Checkpoint Homolog (CHEK1) ELISA Kit for Human

This gene encodes a component of a heterotrimeric cell cycle checkpoint complex, known as the 9-1-1 complex, that is activated to stop cell cycle progression in response to DNA damage or incomplete DNA replication. The 9-1-1 complex is recruited by RAD17 to affected sites where it may attract specialized DNA polymerases and other DNA repair effectors. Alternatively spliced transcript variants of this gene have been described. [provided by RefSeq, Jan 2009]

RAD1: Component of the 9-1-1 cell-cycle checkpoint response complex that plays a major role in DNA repair. The 9-1-1 complex is recruited to DNA lesion upon damage by the RAD17-replication factor C (RFC) clamp loader complex. Acts then as a sliding clamp platform on DNA for several proteins involved in long-patch base excision repair (LP-BER). The 9-1-1 complex stimulates DNA polymerase beta (POLB) activity by increasing its affinity for the 3'-OH end of the primer-template and stabilizes POLB to those sites where LP-BER proceeds; endonuclease FEN1 cleavage activity on substrates with double, nick, or gap flaps of distinct sequences and lengths; and DNA ligase I (LIG1) on long-patch base excision repair substrates. The 9-1-1 complex is necessary for the recruitment of RHNO1 to sites of double-stranded breaks (DSB) occurring during the S phase. Isoform 1 possesses 3'->5' double stranded DNA exonuclease activity. Belongs to the rad1 family. 3 isoforms of the human protein are produced by alternative splicing.

Protein type: Deoxyribonuclease; EC 3.1.11.2; Cell cycle regulation; DNA repair, damage

Chromosomal Location of Human Ortholog: 5p13.2

Cellular Component: nucleoplasm; intracellular membrane-bound organelle; chromosome; nucleus

Molecular Function: protein binding; damaged DNA binding; exodeoxyribonuclease III activity; 3'-5' exonuclease activity

Biological Process: meiotic recombination checkpoint; substantia nigra development; DNA damage checkpoint; DNA catabolic process, exonucleolytic; DNA repair; DNA replication; response to DNA damage stimulus