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Article: Characterization of cells and gene-targeted mice deficient for the p53-binding kinase homeodomain-interacting protein kinase 1 (HIPK1)

TitleCharacterization of cells and gene-targeted mice deficient for the p53-binding kinase homeodomain-interacting protein kinase 1 (HIPK1)
Authors
Issue Date2003
Citation
Proceedings of the National Academy of Sciences of the United States of America, 2003, v. 100, n. 9, p. 5431-5436 How to Cite?
AbstractThe tumor suppressor p53 is regulated in part by binding to cellular proteins. We used p53 as bait in the yeast two-hybrid system and isolated homeodomain-interacting protein kinase 1 (HIPK1) as a p53-binding protein. Deletion analysis showed that amino acids 100-370 of p53 and amino acids 885-1093 of HIPK1 were sufficient for HIPK1-p53 interaction. HIPK1 was capable of autophosphorylation and specific serine phosphorylation of p53. The HIPK1 gene was highly expressed in human breast cancer cell lines and oncogenically transformed mouse embryonic fibroblasts. HIPK1 was localized to human chromosome band 1p13, a site frequently altered in cancers. Gene-targeted HIPK1-/- mice were grossly normal but oncogenically transformed HIPK1 -/- mouse embryonic fibroblasts exhibited reduced transcription of Mdm2 and were more susceptible than transformed HIPKI+/+ cells to apoptosis induced by DNA damage. Carcinogen-treated HIPK1 -/- mice developed fewer and smaller skin tumors than HIPK1+/+ mice. HIPK1 may thus play a role in tumorigenesis, perhaps by means of the regulation of p53 and/or Mdm2.
Persistent Identifierhttp://hdl.handle.net/10722/291636
ISSN
2023 Impact Factor: 9.4
2023 SCImago Journal Rankings: 3.737
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorKondo, Seiji-
dc.contributor.authorLu, Ying-
dc.contributor.authorDebbas, Michael-
dc.contributor.authorLin, Athena W.-
dc.contributor.authorSarosi, Ildiko-
dc.contributor.authorItie, Annick-
dc.contributor.authorWakeham, Andrew-
dc.contributor.authorTuan, Jo Ann-
dc.contributor.authorSaris, Chris-
dc.contributor.authorElliott, Gary-
dc.contributor.authorMa, Weili-
dc.contributor.authorBenchimol, Samuel-
dc.contributor.authorLowell, Scott W.-
dc.contributor.authorMak, Tak Wah-
dc.contributor.authorThukral, Sushil K.-
dc.date.accessioned2020-11-17T14:54:47Z-
dc.date.available2020-11-17T14:54:47Z-
dc.date.issued2003-
dc.identifier.citationProceedings of the National Academy of Sciences of the United States of America, 2003, v. 100, n. 9, p. 5431-5436-
dc.identifier.issn0027-8424-
dc.identifier.urihttp://hdl.handle.net/10722/291636-
dc.description.abstractThe tumor suppressor p53 is regulated in part by binding to cellular proteins. We used p53 as bait in the yeast two-hybrid system and isolated homeodomain-interacting protein kinase 1 (HIPK1) as a p53-binding protein. Deletion analysis showed that amino acids 100-370 of p53 and amino acids 885-1093 of HIPK1 were sufficient for HIPK1-p53 interaction. HIPK1 was capable of autophosphorylation and specific serine phosphorylation of p53. The HIPK1 gene was highly expressed in human breast cancer cell lines and oncogenically transformed mouse embryonic fibroblasts. HIPK1 was localized to human chromosome band 1p13, a site frequently altered in cancers. Gene-targeted HIPK1-/- mice were grossly normal but oncogenically transformed HIPK1 -/- mouse embryonic fibroblasts exhibited reduced transcription of Mdm2 and were more susceptible than transformed HIPKI+/+ cells to apoptosis induced by DNA damage. Carcinogen-treated HIPK1 -/- mice developed fewer and smaller skin tumors than HIPK1+/+ mice. HIPK1 may thus play a role in tumorigenesis, perhaps by means of the regulation of p53 and/or Mdm2.-
dc.languageeng-
dc.relation.ispartofProceedings of the National Academy of Sciences of the United States of America-
dc.titleCharacterization of cells and gene-targeted mice deficient for the p53-binding kinase homeodomain-interacting protein kinase 1 (HIPK1)-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1073/pnas.0530308100-
dc.identifier.pmid12702766-
dc.identifier.pmcidPMC154362-
dc.identifier.scopuseid_2-s2.0-0037627405-
dc.identifier.volume100-
dc.identifier.issue9-
dc.identifier.spage5431-
dc.identifier.epage5436-
dc.identifier.isiWOS:000182612600084-
dc.identifier.issnl0027-8424-

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