| First Author | Sandoval R | Year | 2006 |
| Journal | Exp Cell Res | Volume | 312 |
| Issue | 13 | Pages | 2465-75 |
| PubMed ID | 16730350 | Mgi Jnum | J:111333 |
| Mgi Id | MGI:3653780 | Doi | 10.1016/j.yexcr.2006.04.002 |
| Citation | Sandoval R, et al. (2006) A mutant allele of BARA/LIN-9 rescues the cdk4-/- phenotype by releasing the repression on E2F-regulated genes. Exp Cell Res 312(13):2465-75 |
| abstractText | It has been proposed that C. elegans LIN-9 functions downstream of CDK4 in a pathway that regulates cell proliferation. Here, we report that mammalian BARA/LIN-9 is a predominantly nuclear protein that inhibits cell proliferation. More importantly, we demonstrate that BARA/LIN-9 also acts downstream of cyclin D/CDK4 in mammalian cells since (i) its antiproliferative effect is partially blocked by coexpression of cyclin D1, and (ii) a mutant form that lacks the first 84 amino acids rescues several phenotypic alterations observed in mice null for cdk4. Interestingly, mutation of BARA/LIN-9 restores the expression of E2F target genes in CDK4 null MEFs, indicating that the wild-type protein plays a role in the expression of genes required for the G1/S transition. |
