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Mouse Anti-MLH3 Recombinant Antibody (CBFYM-2295) (CBMAB-M2480-FY)

This product is mouse antibody that recognizes MLH3. The antibody CBFYM-2295 can be used for immunoassay techniques such as: WB, IP, IF, ELISA.
See all MLH3 antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
CBFYM-2295
Application
WB, IP, IF, ELISA

Basic Information

Specificity
Human
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
MUTL HOMOLOG 3
Introduction
This gene is a member of the MutL-homolog family of DNA mismatch repair genes. MLH genes are implicated in maintaining genomic integrity during DNA replication and after meiotic recombination. The protein encoded by this gene functions as a heterodimer with other family members. Somatic mutations in this gene frequently occur in tumors exhibiting microsatellite instability, and germline mutations have been linked to hereditary nonpolyposis colorectal cancer type 7. Several alternatively spliced transcript variants have been identified, but the full-length nature of only two transcript variants has been determined.
Entrez Gene ID
27030
UniProt ID
Q9UHC1
Alternative Names
MutL Homolog 3; DNA Mismatch Repair Protein Mlh3; MutL (E. Coli) Homolog 3; MutL Homolog 3 (E. Coli); MutL Protein Homolog 3; HNPCC7
Function
Probably involved in the repair of mismatches in DNA.
Biological Process
Female meiosis I Source: Ensembl
Male meiotic nuclear division Source: Ensembl
Mismatch repair Source: GO_Central
Protein localization Source: Ensembl
Reciprocal meiotic recombination Source: UniProtKB
Synaptonemal complex assembly Source: Ensembl
Cellular Location
Nucleus
Involvement in disease
Hereditary non-polyposis colorectal cancer 7 (HNPCC7):
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. HNPCC is reported to be the most common form of inherited colorectal cancer in the Western world. Clinically, HNPCC 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 HNPCC 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 HNPCC' or 'incomplete HNPCC' 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.
Colorectal cancer (CRC):
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.

Nawaz, S., Ullah, M. I., Hamid, B. S., Nargis, J., Nawaz, M., Hussain, S., & Ahmad, W. (2021). A loss-of-function variant in DNA mismatch repair gene MLH3 underlies severe oligozoospermia. Journal of Human Genetics, 66(7), 725-730.

Furman, C. M., Elbashir, R., & Alani, E. (2021). Expanded roles for the MutL family of DNA mismatch repair proteins. Yeast, 38(1), 39-53.

Dai, J., Sanchez, A., Adam, C., Ranjha, L., Reginato, G., Chervy, P., ... & Charbonnier, J. B. (2021). Molecular basis of the dual role of the Mlh1-Mlh3 endonuclease in MMR and in meiotic crossover formation. Proceedings of the National Academy of Sciences, 118(23), e2022704118.

Kadyrova, L. Y., Gujar, V., Burdett, V., Modrich, P. L., & Kadyrov, F. A. (2020). Human MutLγ, the MLH1–MLH3 heterodimer, is an endonuclease that promotes DNA expansion. Proceedings of the National Academy of Sciences, 117(7), 3535-3542.

Rahman, M. M., Mohiuddin, M., Keka, I. S., Yamada, K., Tsuda, M., Sasanuma, H., ... & Takeda, S. (2020). Genetic evidence for the involvement of mismatch repair proteins, PMS2 and MLH3, in a late step of homologous recombination. Journal of Biological Chemistry, 295(51), 17460-17475.

Cannavo, E., Sanchez, A., Anand, R., Ranjha, L., Hugener, J., Adam, C., ... & Cejka, P. (2020). Regulation of the MLH1–MLH3 endonuclease in meiosis. Nature, 586(7830), 618-622.

Olkinuora, A., Nieminen, T. T., Mårtensson, E., Rohlin, A., Ristimäki, A., Koskenvuo, L., ... & Borg, Å. (2019). Biallelic germline nonsense variant of MLH3 underlies polyposis predisposition. Genetics in Medicine, 21(8), 1868-1873.

Toledo, M., Sun, X., Brieño-Enríquez, M. A., Raghavan, V., Gray, S., Pea, J., ... & Cohen, P. E. (2019). A mutation in the endonuclease domain of mouse MLH3 reveals novel roles for MutLγ during crossover formation in meiotic prophase I. PLoS genetics, 15(6), e1008177.

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For research use only. Not intended for any clinical use.

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