|Application ||WB, IHC|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||95797 Da|
|Application & Usage||Western blotting (0.5-4 µg/ml), immunoprecipitation (10-20 µg/ml) and Immunohistochemistry (10-20 µg/ml). However, the optimal concentrations should be determined individually.|
|Other Names||HNPCC4 , PMS2CL , PMSL2 , DNA mismatch repair gene homologue H_DJ0042M02.9|
|Formulation||100 µg (0.5 mg/ml) peptide affinity purified rabbit polyclonal antibody in phosphate-buffered saline (PBS) containing 30% glycerol, 0.5% BSA, and 0.01% thimerosal.|
|Handling||The antibody solution should be gently mixed before use.|
|Reconstitution & Storage||-20 °C|
|Precautions||PMS2 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Component of the post-replicative DNA mismatch repair system (MMR). Heterodimerizes with MLH1 to form MutL alpha. 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.|
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Inherited mutations in the MSH2 and MLH1 homologs of the bacterial DNA mismatch repair genes MutS and MutL were initially demonstrated at high frequency in HNPCC and were shown to be associated with microsatellite instability. The demonstration that 10-45% of pancreatic, gastric, breast, ovarian and small cell lung cancers also display microsatellite instability has been interpreted to s µggest that DNA mismatch repair is not restricted to HNPCC tumors but is a common feature in tumor initiation or progression. Two additional homologs of the prokaryotic MutL gene, designated PMS1 and PMS2, have been identified and shown to be mutated in the germline of HNPCC patients.
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