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mouse anti-MLH-1 monoclonal antibody (G168-728) 6257

$160.00$528.00

Antibody summary

  • Mouse monoclonal to MLH-1
  • Suitable for: Immunohistochemistry (formalin-fixed, paraffin-embedded tissues)
  • Reacts with: Human
  • Isotype:IgG1
  • Control: Colon carcinoma
  • Visualization: Nuclear
  • 0.1, 0.5, 1.0 mL concentrated, 7 mL prediluted
SKU: 6257parent Category: Tags: , ,
Weight1 lbs
Dimensions9 × 5 × 2 in
host

mouse

isotype

IgG1

clonality

monoclonal

concentration

concentrate, predilute

applications

IHC

reactivity

human

available size

0.1 mL, 0.5 mL, 1 mL concentrated, 7 mL prediluted

mouse anti-MLH-1 monoclonal antibody G168-728 6257

antibody
Database link:
human P40692
Tested applications
IHC
Recommended dilutions
As directed
Immunogen
N-terminal fragment of human Mi protein
Size and concentration
7 mL prediluted or 0.1, 0.5, 1.0 mL and concentrated
Form
liquid
Storage Instructions
2-8°C for short term, for longer term at -20°C. Avoid freeze / thaw cycles.
Purity
affinity purified
Clonality
monoclonal
Isotype
IgG1
Compatible secondaries
goat anti-mouse IgG, H&L chain specific, peroxidase conjugated polyclonal antibody 5486
goat anti-mouse IgG, H&L chain specific, biotin conjugated, Conjugate polyclonal antibody 2685
goat anti-mouse IgG, H&L chain specific, FITC conjugated polyclonal antibody 7854
goat anti-mouse IgG, H&L chain specific, peroxidase conjugated polyclonal antibody, crossabsorbed 1706
goat anti-mouse IgG, H&L chain specific, biotin conjugated polyclonal antibody, crossabsorbed 1716
goat anti-mouse IgG, H&L chain specific, FITC conjugated polyclonal antibody, crossabsorbed 1721
Isotype control
Mouse monoclonal IgG1 - Isotype Control
target relevance
Protein names
DNA mismatch repair protein Mlh1 (MutL protein homolog 1)
Protein family
DNA mismatch repair MutL/HexB family
Mass
84601Da
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. .
Subellular location
Nucleus . Chromosome . Note=Recruited to chromatin in a MCM9-dependent manner. .
Tissues
Colon, lymphocytes, breast, lung, spleen, testis, prostate, thyroid, gall bladder and heart.
Structure
Component of the DNA mismatch repair (MMR) complex composed at least of MSH2, MSH3, MSH6, PMS1 and MLH1 (PubMed:26300262). Heterodimer of MLH1 and PMS2 (MutL alpha), MLH1 and PMS1 (MutL beta) or MLH1 and MLH3 (MutL gamma). Forms a ternary complex with MutS alpha (MSH2-MSH6) or MutS beta (MSH2-MSH3). Part of the BRCA1-associated genome surveillance complex (BASC), which contains BRCA1, MSH2, MSH6, MLH1, ATM, BLM, PMS2 and the RAD50-MRE11-NBS1 protein complex (PubMed:10783165). This association could be a dynamic process changing throughout the cell cycle and within subnuclear domains (PubMed:10097147). Interacts with MCM9; the interaction recruits MLH1 to chromatin (PubMed:26300262). Interacts with MCM8 (PubMed:26300262). Interacts with PMS2 (PubMed:11427529, PubMed:22753075). Interacts with MBD4 (PubMed:10097147). Interacts with EXO1 (PubMed:11427529, PubMed:11429708, PubMed:12414623, PubMed:14676842, PubMed:22753075). Interacts with MTMR15/FAN1 (PubMed:20603073). .
Involvement in disease
Lynch syndrome 2 (LYNCH2) [MIM:609310]: A form of Lynch syndrome, an autosomal dominant disease associated with marked increase in cancer susceptibility. It is characterized by a familial predisposition to early-onset colorectal carcinoma (CRC) and extra-colonic tumors of the gastrointestinal, urological and female reproductive tracts. Lynch syndrome is reported to be the most common form of inherited colorectal cancer in the Western world. Clinically, it is often divided into two subgroups. Type I is characterized by hereditary predisposition to colorectal cancer, a young age of onset, and carcinoma observed in the proximal colon. Type II is characterized by increased risk for cancers in certain tissues such as the uterus, ovary, breast, stomach, small intestine, skin, and larynx in addition to the colon. Diagnosis of classical Lynch syndrome is based on the Amsterdam criteria: 3 or more relatives affected by colorectal cancer, one a first degree relative of the other two; 2 or more generation affected; 1 or more colorectal cancers presenting before 50 years of age; exclusion of hereditary polyposis syndromes. The term 'suspected Lynch syndrome' or 'incomplete Lynch syndrome' can be used to describe families who do not or only partially fulfill the Amsterdam criteria, but in whom a genetic basis for colon cancer is strongly suspected. . Note=The disease is caused by variants affecting the gene represented in this entry.; Mismatch repair cancer syndrome 1 (MMRCS1) [MIM:276300]: An autosomal recessive form of mismatch repair cancer syndrome, a childhood cancer predisposition syndrome encompassing a broad tumor spectrum. This includes hematological malignancies, central nervous system tumors, Lynch syndrome-associated malignancies such as colorectal tumors as well as multiple intestinal polyps, embryonic tumors and rhabdomyosarcoma. Multiple cafe-au-lait macules, a feature reminiscent of neurofibromatosis type 1, are often found as first manifestation of the underlying cancer. . Note=The disease is caused by variants affecting the gene represented in this entry.; Muir-Torre syndrome (MRTES) [MIM:158320]: Rare autosomal dominant disorder characterized by sebaceous neoplasms and visceral malignancy. . Note=The disease is caused by variants affecting the gene represented in this entry.; Note=Defects in MLH1 may contribute to lobular carcinoma in situ (LCIS), a non-invasive neoplastic disease of the breast.; Endometrial cancer (ENDMC) [MIM:608089]: A malignancy of endometrium, the mucous lining of the uterus. Most endometrial cancers are adenocarcinomas, cancers that begin in cells that make and release mucus and other fluids. Note=Disease susceptibility is associated with variants affecting the gene represented in this entry.; Note=Some epigenetic changes can be transmitted unchanged through the germline (termed 'epigenetic inheritance'). Evidence that this mechanism occurs in humans is provided by the identification of individuals in whom 1 allele of the MLH1 gene is epigenetically silenced throughout the soma (implying a germline event). These individuals are affected by Lynch syndrome but does not have identifiable mutations in MLH1, even though it is silenced, which demonstrates that an epimutation can phenocopy a genetic disease.; Colorectal cancer (CRC) [MIM:114500]: A complex disease characterized by malignant lesions arising from the inner wall of the large intestine (the colon) and the rectum. Genetic alterations are often associated with progression from premalignant lesion (adenoma) to invasive adenocarcinoma. Risk factors for cancer of the colon and rectum include colon polyps, long-standing ulcerative colitis, and genetic family history. . Note=Disease susceptibility is associated with variants affecting the gene represented in this entry.
Target Relevance information above includes information from UniProt accession: P40692
The UniProt Consortium

Data

Human colon adenocarcinoma with Lynch syndrome stained with anti-MLH-1 antibody using peroxidase-conjugate and DAB chromogen. Note absence of nuclear staining of tumor cells whereas the background non tumor cells are positive.
Human colon adenocarcinoma with Lynch syndrome stained with anti-MLH-1 antibody using peroxidase-conjugate and DAB chromogen. Note absence of nuclear staining of tumor cells whereas the background non tumor cells are positive.

Publications

Published literature highly relevant to the biological target of this product and referencing this antibody or clone are retrieved from PubMed database provided by The United States National Library of Medicine at the National Institutes of Health.




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Protocols

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Documents

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