DNA helicase B (HELB)

DNA helicase B (HELB) is a conserved DNA-dependent ATPase and 5′–3′ DNA helicase in higher eukaryotes, particularly humans, where it plays essential roles in the initiation of DNA replication and the cellular responses to replication stress and DNA damage. HELB localizes to the nucleus in the G1 phase to participate in assembly of the replication pre-initiation complex via interactions with DNA polymerase α-primase, CDC45, and TOPBP1. Upon CDK2-mediated phosphorylation at the G1-S transition, HELB is exported to the cytosol but can relocalize to chromatin in response to replication stress or DNA damage. HELB contributes to genomic stability by promoting replication origin firing, stimulating RNA primer synthesis, and regulating homologous recombination through inhibition of long-range resection at DNA double-strand breaks. Dysregulation of HELB has been observed in some cancers, suggesting a role in tumorigenesis. Mutations in HELB or altered expression can compromise DNA replication and DNA repair fidelity, making it a potential biomarker for replication stress and therapeutic target in cancer biology[1][4][7][6].

Other names

DNA helicase BHELBhDHBDHBhelicase (DNA) B