Rabbit anti-Human HUS1 Polyclonal Antibody

Uniprot Id

O60921

Target Species

Human

Target Name

HUS1

Target Full Name

Checkpoint protein HUS1

Target Function

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.

Target Subcellular Location

Nucleus. Cytoplasm, cytosol.

Target Protein Families

HUS1 family

Target Tissue Specificity

Ubiquitous.

Target Research Area

Epigenetics and Nuclear Signaling

Target Synonyms

Checkpoint protein HUS1; hHUS1; HUS1 (S. pombe) checkpoint homolog; Hus1; HUS1 checkpoint homolog (S. pombe); HUS1 Checkpoint Protein; HUS1 protein; HUS1+ - like protein; HUS1_HUMAN; Hydroxyurea-sensitive 1, S. pombe, homolog of

Target Background

The protein encoded by this gene is a component of an evolutionarily conserved, genotoxin-activated checkpoint complex that is involved in the cell cycle arrest in response to DNA damage. This protein forms a heterotrimeric complex with checkpoint proteins RAD9 and RAD1. In response to DNA damage, the trimeric complex interacts with another protein complex consisting of checkpoint protein RAD17 and four small subunits of the replication factor C (RFC), which loads the combined complex onto the chromatin. The DNA damage induced chromatin binding has been shown to depend on the activation of the checkpoint kinase ATM, and is thought to be an early checkpoint signaling event. Alternative splicing results in multiple transcript variants.