DNA Mismatch Repair Protein Mlh1 (MLH1) Antibody

MLH1 antibody

Heterodimerizes with PMS2 to form MutL alpha, a component of the post-replicative DNA mismatch repair system(MMR). DNA repair is initiated by MutS alpha(MSH2-MSH6) or MutS beta(MSH2-MSH6) binding to a dsDNA mismatch, then MutL alpha is recruited to the heteroduplex. Assembly of the MutL-MutS-heteroduplex ternary complex in presence of RFC and PCNA is sufficient to activate endonuclease activity of PMS2. 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. Heterodimerizes with MLH3 to form MutL gamma which plays a role in meiosis.

Recombinant Human MLH1

DNA Mismatch Repair Protein Mlh1 (MLH1) Antibody

MLH1 Antibody is a Rabbit Polyclonal antibody against MLH1. Mismatch repair (MMR), a conserved process that involves correcting errors made during DNA synthesis, is crucial to the maintenance of genomic integrity. MLH1 is the human homologue of the E. coli MMR gene mutL. MMR requires recognition of a base mismatch or insertion/deletion loop by a MutS homolog followed by recruitment of a MutL heterodimeric complex consisting of MLH1 and PMS1 (MutL-α), PMS2 (MutL-β) or MLH3 (MutL-γ). Other factors required for MMR in eukaryotes are EXO1, PCNA, RFC, RPA, DNA polymerases and DNA ligase (reviewed in 1). Inactivation of the MLH1 gene causes genome instability and predisposition to cancer (2-5). The MLH1 gene is frequently mutated in hereditary nonpolyposis colon cancer (HNPCC) (6). MLH1 also plays a role in meiotic recombination (7). 1.Modrich, P. (2006) J Biol Chem 281, 30305-9. 2.Seng, T.J. et al. (2008) Br J Cancer 99, 375-82. 3.Harley, I. et al. (2008) Gynecol Oncol 109, 384-7. 4.Mao, G. et al. (2008) J Biol Chem 283, 3211-6. 5.Hubner, R.A. and Houlston, R.S. (2007) J Natl Cancer Inst 99, 1490; author reply 1490-1. 6.Vasen, H.F. (2005) Fam Cancer 4, 219-25. 7.Argueso, J.L. et al. (2003) Mol Cell Biol 23, 873-86.