| First Author | Tsuji K | Year | 2002 |
| Journal | J Biol Chem | Volume | 277 |
| Issue | 4 | Pages | 2951-7 |
| PubMed ID | 11706030 | Mgi Jnum | J:114013 |
| Mgi Id | MGI:3688023 | Doi | 10.1074/jbc.M108535200 |
| Citation | Tsuji K, et al. (2002) Differential effect of ik3-1/cables on p53- and p73-induced cell death. J Biol Chem 277(4):2951-7 |
| abstractText | ik3-1/Cables is associated with cdk3 in self-replicating cells. In postmitotic neurons, it may serve as an adaptor molecule, functionally connecting c-abl and cdk5, and supporting neurite growth. Here we report that ik3-1 binds to p53 and p73 in vivo. Ectopically expressed ik3-1 potentiates p53-induced cell death but not p73-induced cell death in U2OS cells. On the contrary, coexpression of ik3-1-DeltaC, an ik3-1 deletion mutant lacking the C-terminal 139 [corrected] amino acids (corresponding to the cyclin box-homologous region), inhibits p73-induced cell death but not p53-induced cell death. ik3-1-DeltaC-mediated inhibition of p73-induced cell death are partially attenuated by overexpression of ik3-1. These data indicate that ik3-1 is not only a regulator for p53-induced cell death but also an essential regulator for p73-induced cell death, and ik3-1-DeltaC competes with ik3-1 only in p73-induced cell death. Furthermore, functional domains of p53 responsible for its interaction with ik3-1 are partially different from those of p73. In conclusion, we found that ik3-1, a putative component of cell cycle regulation, is functionally connected with p53 and p73, but in distinct fashions. |
