Analysis of the human RAD51L1 promoter region and its activation by UV light

Lan Peng, Michael C. Rice, Eric B. Kmiec

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

The human REC2/RAD51B gene (HGMW-approved symbol RAD51L1) encodes a 350- amino-acid protein with regional homologies to members of the RAD52 epistasis group. It is induced by DNA-damaging agents, and the overexpression of this gene product causes G1/S cell cycle arrest. In this report, the promoter region, containing the UV-responsive element, is revealed. Deletion analyses of a 1699-base fragment at the 5' end of the human REC2/RAD51B cDNA identified a 116-base sequence that appears to be responsible for radiation induction. This fragment contains many DNA sequences that have been identified in the promoter regions of other radiation-inducible genes in yeast and humans. Within this region are 'consensus' binding sites for both the AP2 and the p53 proteins that may act to regulate the expression of the human REC2/RAD51B gene. Five putative transcripts have been identified from regions 5' of the promoter element that splice near the ATG translation start site. None of the transcripts contain the UV-inducible element nor the consensus transcription factor binding sites.

Original languageEnglish (US)
Pages (from-to)529-541
Number of pages13
JournalGenomics
Volume54
Issue number3
DOIs
StatePublished - Dec 15 1998

Fingerprint

Ultraviolet Rays
Genetic Promoter Regions
Genes
Binding Sites
Radiation
G1 Phase Cell Cycle Checkpoints
Proteins
Transcription Factors
Complementary DNA
Yeasts
Amino Acids
DNA

ASJC Scopus subject areas

  • Genetics

Cite this

Analysis of the human RAD51L1 promoter region and its activation by UV light. / Peng, Lan; Rice, Michael C.; Kmiec, Eric B.

In: Genomics, Vol. 54, No. 3, 15.12.1998, p. 529-541.

Research output: Contribution to journalArticle

Peng, Lan ; Rice, Michael C. ; Kmiec, Eric B. / Analysis of the human RAD51L1 promoter region and its activation by UV light. In: Genomics. 1998 ; Vol. 54, No. 3. pp. 529-541.
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