Prolonged c-jun expression in irradiated ataxia telangiectasia fibroblasts

摘要: Purpose: Ataxia telangiectasia (AT) is an autosomal recessive disorder associated with radiation sensitivity and anincreased incidence of leukemia, lymphoma, some solid tumors. After exposure to ionizbtg radiation, cells from patients AT demonstrate attenuated G,-phase checkpoint. Because c-jun known reguiate, in part, the exit G, onset DNA replication, we analyzed c@n transcription irradiated .4T fibroblasts. Methods Materials: ATSBI fibroblasts were RNA was extracted assayed for expression by Northern blot analysis. Transcriptional regulation c-&n evaluated use 5’ untrzmslated region jun promoter linked chloramphenicol acetyl transferase (CAT) reporter gene. Deletion mutants RSRF, SP-1, AP-1, CCAAT domains within CAT transfected into AT531 cells. Transfectants irradiated, qua&Bed. x-irradiation, nuclear protein binding electrophoretic mobility shii assay. Results: X-ray-mediated sustained as compared only transient -irradiated normal diploid Mutation either AP-1 or reduced 50% combined deletion both cis-aetingelementsentirely eliminated radiation-mediated transcriptional activation. Electrophoretic gel &ii assay t&e proteins isolated demonstrated their increased sequence at 30 mln after irradiation. Competition excess cold that this specific. These findings distinct induction phorbol esthers RSRF c&-acting element segments upstream -’ 132 base pairs do participate e.j,n but not radiation. Conclusions: Radiation-mediated prolonged regulated combinatorial control domains, induced esthers. Copyright 0 1996 Elsevier Science Inc. Radiation, telangiectasia, c&n, box.