國家衛生研究院 NHRI:Item 3990099045/2360
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    題名: Overexpression of ABIN-2, a negative regulator of NF-kappa B, delays liver regeneration in the ABIN-2 transgenic mice
    其他題名: Overexpression of ABIN-2, a negative regulator of NF-κB, delays liver regeneration in the ABIN-2 transgenic mice
    作者: Li, CC;Chou, CK;Wang, MH;Tsai, TF
    貢獻者: Division of Molecular and Genomic Medicine
    摘要: Activation of NF-kappa B 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-kappa B activation-2, ABIN-2, is an inhibitor of NF-kappa B. 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 8 h post-hepatectomy. To test that the inducible expression of ABIN-2 serves to regulate NF-kappa B 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-kappa B nuclear translocation, which peaked at around 2-4 h 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-kappa B activation during liver regeneration. (c) 2006 Elsevier Inc. All rights reserved.
    關鍵詞: Biochemistry & Molecular Biology;Biophysics
    日期: 2006-03-31
    關聯: Biochemical and Biophysical Research Communications. 2006 Mar;342(1):300-309.
    Link to: http://dx.doi.org/10.1016/j.bbrc.2006.01.114
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0006-291X&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000235793800041
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=32644460310
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