UV-induced DNA damage is an intermediate step in UV-induced expression of human immunodeficiency virus type 1, collagenase, c-fos, and metallothionein.

• DOI: 10.1128/mcb.9.11.5169
• Publication Date: 2015-10-01T21:49:03Z
• Authors: B Stein; H J Rahmsdorf; A Steffen; M Litfin; P Herrlich
• Keywords: Adult; Male; 0301 basic medicine; 570; Proto-Oncogene Proteins c-jun; Molecular Sequence Data; 03 medical and health sciences; Proto-Oncogene Proteins; Proto-Oncogenes; Animals; Humans; info:eu-repo/classification/ddc/570; Base Sequence; biology; Fibroblasts; Life sciences; 3. Good health; DNA-Binding Proteins; Enhancer Elements, Genetic; Microbial Collagenase; Gene Expression Regulation; DNA, Viral; HIV-1; Metallothionein; ddc:570; Proto-Oncogene Proteins c-fos; DNA Damage; HeLa Cells

UV irradiation of human and murine cells enhances the transcription several genes. Here we report on primary target relevant absorption, pathways leading to gene activation, elements receiving UV-induced signal in immunodeficiency virus type 1 (HIV-1) long terminal repeat, coding for collagenase, cellular oncogene fos. In order induce expression radiation needs be absorbed by DNA cause damage kind that cannot repaired from patients with xeroderma pigmentosum group A. activation three genes is mediated major enhancer (located between nucleotide positions -105 -79 HIV-1, -72 -65 collagenase gene, -320 -299 fos). These share no apparent sequence motif bind different trans-acting proteins; a member NF kappa B family binds HIV-1 enhancer, heterodimer Jun Fos (AP-1) serum response factors p67 p62 DNA-binding activities recognizing enhancers are augmented extracts UV-treated cells. The increase activity due posttranslational modification. While AP-1 resides nucleus must modulated there, activated cytoplasm, indicating existence cytoplasmic transduction pathway triggered damage. addition new synthesis induced radiation.