cellular
• after Cre retrovirus infection (to delete the floxed allele), primary mouse embryonic fibroblasts (MEFs) derived from E13.5 embryos show significantly decreased cell proliferation relative to wild-type MEFs
• no differences in oncogene-induced cellular replicative senescence or apoptosis are observed
• defect in MEF proliferation can be rescued by beta-TrCP2 overexpression, but not by beta-TrCP1 overexpression
• arrest in MEF proliferation is induced by stabilization and abnormal accumulation of Cdkn2a (also known as p19ARF)
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