Cancer Protein Description
This report provides a detailed description of a selected cancer protein with information collected from various sources, including UniProt, the Wellcome Trust Sanger Institute’s Catalogue of Somatic Mutations in Cancer (COSMIC), and the Atlas of Genetics and Cytogenetics in Oncology and Haematology.
| Protein Name: | HIPK2 |
| Gene Name: | HIPK2 |
| Protein Full Name: | Homeodomain-interacting protein kinase 2 |
| Alias: | EC 2.7.11.1; Homeodomain interacting protein kinase 2; Kinase HIPK2; NBAK1; Nuclear body associated kinase 1; Sialophorin tail associated nuclear serine,threonine kinase; Sialophorin tail associated nuclear serine/threonine kinase; STANK |
| Mass (Da): | 130966 |
| Number AA: | 1198 |
| UniProt ID: | Q9H2X6 |
| Locus ID: | 28996 |
| COSMIC ID: | HIPK2 |
| Gene location on chromosome: | 7q34 |
| Cancer protein type: | TSP |
| Effect of cancer mutation on protein: | UNCLEAR |
| Effect of active protein on cancer: | INHIBITS |
| Number of cancer specimens: | 20588 |
| Percent of cancer specimens with mutations: | 0.93 |
| Deregulated in translocations: | PEBP2-beta-SMMHC fusion protein in AML(RUNX1)-associated leukemias; A frequent amplification of HIPK2 along with BRAF rearrangements in JPA (35 out of 53 cases) through 7q34 duplication was reported |
| Normal role description: | HIPK2 is a protein-serine/threonine kinase that interacts with numerous transcription factors (such as p53, AML1(RUNX1), PAX6, c-MYB or NK3) as well as transcriptional regulators (such as CBP, p300, Groucho, CtBP, HMGA1 or Smads). In this way HIPK2 can activate or repress transcription and thereby influence differentiation, development and the DNA damage response. HIPK2 can promote the apoptotic program via p53-dependent and -independent pathways through phosphorylation of p53 at Ser46 or phosphorylation of the anti-apoptotic co-repressor CtBP at Ser422 (both actions leading to the transcription of pro-apoptotic target genes). In most cancer systems appears to repress growth and prevent tumorigenesis. In cervical cancer was described to be upregulated but this may represent a compensation of normal cellular machinery |