The Endocrine Society
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Các bài báo tiêu biểu
Control by Basal Phosphorylation of Cell Cycle-Dependent, Hormone-Induced Glucocorticoid Receptor Hyperphosphorylation
Tập 11 Số 3 - Trang 305-311 - 1997
High Level Expression of Wild Type and Variant Mouse Glucocorticoid Receptors in Chinese Hamster Ovary Cells
Tập 4 Số 1 - Trang 162-170 - 1990
In vivo regulation of central nervous system progesterone receptors: cocaine induces steroid-dependent behavior through dopamine transporter modulation of D5 receptors in rats
Tập 10 Số 12 - Trang 1595-1604 - 1996
Identification of a Gene Induced by Glucocorticoids in Murine T-Cells: A Potential G Protein-Coupled Receptor
Tập 5 Số 9 - Trang 1331-1338 - 1991
Antiandrogen Effects of Mifepristone on Coactivator and Corepressor Interactions with the Androgen Receptor
Tập 18 Số 1 - Trang 70-85 - 2004
Autophagy Deficiency by Hepatic FIP200 Deletion Uncouples Steatosis From Liver Injury in NAFLD Nonalcoholic fatty liver disease is a metabolic disorder commonly associated with obesity. A subset of nonalcoholic fatty liver disease patients further develops nonalcoholic steatohepatitis that is characterized by chronic liver injury, inflammation, and fibrosis. Recent work has implicated the autophagy pathway in the mobilization and oxidation of triglycerides from lipid droplets. However, whether impaired autophagy in hepatocytes drives excess fat accumulation in the liver remains controversial. In addition, the role of autophagy in protecting the liver from gut endotoxin-induced injury has not been elucidated. Here we generated mice with liver-specific autophagy deficiency by the conditional deletion of focal adhesion kinase family kinase-interacting protein of 200 kDa (also called Rb1cc1), a core subunit of the mammalian autophagy related 1 complex. To our surprise, mice lacking FIP200 in hepatocytes were protected from starvation- and high-fat diet-induced fat accumulation in the liver and had decreased expression of genes involved in lipid metabolism. Activation of the de novo lipogenic program by liver X receptor was impaired in FIP200-deficient livers. Furthermore, liver autophagy was stimulated by exposure to low doses of lipopolysaccharides and its deficiency-sensitized mice to endotoxin-induced liver injury. Together these studies demonstrate that hepatocyte-specific autophagy deficiency per se does not exacerbate hepatic steatosis. Instead, autophagy may play a protective role in the liver after exposure to gut-derived endotoxins and its blockade may accelerate nonalcoholic steatohepatitis progression.
Tập 27 Số 10 - Trang 1643-1654 - 2013
Macrophage-Secreted Factors Promote a Profibrotic Phenotype in Human Preadipocytes
Tập 23 Số 1 - Trang 11-24 - 2009
Structural Requirements of the Glucocorticoid and Retinoic Acid Response Units in the Phosphoenolpyruvate Carboxykinase Gene Promoter
Tập 12 Số 10 - Trang 1487-1498 - 1998