| First Author | Trapasso F | Year | 2009 |
| Journal | DNA Cell Biol | Volume | 28 |
| Issue | 4 | Pages | 161-7 |
| PubMed ID | 19364276 | Mgi Jnum | J:156574 |
| Mgi Id | MGI:4420885 | Doi | 10.1089/dna.2008.0778 |
| Citation | Trapasso F, et al. (2009) Targeted disruption of the murine homeodomain-interacting protein kinase-2 causes growth deficiency in vivo and cell cycle arrest in vitro. DNA Cell Biol 28(4):161-7 |
| abstractText | The homeodomain-interacting protein kinase 2 (HIPK2) protein is a member of a recently identified family of nuclear protein kinases that are well conserved in various organisms. HIPK2 can bind to several homeotic factors and to a series of proteins involved in the regulation of cell survival and proliferation in response to morphogenetic and genotoxic signals. Here we report Hipk2-targeted disruption in mouse; Hipk2(-/-) mice are viable and fertile but significantly smaller than their wild-type littermates. This feature is present at birth and retained throughout the mouse adulthood. Mouse embryo fibroblasts from Hipk2(-/-) mice show a reduced proliferation rate, compared to the wild-type counterparts, with accumulation in the G0/G1 phase of the cell cycle and altered levels of the cell cycle regulators cyclin D and CDK6. Restoration of wild-type HIPK2 expression in Hipk2(-/-) cells rescues the normal phenotype supporting a role for HIPK2 in the regulation of cell proliferation. |
