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Small inducible cytokine subfamily B member 16
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[C1q/TNF-related protein 6] This protein is a member of the CRTP family (see: C1q family) (Wong et al, 2004). It is characterized by the presence of a C1q domain as found in complement factor C1q. The approved gene symbol for this protein is C1QTNF6 [Complement C1q tumor necrosis factor-related protein 6, C1q and tumor necrosis factor related protein 6]. A databank synonym is ZACRP6.
Wong et al (2010) have reported that CTRP6 is a secreted glycoprotein. Like adiponectin secreted CTRP6 is a trimer that can form higher-order oligomeric complexes via disulfide bonding. Besides forming homo-oligomers, CTRP6 can also form heterooligomers with CTRP1. High levels of CTRP6 are expressed in the placenta and the eye. Expression levels of CTRP6 are up-regulated in 8-week-old obese (ob/ob) mice relative to lean controls. Treatment of mice with rosiglitazone decreases CTRP6 transcript levels. CTRP6 circulates in the blood and may act as an endocrine hormone. Serum levels of CTRP6 are increased in knock-out mice lacking expression of adiponectin.
Lee et al (2010) have reported that CTRP6 plays a role in fatty acid metabolism. It mediates the phosphorylation and activation of the 5'-AMP-activated protein kinase (AMPK) in skeletal muscle cells and also induces the phosphorylation of acetyl coenzyme A carboxylase and fatty acid oxidation in myocytes.
Kim et al (2010) have shown that CTRP6 induces the expression of the potent anti-inflammatory cytokine IL10 in macrophages.
Chang et al (2006) have identified CRTF6 as one of the host genes that can limit replication of ASFV (African Swine Fever virus) that causes acute haemorrhagic fever in domestic pigs.
Takeuchi et al (2011) have reported overexpression of CTRP6 in 21/30 hepatocellular carcinomas. CTRP6 is detected in tumor cells but not in non-cancerous liver tissues. It also localizes on the tumor endothelial cells in close proximity hepatocellular carcinoma cells expressing the protein. Recombinant CTRP6 increases the level of active phosphorylated Akt molecules in cultured vascular endothelial cells. Enforced expression of CTRP6 markedly reduces the central hypovascular necrosis areas of transplanted HepG2 hepatocellular carcinoma cells. Thus, CTRP6 may contribute to tumor angiogenesis by activating the Akt pathway in many hepatocellular carcinomas.
Copyright © 2012 by H IBELGAUFTS. All rights reserved.
ENTRY LAST MODIFIED: September 2010
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