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Título

Mice lacking bi-1 gene show accelerated liver regeneration

AutorBruey, Jean-Marie; Kress, Christina; Zapata, Juan M. ; Reed, John C.
Palabras claveBI-1
Cell cycle
Calcineurin
Bcl-2
Regeneration
Fecha de publicación2007
EditorAmerican Association for Cancer Research
CitaciónCancer Research 67(4): 1442-1450 (2007)
ResumenThe 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 Ca2+ 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 p27Kip1. Dephosphorylation and nuclear translocation of nuclear factor of activated T cells 1 (NFAT1), a substrate of the Ca2+-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.
DescripciónEl pdf del artículo es la versión pre-print.-- et al.
Versión del editorhttp://dx.doi.org/10.1158/0008-5472.CAN-06-0850
URIhttp://hdl.handle.net/10261/91746
DOI10.1158/0008-5472.CAN-06-0850
ISSN0008-5472
E-ISSN1538-7445
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