| http://purl.uniprot.org/citations/17376776 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/17376776 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/17376776 | http://www.w3.org/2000/01/rdf-schema#comment | "Protein phosphatase 5 (Ppp5), a tetratricopeptide repeat domain protein, has been implicated in multiple cellular functions, including cellular proliferation, migration, differentiation and survival, and cell cycle checkpoint regulation via the ataxia telangiectasia mutated/ATM and Rad3-related (ATM/ATR) signal pathway. However, the physiological functions of Ppp5 have not been reported. To confirm the role of Ppp5 in cell cycle checkpoint regulation, we generated Ppp5-deficient mice and isolated mouse embryonic fibroblast (MEF) cells from Ppp5-deficient and littermate control embryos. Although Ppp5-deficient mice can survive through embryonic development and postnatal life and MEF cells from the Ppp5-deficient mice maintain normal replication checkpoint induced by hydroxyurea, Ppp5-deficient MEF cells display a significant defect in G(2)/M DNA damage checkpoint in response to ionizing radiation (IR). To determine whether this defect in IR-induced G(2)/M checkpoint is due to altered ATM-mediated signaling, we measured ATM kinase activity and ATM-mediated downstream events. Our data demonstrated that IR-induced ATM kinase activity is attenuated in Ppp5-deficient MEFs. Phosphorylation levels of two known ATM substrates, Rad17 and Chk2, were significantly reduced in Ppp5-deficient MEFs in response to IR. Furthermore, DNA damage-induced Rad17 nuclear foci were dramatically reduced in Ppp5-deficient MEFs. These results demonstrate a direct regulatory linkage between Ppp5 and activation of the ATM-mediated G(2)/M DNA damage checkpoint pathway in vivo."xsd:string |
| http://purl.uniprot.org/citations/17376776 | http://purl.org/dc/terms/identifier | "doi:10.1074/jbc.c700019200"xsd:string |
| http://purl.uniprot.org/citations/17376776 | http://purl.org/dc/terms/identifier | "doi:10.1074/jbc.c700019200"xsd:string |
| http://purl.uniprot.org/citations/17376776 | http://purl.uniprot.org/core/author | "Chen H."xsd:string |
| http://purl.uniprot.org/citations/17376776 | http://purl.uniprot.org/core/author | "Chen H."xsd:string |
| http://purl.uniprot.org/citations/17376776 | http://purl.uniprot.org/core/author | "Li D."xsd:string |
| http://purl.uniprot.org/citations/17376776 | http://purl.uniprot.org/core/author | "Li D."xsd:string |
| http://purl.uniprot.org/citations/17376776 | http://purl.uniprot.org/core/author | "Bao S."xsd:string |
| http://purl.uniprot.org/citations/17376776 | http://purl.uniprot.org/core/author | "Bao S."xsd:string |
| http://purl.uniprot.org/citations/17376776 | http://purl.uniprot.org/core/author | "Yong W."xsd:string |
| http://purl.uniprot.org/citations/17376776 | http://purl.uniprot.org/core/author | "Yong W."xsd:string |
| http://purl.uniprot.org/citations/17376776 | http://purl.uniprot.org/core/author | "Shou W."xsd:string |
| http://purl.uniprot.org/citations/17376776 | http://purl.uniprot.org/core/author | "Shou W."xsd:string |
| http://purl.uniprot.org/citations/17376776 | http://purl.uniprot.org/core/author | "Sanchez E.R."xsd:string |
| http://purl.uniprot.org/citations/17376776 | http://purl.uniprot.org/core/author | "Sanchez E.R."xsd:string |
| http://purl.uniprot.org/citations/17376776 | http://purl.uniprot.org/core/date | "2007"xsd:gYear |
| http://purl.uniprot.org/citations/17376776 | http://purl.uniprot.org/core/date | "2007"xsd:gYear |
| http://purl.uniprot.org/citations/17376776 | http://purl.uniprot.org/core/name | "J. Biol. Chem."xsd:string |
| http://purl.uniprot.org/citations/17376776 | http://purl.uniprot.org/core/name | "J. Biol. Chem."xsd:string |
| http://purl.uniprot.org/citations/17376776 | http://purl.uniprot.org/core/pages | "14690-14694"xsd:string |
| http://purl.uniprot.org/citations/17376776 | http://purl.uniprot.org/core/pages | "14690-14694"xsd:string |
| http://purl.uniprot.org/citations/17376776 | http://purl.uniprot.org/core/title | "Mice lacking protein phosphatase 5 are defective in ataxia telangiectasia mutated (ATM)-mediated cell cycle arrest."xsd:string |
| http://purl.uniprot.org/citations/17376776 | http://purl.uniprot.org/core/title | "Mice lacking protein phosphatase 5 are defective in ataxia telangiectasia mutated (ATM)-mediated cell cycle arrest."xsd:string |