|  Help  |  About  |  Contact Us

Publication : Overexpression of ABIN-2, a negative regulator of NF-kappaB, delays liver regeneration in the ABIN-2 transgenic mice.

First Author  Li CC Year  2006
Journal  Biochem Biophys Res Commun Volume  342
Issue  1 Pages  300-9
PubMed ID  16480954 Mgi Jnum  J:105880
Mgi Id  MGI:3616926 Doi  10.1016/j.bbrc.2006.01.114
Citation  Li CC, et al. (2006) Overexpression of ABIN-2, a negative regulator of NF-kappaB, delays liver regeneration in the ABIN-2 transgenic mice. Biochem Biophys Res Commun 342(1):300-9
abstractText  Activation of NF-kappaB is one of the earliest responses at the start of liver regeneration, and is required for hepatocyte cell cycle progression. The A20-binding inhibitor of NF-kappaB activation-2, ABIN-2, is an inhibitor of NF-kappaB. However, its effects on hepatocyte cell cycle progression are not known and its involvement in liver regeneration has not been explored. In this study, the temporal expression pattern of the mouse ABIN-2 was studied during liver regeneration induced by partial hepatectomy. We demonstrate that ABIN-2 is rapidly and transiently induced, and expression peaked at around 8h post-hepatectomy. To test that the inducible expression of ABIN-2 serves to regulate NF-kappaB during liver regeneration, transgenic mice overexpressing human ABIN-2 protein in the liver were generated. Our transgenic data demonstrated that overexpression of ABIN-2 inhibited NF-kappaB nuclear translocation, which peaked at around 2-4h post-hepatectomy, and this led to an impairment of the G1/S transition as well as a delay in hepatocyte cell cycle progression of the regenerating liver. In addition, overexpression of ABIN-2 specifically inhibited endogenous ABIN-2 mRNA induction, suggesting a negative feedback mechanism for ABIN-2 expression. In conclusion, ABIN-2 may function as a negative regulator that downregulates NF-kappaB activation during liver regeneration.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

4 Authors

2 Bio Entities

Trail: Publication

0 Expression