Piu F, Aronheim A, Katz S, Karin M
Department of Pharmacology, Laboratory of Gene Regulation and Signal Transduction, , University of California at San Diego, La Jolla, California 92093-0636, USA.
Mol Cell Biol. 2001 May;21(9):3012-24. doi: 10.1128/MCB.21.9.3012-3024.2001.
Members of the AP-1 transcription factor family, especially c-Jun and c-Fos, have long been known to mediate critical steps in the cellular response to ultraviolet (UV) irradiation. We sought to examine whether two newly discovered members of the AP-1 family, JDP-1 and JDP-2, also participate in the mammalian UV response. Here we report that JDP-2, but not JDP-1, is transiently induced upon UV challenge and that elevated levels of JDP-2 increase cell survival following UV exposure. This protective function of JDP-2 appears to be mediated through repression of p53 expression at the transcriptional level, via a conserved atypical AP-1 site in the p53 promoter.
长期以来，人们一直认为AP-1转录因子家族的成员，尤其是c-Jun和c-Fos，在细胞对紫外线（UV）照射的反应中介导关键步骤。我们试图研究AP-1家族的两个新发现成员JDP-1和JDP-2是否也参与哺乳动物的UV反应。在此我们报告，JDP-2而非JDP-1在UV刺激后被短暂诱导，并且JDP-2水平升高可增加UV照射后的细胞存活率。JDP-2的这种保护功能似乎是通过p53启动子中一个保守的非典型AP-1位点在转录水平上抑制p53表达来介导的。
