Journal
EXPERIMENTAL CELL RESEARCH
Volume 355, Issue 1, Pages 40-46Publisher
ELSEVIER INC
DOI: 10.1016/j.yexcr.2017.03.033
Keywords
Non-alcoholic fatty liver disease (NAFLD); Casein kinase 2 interacting protein-1 (CKIP-1); c-Jun NH2-terminal kinase 1 (JNK1); Insulin receptor substrate-1(IRS-1); High fat diet (HFD)
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Funding
- Scientific Research Common Program of Beijing Municipal Commission of Education [km201510025017]
- National Natural Science Foundation of China [81570515, 31470035]
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Casein kinase 2 interacting protein-1(CRIF-1) is widely expressed in a variety of tissues and cells, and plays an important role in various critical cellular and physiological processes including cell growth, apoptosis, differentiation, cytoskeleton and bone formation. Here, we found: (1) CHIP-1 deficient mice exhibited increased body weight, liver weight, number and size of lipid droplets, and TG content comparing with WT mice after being exposed to high fat diet (HFD); (2) the levels of serum insulin, liver glycogen, phosphorylated C-Jun-N-terminal kinase-1 (pJNK1) and phosphorylated insulin receptor substrate -1(pIRS1) in CHIP-1(-/-) mice were higher than those of WT mice; (3) CHIP-1 interacted with JNK1 in vitro. Our results indicate that CHIP-1 deficiency in mice aggravates HFD-induced fatty liver by upregulating JNK1 phosphorylation and further upregulating IRS-1 phosphorylation and RI.
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