Searching across hundreds of databases

Our searching services are busy right now. Your search will reload in five seconds.

Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

PML tumor suppressor is regulated by HIPK2-mediated phosphorylation in response to DNA damage.

Oncogene | Feb 5, 2009

The promyelocytic leukemia (PML) tumor suppressor protein, a central regulator of cell proliferation and apoptosis, is frequently fused to the retinoic acid receptor-alpha (RARalpha) in acute PML. Here we show the interaction of PML with another tumor suppressor protein, the serine/threonine kinase homeodomain-interacting protein kinase (HIPK2). In response to DNA damage, HIPK2 phosphorylates PML at serines 8 and 38. Although HIPK2-mediated phosphorylation of PML occurs early during the DNA damage response, the oncogenic PML-RARalpha fusion protein is phosphorylated with significantly delayed kinetics. DNA damage or HIPK2 expression leads to the stabilization of PML and PML-RARalpha proteins. The N-terminal phosphorylation sites contribute to the DNA damage-induced PML SUMOylation and are required for the ability of PML to cooperate with HIPK2 for the induction of cell death.

Pubmed ID: 19015637 RIS Download

Mesh terms: Carrier Proteins | Cell Death | Cells, Cultured | DNA Damage | Genes, Tumor Suppressor | Humans | Nuclear Proteins | Phosphorylation | Promyelocytic Leukemia Protein | Protein Binding | Protein Processing, Post-Translational | Protein Stability | Protein Structure, Tertiary | Protein-Serine-Threonine Kinases | SUMO-1 Protein | Serine | Transcription Factors | Tumor Suppressor Proteins

Research resources used in this publication

None found

Research tools detected in this publication

None found

Data used in this publication

None found

Associated grants


Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.

We have not found any resources mentioned in this publication.