CYCLOBUTANE PYRIMIDINE DIMERS IN UV-DNA INDUCE RELEASE OF SOLUBLE MEDIATORS THAT ACTIVATE THE HUMAN-IMMUNODEFICIENCY-VIRUS PROMOTER

被引:36
作者
YAROSH, DB [1 ]
ALAS, L [1 ]
KIBITEL, J [1 ]
OCONNOR, A [1 ]
CARRIER, F [1 ]
FORNACE, AJ [1 ]
机构
[1] NCI,MOLEC PHARMACOL LAB,BETHESDA,MD 20892
关键词
D O I
10.1111/1523-1747.ep12476573
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
Ultraviolet (UV) irradiation of human cells induced expression of a stably maintained fusion gene consisting of the human immunodeficiency virus long terminal repeat promoter controlling the bacterial chloramphenicol acetyltransferase gene. Two experiments demonstrated that DNA damage can initiate induction: UV induction was greater in DNA repair-deficient cells from a xeroderma pigmentosum patient than in repair-proficient cells, and transfection of UV-irradiated DNA into unirradiated cells activated gene expression. increased repair of cyclobutane pyrimidine dimers by T4 endonuclease V abrogated viral gene activation, suggesting that dimers in DNA are one signal leading to increased gene expression. This signal was spread from UV-irradiated cells to unirradiated cells by co-cultivation, implicating the release of soluble factors. Irradiation of cells from DNA repair-deficiency diseases resulted in greater release of soluble factors than irradiation of cells from unaffected individuals. These results suggest that UV-induced cyclobutane pyrimidine dimers can activate the human immunodeficiency virus promoter at least in part by a signal-transduction pathway that includes secretion of soluble mediators.
引用
收藏
页码:790 / 794
页数:5
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