HELB
Function
5'-3' DNA helicase involved in DNA damage response by acting as an inhibitor of DNA end resection (PubMed:25617833, PubMed:26774285). Recruitment to single-stranded DNA (ssDNA) following DNA damage leads to inhibit the nucleases catalyzing resection, such as EXO1, BLM and DNA2, possibly via the 5'-3' ssDNA translocase activity of HELB (PubMed:26774285). As cells approach S phase, DNA end resection is promoted by the nuclear export of HELB following phosphorylation (PubMed:26774285). Acts independently of TP53BP1 (PubMed:26774285). Unwinds duplex DNA with 5'-3' polarity. Has single-strand DNA-dependent ATPase and DNA helicase activities. Prefers ATP and dATP as substrates (PubMed:12181327). During S phase, may facilitate cellular recovery from replication stress (PubMed:22194613).
Post-translational modifications
Phosphorylated at Ser-967 by CDK2 during the G1/S transition, resulting in its nuclear export into the cytoplasm (PubMed:15146062, PubMed:26774285). As S phase progresses, its exclusion from the nucleus promotes the activation of long-range resection (PubMed:26774285).
Sequence Similarities
Belongs to the RecD family. HELB subfamily.
Tissue Specificity
Highly expressed in testis and thymus and weakly in liver, spleen, kidney and brain.
Cellular localization
- Nucleus
- Cytoplasm
- Chromosome
- Predominantly nuclear (PubMed:15146062). Phosphorylation at Ser-967 by CDK2 during the G1/S transition results in its nuclear export into the cytoplasm as cells approach and progress through S phase (PubMed:15146062). Following DNA damage, recruited to sites of double-strand breaks by the RPA complex (PubMed:26774285). Recruited to chromatin following DNA damage induced by UV irradiation, or camptothecin or hydroxyurea treatment (PubMed:22194613).
Alternative names
DNA helicase B, hDHB, HELB