|Application ||WB, E|
|Calculated MW||84601 Da|
|Antigen Region||458-489 aa|
|Other Names||DNA mismatch repair protein Mlh1, MutL protein homolog 1, MLH1, COCA2|
|Target/Specificity||This MLH1 antibody is generated from mice immunized with a KLH conjugated synthetic peptide between 458-489 amino acids from the Central region of human MLH1.|
|Format||Mouse monoclonal antibody supplied in crude ascites with 0.09% (W/V) sodium azide.|
|Storage||Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||MLH1 Antibody (Center) (Ascites) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||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-MSH3) 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.|
|Tissue Location||Colon, lymphocytes, breast, lung, spleen, testis, prostate, thyroid, gall bladder and heart|
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Provided below are standard protocols that you may find useful for product applications.
This gene was identified as a locus frequently mutated in hereditary nonpolyposis colon cancer (HNPCC). It is a human homolog of the E. coli DNA mismatch repair gene mutL, consistent with the characteristic alterations in microsatellite sequences (RER+phenotype) found in HNPCC. Alternative splicing results in multiple transcript variants encoding distinct isoforms. Additional transcript variants have been described, but their full-length natures have not been determined.
Ling, Z.Q., et al. Cancer Lett. 297(2):244-251(2010)
Qi, Y., et al. J. Biol. Chem. 285(43):33010-33017(2010)
Borras, E., et al. Cancer Res. 70(19):7379-7391(2010)
Mangoni, M., et al. Int. J. Radiat. Oncol. Biol. Phys. (2010) In press :
Ho-Pun-Cheung, A., et al. Pharmacogenomics J. (2010) In press :
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