References
Query Results -- Details
MGI Accession ID: MGI:3715684
J Number: J:122882
Other Accession IDs:
Title: Reduction of apoptosis in Rb-deficient embryos via Abl knockout.
Authors: Borges HL; Hunton IC; Wang JY
Journal: Oncogene
Volume: 26
Issue: 26
Date: 2007 May 31
Year: 2007
Pages: 3868-77
Review Status: Peer Reviewed
Abstract:
The retinoblastoma protein RB regulates cell proliferation, differentiation and apoptosis. Homozygous knockout of Rb in mice causes embryonic lethality owing to placental defects that result in excessive apoptosis. RB binds to a number of cellular proteins including the nuclear Abl protein and inhibits its tyrosine kinase activity. Ex vivo experiments have shown that genotoxic or inflammatory stress can activate Abl kinase to stimulate apoptosis. Employing the Rb-null embryos as an in vivo model of apoptosis, we have shown that the genetic ablation of Abl can reduce apoptosis in the developing central nervous system and the embryonic liver. These results are consistent with the inhibitory interaction between RB and Abl, and provide in vivo evidence for the proapoptotic function of Abl.
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