| First Author | Zhan Y | Year | 2017 |
| Journal | Exp Cell Res | Volume | 355 |
| Issue | 1 | Pages | 40-46 |
| PubMed ID | 28351752 | Mgi Jnum | J:260914 |
| Mgi Id | MGI:6152093 | Doi | 10.1016/j.yexcr.2017.03.033 |
| Citation | Zhan Y, et al. (2017) Deficiency of CKIP-1 aggravates high-fat diet-induced fatty liver in mice. Exp Cell Res 355(1):40-46 |
| abstractText | Casein kinase 2 interacting protein-1(CKIP-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) CKIP-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 CKIP-1(-/-) mice were higher than those of WT mice; (3) CKIP-1 interacted with JNK1 in vitro. Our results indicate that CKIP-1 deficiency in mice aggravates HFD-induced fatty liver by upregulating JNK1 phosphorylation and further upregulating IRS-1 phosphorylation and RI. |
