WFRF:(Bekker Jensen S)
Sökning: WFRF:(Bekker Jensen S) > Nucleotide excision...
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| Fältnamn | Indikatorer | Metadata |
|---|---|---|
| 000 | 02701naa a2200361 4500 | |
| 001 | oai:prod.swepub.kib.ki.se:119365080 | |
| 003 | SwePub | |
| 008 | 240913s2009 | |||||||||||000 ||eng| | |
| 024 | 7 | a http://kipublications.ki.se/Default.aspx?queryparsed=id:1193650802 URI |
| 024 | 7 | a https://doi.org/10.1083/jcb.2009021502 DOI |
| 040 | a (SwePub)ki | |
| 041 | a engb eng | |
| 042 | 9 SwePub | |
| 072 | 7 | a ref2 swepub-contenttype |
| 072 | 7 | a art2 swepub-publicationtype |
| 100 | 1 | a Marteijn, JA4 aut |
| 245 | 1 0 | a Nucleotide excision repair-induced H2A ubiquitination is dependent on MDC1 and RNF8 and reveals a universal DNA damage response |
| 264 | c 2009-09-21 | |
| 264 | 1 | b Rockefeller University Press,c 2009 |
| 520 | a Chromatin modifications are an important component of the of DNA damage response (DDR) network that safeguard genomic integrity. Recently, we demonstrated nucleotide excision repair (NER)–dependent histone H2A ubiquitination at sites of ultraviolet (UV)-induced DNA damage. In this study, we show a sustained H2A ubiquitination at damaged DNA, which requires dynamic ubiquitination by Ubc13 and RNF8. Depletion of these enzymes causes UV hypersensitivity without affecting NER, which is indicative of a function for Ubc13 and RNF8 in the downstream UV–DDR. RNF8 is targeted to damaged DNA through an interaction with the double-strand break (DSB)–DDR scaffold protein MDC1, establishing a novel function for MDC1. RNF8 is recruited to sites of UV damage in a cell cycle–independent fashion that requires NER-generated, single-stranded repair intermediates and ataxia telangiectasia–mutated and Rad3-related protein. Our results reveal a conserved pathway of DNA damage–induced H2A ubiquitination for both DSBs and UV lesions, including the recruitment of 53BP1 and Brca1. Although both lesions are processed by independent repair pathways and trigger signaling responses by distinct kinases, they eventually generate the same epigenetic mark, possibly functioning in DNA damage signal amplification. | |
| 700 | 1 | a Bekker-Jensen, S4 aut |
| 700 | 1 | a Mailand, N4 aut |
| 700 | 1 | a Lans, H4 aut |
| 700 | 1 | a Schwertman, P4 aut |
| 700 | 1 | a Gourdin, AM4 aut |
| 700 | 1 | a Dantuma, NPu Karolinska Institutet4 aut |
| 700 | 1 | a Lukas, J4 aut |
| 700 | 1 | a Vermeulen, W4 aut |
| 710 | 2 | a Karolinska Institutet4 org |
| 773 | 0 | t The Journal of cell biologyd : Rockefeller University Pressg 186:6, s. 835-847q 186:6<835-847x 1540-8140x 0021-9525 |
| 856 | 4 | u http://jcb.rupress.org/content/186/6/835.full.pdf |
| 856 | 4 8 | u http://kipublications.ki.se/Default.aspx?queryparsed=id:119365080 |
| 856 | 4 8 | u https://doi.org/10.1083/jcb.200902150 |
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- Marteijn, JA
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