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A20 protects mice from lethal radical hepatectomy by promoting hepatocyte proliferation via a p21waf1-dependent mechanism.

A20 protects mice from lethal radical hepatectomy by promoting hepatocyte proliferation via a p21waf1-dependent mechanism. Research Abstract Details 

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  • A20 protects mice from lethal radical hepatectomy by promoting hepatocyte proliferation via a p21waf1-dependent mechanism. Abstract Text:

    The liver has a remarkable regenerative capacity, allowing recovery following injury. Regeneration after injury is contingent on maintenance of healthy residual liver mass, otherwise fulminant hepatic failure (FHF) may arise. Understanding the protective mechanisms safeguarding hepatocytes and promoting their proliferation is critical for devising therapeutic strategies for FHF. We demonstrate that A20 is part of the physiological response of hepatocytes to injury. In particular, A20 is significantly upregulated in the liver following partial hepatectomy. A20 protects hepatocytes from apoptosis and ongoing inflammation by inhibiting NF-kappaB. Hepatic expression of A20 in BALB/c mice dramatically improves survival following extended and radical lethal hepatectomy. A20 expression in the liver limits hepatocellular damage hence maintains bilirubin clearance and the liver synthetic function. In addition, A20 confers a proliferative advantage to hepatocytes via decreased expression of the cyclin-dependent kinase inhibitor p21(waf1). In conclusion, A20 provides a proliferative advantage to hepatocytes. By combining anti-inflammatory, antiapoptotic and pro-proliferative functions, A20-based therapies could be beneficial in prevention and treatment of FHF.

    A20 protects mice from lethal radical hepatectomy by promoting hepatocyte proliferation via a p21waf1-dependent mechanism. Publishing Authors By Initials

    For similar zinc fingers research abstracts see: zinc fingers research

    PUBMED ID PMID:

    MEDLINE DATE:

    A20 protects mice from lethal radical hepatectomy by promoting hepatocyte proliferation via a p21waf1-dependent mechanism. Journal Published:

    PUBLICATION TYPE: Research Support, U.S. Gov't,

    Journal: Hepatology (Baltimore, Md.)

    VOLUME: 42

    Page Numbers: 156-64

    Journal Abbreviation: Hepatology

    ISSN: 0270-9139

    DAY: 16

    MONTH: Jul

    YEAR: 2005

    A20 protects mice from lethal radical hepatectomy by promoting hepatocyte proliferation via a p21waf1-dependent mechanism. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 8302946

    A20 protects mice from lethal radical hepatectomy by promoting hepatocyte proliferation via a p21waf1-dependent mechanism. Keywords Mesh Terms:

    KEYWORDS: Zinc Fingers

    MESH TERMS: genetics

    Chemical & Substance for Abstract: A20 protects mice from lethal radical hepatectomy by promoting hepatocyte proliferation via a p21waf1-dependent mechanism. Information

    Substance Name: Tnfaip3 protein, mouse

    Registry Number: EC 3.4.22.-

    Grant and Affiliation Information for A20 protects mice from lethal radical hepatectomy by promoting hepatocyte proliferation via a p21waf1-dependent mechanism.

    AFFILIATION: Immunobiology Research Center, Division of Vascular Surgery, and the Transplant Center, Department of Surgery, Harvard Medical School, Boston, MA 02215, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NHLBI

    GRANT: T32 HL07734

    ACRONYM: HL

    MEDLINETA: Hepatology

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

    Number Hits: 0

    A20 protects mice from lethal radical hepatectomy by promoting hepatocyte proliferation via a p21waf1-dependent mechanism Related Publications

     

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