalih NSAIL (diklofenaka, naproksena i ketoprofena) smanjivao vijabilitet U251 ćelija humanog glioblastoma. Antigliomski efekat indometacina je bio povezan sa ekspresijom tumor supresorskog proteina p21 i zastojem ćelijskog ciklusa u G2M fazi, indukcijom oksidativnog stresa, depolarizacijom mitohondrija, aktivacijom kaspaza i indukcijom apoptoze. Indometacin je jedini od ispitivanih NSAIL povećavao fosforilaciju AMPK i nishodnih molekula koje ona fosforiliše, Raptor-a i acetil-CoA karboksilaze (ACC). Aktivaciju AMPK pratilo je smanjenje fosforilacije mTOR i molekula čiju aktivnost mTORC1 reguliše, kao što su ribozomalna p70S6 kinaza (S6K) i PRAS40 (Ser183). Genetska inhibicija AMPK RNK interferencijom, kao i tretman ćelija aktivatorom mTORC1 leucinom doveli su do delimičnog poništavanja citotoksičnih efekata izazvanih indometacinom. Sa druge strane, farmakološki aktivatori AMPK metformin i AICAR su poput indometacina ispoljavali antigliomski efekat inhibicijom mTORC1. Aktivacija AMPK u ćelijama tretiranim indometacinom korelirala je sa smanjenjem ćelijskog ATP i porastom AMP/ATP odnosa, ali je bila nezavisna od inhibicije COX i povećanja intraćelijskog nivoa kalcijuma. Takođe, citotoksični efekat indometacina na ćelije primarne kulture glioblastoma bio je posredovan aktivacijom AMPK/Raptor/ACC i inhibicijom mTORC1/S6K signalnih molekula...

Advisors/Committee Members: Trajković, Vladimir, 1967-, 12751207.

Subjects/Keywords: glioma; NSAID; indomethacin; AMPK; mTOR; apoptosis; autophagy

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

APA (6^th Edition):

Pantović, Aleksandar, 1982-, 5. (2020). Uloga adenozin-monofosfatom aktivirane protein-kinaze i mTOR kompleksa 1 u in vitro citotoksičnom dejstvu nesteroidnih anti-inflamatornih lekova na ćelije glioma. (Thesis). Univerzitet u Beogradu. Retrieved from https://fedorabg.bg.ac.rs/fedora/get/o:23025/bdef:Content/get

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

Chicago Manual of Style (16^th Edition):

Pantović, Aleksandar, 1982-, 59207177. “Uloga adenozin-monofosfatom aktivirane protein-kinaze i mTOR kompleksa 1 u in vitro citotoksičnom dejstvu nesteroidnih anti-inflamatornih lekova na ćelije glioma.” 2020. Thesis, Univerzitet u Beogradu. Accessed March 01, 2021. https://fedorabg.bg.ac.rs/fedora/get/o:23025/bdef:Content/get.

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

MLA Handbook (7^th Edition):

Pantović, Aleksandar, 1982-, 59207177. “Uloga adenozin-monofosfatom aktivirane protein-kinaze i mTOR kompleksa 1 u in vitro citotoksičnom dejstvu nesteroidnih anti-inflamatornih lekova na ćelije glioma.” 2020. Web. 01 Mar 2021.

Vancouver:

Pantović, Aleksandar, 1982- 5. Uloga adenozin-monofosfatom aktivirane protein-kinaze i mTOR kompleksa 1 u in vitro citotoksičnom dejstvu nesteroidnih anti-inflamatornih lekova na ćelije glioma. [Internet] [Thesis]. Univerzitet u Beogradu; 2020. [cited 2021 Mar 01]. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:23025/bdef:Content/get.

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

Council of Science Editors:

Pantović, Aleksandar, 1982- 5. Uloga adenozin-monofosfatom aktivirane protein-kinaze i mTOR kompleksa 1 u in vitro citotoksičnom dejstvu nesteroidnih anti-inflamatornih lekova na ćelije glioma. [Thesis]. Univerzitet u Beogradu; 2020. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:23025/bdef:Content/get

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

Open Access Theses and Dissertations