<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Episkopou, H.</style></author><author><style face="normal" font="default" size="100%">Kyrtopoulos, S.A.</style></author><author><style face="normal" font="default" size="100%">Sfikakis, P.P.</style></author><author><style face="normal" font="default" size="100%">Fousteri, M.</style></author><author><style face="normal" font="default" size="100%">Dimopoulos, M.A.</style></author><author><style face="normal" font="default" size="100%">Mullenders, L.H.F.</style></author><author><style face="normal" font="default" size="100%">Souliotis, V.L.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Association between transcriptional activity, local chromatin structure, and the efficiencies of both subpathways of nucleotide excision repair of melphalan adducts</style></title><secondary-title><style face="normal" font="default" size="100%">Cancer Research</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2009</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2009</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">https://www.scopus.com/inward/record.uri?eid=2-s2.0-66249147593&amp;doi=10.1158%2f0008-5472.CAN-08-3489&amp;partnerID=40&amp;md5=aa401bf07fa514cf02685ea0d0c7610c</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">69</style></volume><pages><style face="normal" font="default" size="100%">4424 - 4433</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">The repair of melphalan-induced N-alkylpurine monoadducts and interstrand cross-links was examined in different repair backgrounds, focusing on four genes (β-actin, p53, N-ras, and δ-globin) with dissimilar transcription activities. Adducts were found to be substrates for both global genome repair (GGR) and transcription-coupled repair (TCR), with TCR being less efficient than GGR. In nucleotide excision repair-deficient cells, adducts accumulated to similar levels in all four genes. The repair efficiency in different gene loci varied in a qualitatively and quantitatively similar way in both GGR-deficient and TCR-deficient backgrounds and correlated with transcriptional activity and local chromatin condensation. No strand-specific repair was found in GGR +/TCR+ cells, implying that GGR dominated. Adducts were lost over two sharply demarcated phases: a rapid phase resulting in the removal within 1 hour of up to ∼80% of the adducts, and a subsequent phase with t1/2 ∼36 to 48 hours. Following pretreatment of cells with α-amanitin, the rate of transcription, the state of chromatin condensation, and the repair efficiencies (both TCR and GGR) of the transcribed β-actin, p53, and N-ras genes became similar to those of the nontranscribed δ-globin gene. In conclusion, a continuous, parallel variation of the state of transcription and local chromatin condensation, on one hand, and the rates of both GGR and TCR, on the other hand, have been shown. ©2009 American Association for Cancer Research.</style></abstract><issue><style face="normal" font="default" size="100%">10</style></issue><notes><style face="normal" font="default" size="100%">Cited By :12Export Date: 21 February 2017</style></notes></record></records></xml>