Lane 1: MCF-7 cell lysate
Lane 2: Hela cell lysate
Recombinant Rabbit monoclonal primary
Recombinant PMS2 Monoclonal Antibody (ET1605-1)
MCF-7 cell lysate, Hela cell lysate, Hela, human colon carcinoma tissue, human breast carcinoma tissue.
Store at +4C after thawing. Aliquot store at -20C. Avoid repeated freeze / thaw cycles.
1*TBS (pH7.4), 0.05% BSA, 40% Glycerol. Preservative: 0.05% Sodium Azide.
Protein A affinity purified.
DNA mismatch repair gene homologue antibody; DNA mismatch repair protein PMS2 antibody; H_DJ0042M02.9 antibody; HNPCC4 antibody; Mismatch repair endonuclease PMS2 antibody; Mismatch repair gene PMSL2 antibody; PMS 2 antibody; PMS1 protein homolog 2 antibody; PMS2 antibody; PMS2 postmeiotic segregation increased 2 antibody; PMS2 postmeiotic segregation increased 2 (S. cerevisiae) antibody; PMS2_HUMAN antibody; PMS2CL antibody; PMSL2 antibody; Postmeiotic segregation increased, S. cerevisiae, 2 antibody
Belongs to the DNA mismatch repair MutL/HexB family.
Component of the post-replicative DNA mismatch repair system (MMR). It introduces single-strand breaks near the mismatch and thus generates new entry points for the exonuclease EXO1 to degrade the strand containing the mismatch. DNA methylation would prevent cleavage and therefore assure that only the newly mutated DNA strand is going to be corrected. MutL alpha (MLH1-PMS2) interacts physically with the clamp loader subunits of DNA polymerase III, suggesting that it may play a role to recruit the DNA polymerase III to the site of the MMR. Also implicated in DNA damage signaling, a process which induces cell cycle arrest and can lead to apoptosis in case of major DNA damages. The finding that mutations in DNA mismatch repair genes are associated with hereditary nonpolyposis colorectal cancer (HNPCC) has resulted in considerable interest in the understanding of the mechanism of DNA mismatch repair. Initially, inherited mutations in the MSH2 and MLH1 homologs of the bacterial DNA mismatch repair genes MutS and MutL were demonstrated at high frequency in HNPCC and were shown to be associated with microsatellite instability. The demonstration that 10 to 45% of pancreatic, gastric, breast, ovarian and small cell lung cancers also display microsatellite instability has been interpreted to suggest that DNA mismatch repair is not restricted to HNPCC tumors but is a common feature in tumor initiation or progression.