title: Differential expression of a novel gene BRE (TNFRSF1A modulator/BRCC45) in response to stress and biological signals.
abstract: Stress-responsive genes play critical roles in many biological functions that includes apoptosis, survival, differentiation and regeneration. We have identified a novel stress-responsive gene called BRE which interacts with TNF-receptor-1 and blocks the apoptotic effect of TNF-alpha. BRE enhances tumor growth in vivo and is up-regulated in hepatocellular and esophageal carcinomas. BRE also regulates the ubiquitination of the DNA repair complex BRCC, and the synthesis of steroid hormones. Here, we examined BRE-mRNA in cells after treatments with UV and ionizing radiation (IR). UV and IR treatment alone suppressed BRE-mRNA levels by more than 90% at 24 h, while hydroxyurea, fluorodeoxyuridine, aphidicolin, known inhibitors of S-phase DNA synthesis, had no significant effect. BRE protein expression was unaltered in cells treated with TNF-alpha, Interleukin-1 and Dexamethasone, while a threefold increase was observed following chorionic gonadotropin exposure. Although BRE plays a regulatory role in many different pathways, yet its expression is apparently under very stringent control.
authors.affiliation: Key Joint CUHK-JiNan University Laboratories for Regenerative Medicine, Ministry of Education, JiNan University, Guang Zhou, Guang Dong, China. chanjyh01@hotmail.com
authors.forename: John Yeuk-Hon
authors.initials: JY
authors.lastname: Chan
authors.forename: Li
authors.initials: L
authors.lastname: Li
authors.forename: Ji
authors.initials: J
authors.lastname: Miao
authors.forename: Dong-Qing
authors.initials: DQ
authors.lastname: Cai
authors.forename: Kenneth Ka-Ho
authors.initials: KK
authors.lastname: Lee
authors.forename: Yiu-Loon
authors.initials: YL
authors.lastname: Chui
mesh_terms: D016590:Aphidicolin / Q000494:pharmacology; D001685:Biological Factors / Q000494:pharmacology*; D002103:Cadaverine / Q000031:analogs & derivatives / Q000494:pharmacology; D002460:Cell Line; D006063:Chorionic Gonadotropin / Q000494:pharmacology; D000072481:DNA Ligase ATP; D011088:DNA Ligases / Q000235:genetics / Q000378:metabolism; D003907:Dexamethasone / Q000494:pharmacology; D004121:Dimethyl Sulfoxide / Q000494:pharmacology; D005468:Fluorodeoxyuridylate / Q000494:pharmacology; D005786:Gene Expression Regulation / Q000187:drug effects* / Q000528:radiation effects; D006801:Humans; D006918:Hydroxyurea / Q000494:pharmacology; D007375:Interleukin-1 / Q000494:pharmacology; D009419:Nerve Tissue Proteins / Q000235:genetics* / Q000378:metabolism; D009687:Nuclear Proteins / Q000235:genetics / Q000378:metabolism; D000071156:Promyelocytic Leukemia Protein; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011839:Radiation, Ionizing; D015398:Signal Transduction / Q000187:drug effects* / Q000528:radiation effects; D013312:Stress, Physiological / Q000187:drug effects* / Q000235:genetics* / Q000528:radiation effects; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology; D025521:Tumor Suppressor Proteins / Q000235:genetics / Q000378:metabolism; D014466:Ultraviolet Rays
chemical_list: C091514:BABAM2 protein, human; D001685:Biological Factors; D006063:Chorionic Gonadotropin; D007375:Interleukin-1; D009419:Nerve Tissue Proteins; D009687:Nuclear Proteins; D000071156:Promyelocytic Leukemia Protein; D012333:RNA, Messenger; D014157:Transcription Factors; D014409:Tumor Necrosis Factor-alpha; D025521:Tumor Suppressor Proteins; D005468:Fluorodeoxyuridylate; C070576:PML protein, human; D016590:Aphidicolin; D003907:Dexamethasone; D011088:DNA Ligases; D000072481:DNA Ligase ATP; C008542:monodansylcadaverine; D002103:Cadaverine; D006918:Hydroxyurea; D004121:Dimethyl Sulfoxide