TITLE

Cyclobutane Pyrimidine Dimers in UV-DNA Induce Release of Soluble Mediators that Activate the Human Immunodeficiency Virus Promoter

AUTHOR(S)
Yarosh, Daniel B.; Alas, Lori; Kibitel, Jeannie; O'Connor, Adrienne; Carrier, France; Fornace Jr., Albert J.
PUB. DATE
June 1993
SOURCE
Journal of Investigative Dermatology;Jun93, Vol. 100 Issue 6, p790
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
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.
ACCESSION #
12476573

 

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