TY - JOUR
AU - Reuven, Nina
AU - Adler, Julia
AU - Porat, Ziv
AU - Polonio-Vallon, Tilman
AU - Hofmann, Thomas
AU - Shaul, Yosef
TI - The Tyrosine Kinase c-Abl Promotes Homeodomain-interacting Protein Kinase 2 (HIPK2) Accumulation and Activation in Response to DNA Damage.
JO - The journal of biological chemistry
VL - 290
IS - 27
SN - 1083-351X
CY - Bethesda, Md.
PB - Soc.
M1 - DKFZ-2017-03399
SP - 16478 - 16488
PY - 2015
AB - The non-receptor tyrosine kinase c-Abl is activated in response to DNA damage and induces p73-dependent apoptosis. Here, we investigated c-Abl regulation of the homeodomain-interacting protein kinase 2 (HIPK2), an important regulator of p53-dependent apoptosis. c-Abl phosphorylated HIPK2 at several sites, and phosphorylation by c-Abl protected HIPK2 from degradation mediated by the ubiquitin E3 ligase Siah-1. c-Abl and HIPK2 synergized in activating p53 on apoptotic promoters in a reporter assay, and c-Abl was required for endogenous HIPK2 accumulation and phosphorylation of p53 at Ser(46) in response to DNA damage by γ- and UV radiation. Accumulation of HIPK2 in nuclear speckles and association with promyelocytic leukemia protein (PML) in response to DNA damage were also dependent on c-Abl activity. At high cell density, the Hippo pathway inhibits DNA damage-induced c-Abl activation. Under this condition, DNA damage-induced HIPK2 accumulation, phosphorylation of p53 at Ser(46), and apoptosis were attenuated. These data demonstrate a new mechanism for the induction of DNA damage-induced apoptosis by c-Abl and illustrate network interactions between serine/threonine and tyrosine kinases that dictate cell fate.
KW - Carrier Proteins (NLM Chemicals)
KW - Tumor Suppressor Protein p53 (NLM Chemicals)
KW - HIPK2 protein, human (NLM Chemicals)
KW - Proto-Oncogene Proteins c-abl (NLM Chemicals)
KW - Protein-Serine-Threonine Kinases (NLM Chemicals)
LB - PUB:(DE-HGF)16
C6 - pmid:25944899
C2 - pmc:PMC4505402
DO - DOI:10.1074/jbc.M114.628982
UR - https://inrepo02.dkfz.de/record/127374
ER -