Mice lacking bi-1 gene show accelerated liver regeneration.

Mice lacking bi-1 gene show accelerated liver regeneration. Research Abstract Details 

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Mice lacking bi-1 gene show accelerated liver regeneration. Abstract Text:

Bailly-Maitre,Emilie Bard-Chapeau, Luciano,Nathalie Droin,Jean-Marie Bruey,Benjamin Faustin,Christina Kress,Juan M Zapata,John C Reed,

The liver has enormous regenerative capacity such that, after partial hepatectomy, hepatocytes rapidly replicate to restore liver mass, thus providing a context for studying in vivo mechanisms of cell growth regulation. Bax inhibitor-1 (BI-1) is an evolutionarily conserved endoplasmic reticulum (ER) protein that suppresses cell death. Interestingly, the BI-1 protein has been shown to regulate Ca(2+) handling by the ER similar to antiapoptotic Bcl-2 family proteins. Effects on cell cycle entry by Bcl-2 family proteins have been described, prompting us to explore whether bi-1-deficient mice display alterations in the in vivo regulation of cell cycle entry using a model of liver regeneration. Accordingly, we compared bi-1(+/+) and bi-1(-/-) mice subjected to partial hepatectomy with respect to the kinetics of liver regeneration and molecular events associated with hepatocyte proliferation. We found that bi-1 deficiency accelerates liver regeneration after partial hepatectomy. Regenerating hepatocytes in bi-1(-/-) mice enter cell cycle faster, as documented by more rapid incorporation of deoxynucleotides, associated with earlier increases in cyclin D1, cyclin D3, cyclin-dependent kinase (Cdk) 2, and Cdk4 protein levels, more rapid hyperphosphorylation of retinoblastoma protein, and faster degradation of p27(Kip1). Dephosphorylation and nuclear translocation of nuclear factor of activated T cells 1 (NFAT1), a substrate of the Ca(2+)-sensitive phosphatase calcineurin, were also accelerated following partial hepatectomy in BI-1-deficient hepatocytes. These findings therefore reveal additional similarities between BI-1 and Bcl-2 family proteins, showing a role for BI-1 in regulating cell proliferation in vivo, in addition to its previously described actions as a regulator of cell survival.

Mice lacking bi-1 gene show accelerated liver regeneration. Publishing Authors By Initials

B Bailly-Maitre,E Bard-Chapeau,F Luciano,N Droin,JM Bruey,B Faustin,C Kress,JM Zapata,JC Reed,

For similar peptides: intercellular signaling peptides and proteins: cytokines: monokines: tumor necrosis factor-alpha research abstracts see: peptides: intercellular signaling peptides and proteins: cytokines: monokines: tumor necrosis factor-alpha research

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Mice lacking bi-1 gene show accelerated liver regeneration. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Cancer research

VOLUME: 67

Page Numbers: 1442-50

Journal Abbreviation: Cancer Res.

ISSN: 0008-5472

DAY: 15

MONTH: Feb

YEAR: 2007

Mice lacking bi-1 gene show accelerated liver regeneration. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 2984705

Mice lacking bi-1 gene show accelerated liver regeneration. Keywords Mesh Terms:

KEYWORDS: Tumor Necrosis Factor-alpha

MESH TERMS: genetics

Chemical & Substance for Abstract: Mice lacking bi-1 gene show accelerated liver regeneration. Information

Substance Name: Cyclin-Dependent Kinase Inhibitor p27

Registry Number: 147604-94-2

Grant and Affiliation Information for Mice lacking bi-1 gene show accelerated liver regeneration.

AFFILIATION: Burnham Institute for Medical Research, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.

Country: United States

AGENCY: United States NIA

GRANT: AG 15393

ACRONYM: AG

MEDLINETA: Cancer Res

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