AMPK activation prevents excess nutrient-induced hepatic lipid accumulation by inhibiting mTORC1 signaling and endoplasmic reticulum stress response-Reference-Cited by-同舟云学术

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AMPK activation prevents excess nutrient-induced hepatic lipid accumulation by inhibiting mTORC1 signaling and endoplasmic reticulum stress response

Published:2014-09 Issue:9 Volume:1842 Page:1844-1854
ISSN:0925-4439
Container-title:Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
language:en
Short-container-title:Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease

Author:

Li Hongliang,Min Qing,Ouyang Changhan,Lee Jiyeon,He Chaoyong,Zou Ming-Hui,Xie Zhonglin

Funder

NIH

American Heart Association Scientist Development Grant

Juvenile Diabetes Research Foundation

Oklahoma Center for the Advancement of Science and Technology

American Diabetes Association

Publisher

Elsevier BV

Subject

Molecular Biology,Molecular Medicine

Reference54 articles.

1. The role of endoplasmic reticulum in hepatic lipid homeostasis and stress signaling;Fu;Cell Metab.,2012

2. Reduction of AMP-activated protein kinase alpha2 increases endoplasmic reticulum stress and atherosclerosis in vivo;Dong;Circulation,2010

3. Endoplasmic reticulum stress causes the activation of sterol regulatory element binding protein-2;Colgan;Int. J. Biochem. Cell Biol.,2007

4. PERK-dependent regulation of lipogenesis during mouse mammary gland development and adipocyte differentiation;Bobrovnikova-Marjon;Proc. Natl. Acad. Sci. U. S. A.,2008

5. Nutrient overload, insulin resistance, and ribosomal protein S6 kinase 1, S6K1;Um;Cell Metab.,2006

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