| http://purl.uniprot.org/citations/14973123 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/14973123 | http://www.w3.org/2000/01/rdf-schema#comment | "Apurinic/apyrimidinic (AP) endonuclease (APE) is a multifunctional protein possessing both DNA repair and redox regulatory activities. In base excision repair (BER), APE is responsible for processing spontaneous, chemical, or monofunctional DNA glycosylase-initiated AP sites via its 5'-endonuclease activity and 3'-"end-trimming" activity when processing residues produced as a consequence of bifunctional DNA glycosylases. In this study, we have fully characterized a mammalian model of APE haploinsufficiency by using a mouse containing a heterozygous gene-targeted deletion of the APE gene (Apex(+/-)). Our data indicate that Apex(+/-) mice are indeed APE-haploinsufficient, as exhibited by a 40-50% reduction (p < 0.05) in APE mRNA, protein, and 5'-endonuclease activity in all tissues studied. Based on gene dosage, we expected to see a concomitant reduction in BER activity; however, by using an in vitro G:U mismatch BER assay, we observed tissue-specific alterations in monofunctional glycosylase-initiated BER activity, e.g. liver (35% decrease, p < 0.05), testes (55% increase, p < 0.05), and brain (no significant difference). The observed changes in BER activity correlated tightly with changes in DNA polymerase beta and AP site DNA binding levels. We propose a mechanism of BER that may be influenced by the redox regulatory activity of APE, and we suggest that reduced APE may render a cell/tissue more susceptible to dysregulation of the polymerase beta-dependent BER response to cellular stress."xsd:string |
| http://purl.uniprot.org/citations/14973123 | http://purl.org/dc/terms/identifier | "doi:10.1074/jbc.m313983200"xsd:string |
| http://purl.uniprot.org/citations/14973123 | http://purl.uniprot.org/core/author | "Nakamura J."xsd:string |
| http://purl.uniprot.org/citations/14973123 | http://purl.uniprot.org/core/author | "Friedberg E.C."xsd:string |
| http://purl.uniprot.org/citations/14973123 | http://purl.uniprot.org/core/author | "Meira L.B."xsd:string |
| http://purl.uniprot.org/citations/14973123 | http://purl.uniprot.org/core/author | "Cabelof D.C."xsd:string |
| http://purl.uniprot.org/citations/14973123 | http://purl.uniprot.org/core/author | "Heydari A.R."xsd:string |
| http://purl.uniprot.org/citations/14973123 | http://purl.uniprot.org/core/author | "Raffoul J.J."xsd:string |
| http://purl.uniprot.org/citations/14973123 | http://purl.uniprot.org/core/date | "2004"xsd:gYear |
| http://purl.uniprot.org/citations/14973123 | http://purl.uniprot.org/core/name | "J Biol Chem"xsd:string |
| http://purl.uniprot.org/citations/14973123 | http://purl.uniprot.org/core/pages | "18425-18433"xsd:string |
| http://purl.uniprot.org/citations/14973123 | http://purl.uniprot.org/core/title | "Apurinic/apyrimidinic endonuclease (APE/REF-1) haploinsufficient mice display tissue-specific differences in DNA polymerase beta-dependent base excision repair."xsd:string |
| http://purl.uniprot.org/citations/14973123 | http://purl.uniprot.org/core/volume | "279"xsd:string |
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