Targeted disruption of the murine homeodomain-interacting protein kinase-2 causes growth deficiency in vivo and cell cycle arrest in vitro

Francesco Trapasso, Rami I. Aqeilan, Rodolfo Iuliano, Rosa Visone, Eugenio Gaudio, Laura Ciuffini, Hansjuerg Alder, Francesco Paduano, Giovanna Maria Pierantoni, Silvia Soddu, Carlo M. Croce, Alfredo Fusco

Research output: Contribution to journalArticlepeer-review

Abstract

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.

Original languageEnglish
Pages (from-to)161-167
Number of pages7
JournalDNA and Cell Biology
Volume28
Issue number4
DOIs
Publication statusPublished - Apr 1 2009

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cell Biology

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