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PMS2 Recombinant Rabbit monoclonal Antibody IgG

SKU: BA113145-100µl
$279.00Price

Fig1: Western blot analysis of PMS2 on Hela cell lysates. Proteins were transferred to a PVDF membrane and blocked with 5% BSA in PBS for 1 hour at room temperature. The primary antibody was used at a 1:1,000 dilution in 5% BSA at room temperature for 2 hours. Goat Anti-Mouse IgG - HRP Secondary Antibody (HA1006) at 1:5,000 dilution was used for 1 hour at room temperature.

Fig2: ICC staining PMS2 in Hela cells (red). Formalin fixed cells were permeabilized with 0.1% Triton X-100 in TBS for 10 minutes at room temperature and blocked with 1% Blocker BSA for 15 minutes at room temperature. Cells were probed with Carbonic anhydrase 2 monoclonal antibody at a dilution of 1:100 for at least 1 hour at room temperature, washed with PBS. Alexa Fluorc™ 488 Goat anti-Mouse IgG was used as the secondary antibody at 1/100 dilution. The nuclear counter stain is DAPI (blue).

Fig3: Immunohistochemical analysis of paraffin-embedded human colon cancer tissue using anti-PMS2 antibody. The section was pre-treated using heat mediated antigen retrieval with sodium citrate buffer (pH6) for 20 mins. The tissues were blocked in 5% BSA for 30 minutes at room temperature, washed with ddH2O and PBS, and then probed with the antibody (ET1605-1) at 1/200 dilution, for 30 minutes at room temperature and detected using an HRP conjugated compact polymer system. DAB was used as the chrogen. Counter stained with hematoxylin and mounted with DPX.

Bon Opus Cat. #BA113145
Size
  • Host Species; Species Reactivity

    Rabbit; Human
  • Immunogen

    Recombinant protein
  • Application Summary

    WB, ICC/IF, IHC, IP, FC
  • Purification; Formulation

    Protein A purified.; 1*TBS (pH7.4), 1%BSA, 40%Glycerol. Preservative: 0.05% Sodium Azide.
  • Background

    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.(ET1605-1)