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Results suggest that Xenopus MBD4 (show MBD4 ELISA Kits)/MLH1 participates in a novel G2 checkpoint that is responsive to DNMT1p levels in developing embryos and cells.
Male mlh1 mutants are sterile and display an arrest in spermatogenesis at metaphase I, resulting in increased testis weight due to accumulation of prophase I spermatocytes.
In zebrafish mlh1 mutant (knock-out) males, a delay of both meiotic divisions occurs rather than complete arrest during meiosis I. Eggs fertilized with mutant sperm develop as malformed embryos and are aneuploid.
Identification and characterization of novel knockout mutants of the three major MMR (show MRC1 ELISA Kits) genes, mlh1, msh2 (show MSH2 ELISA Kits), and msh6 (show MSH6 ELISA Kits), in zebrafish that develop tumors at low frequencies.
a causal relationship between MLH1-deficiency and incidence of oncogenic point mutations in tyrosine kinases driving cell transformation and acquired resistance to kinase-targeted cancer therapies, is reported.
high mutation ofMlh1(-/-)-deficient fetuses has little effect on the fetuses during their early developmental stages, whereas Mlh1(-/-)-deficient fetuses from X-ray irradiated mothers are clearly effected
radiation exposure could further increase the risk of colorectal carcinogenesis induced by inflammation under the conditions of Mlh1 deficiency.
these data identify Mlh1 and Mlh3 as novel critical genetic modifiers of HTT (show HTT ELISA Kits) CAG instability, point to Mlh1 genetic variation as the likely source of the instability difference in B6 and 129 strains
Data indicate that Mlh1 showed only modest methylation was still expressed in both Mlh1(+/-) and Mlh1(+/+) mice.
nickel-smelting fumes upregulated the expression of Mlh1 protein, mouse . This suggest that nickel-smelting fumes could be toxic to cells, inducing cell apoptosis and necrosis.
suggesting a role for the ATPase (show DNAH8 ELISA Kits) activity of MLH1 beyond the activation of the endonuclease functions of its MMR (show MRC1 ELISA Kits) partner PMS2 (show PMS2 ELISA Kits)
Down-regulation of MLH1 is associated with initiation and growth of neuroblastoma (show ARHGEF16 ELISA Kits) and brain tumour multicellular spheroids.
MLH1 can convert DNA nicks and point mutations into double-stranded DNA breaks for both core nonhomologous end-joining factors and alternative end-joining pathways of class-switch recombination.
Data show that the constitutive inactivation of MLH1, resulting Mlh1(Deltaex4/Deltaex4) mouse line, displays complete MMR (show MRC1 ELISA Kits) deficiency and a cancer predisposition phenotype similar to Mlh1-/- mice.
Loss of MLH1 expression is associated with colorectal carcinoma.
the MLH1 c.543C>T silent mutation is considered 'pathogenic'.
Promoter methylation and loss of protein expression of hMLH1 are not parallel processes that occur concurrently. hMLH1 methylation is an early molecular event which occurs even in hyperplastic polyps (HPs (show HPS1 ELISA Kits)). the loss of hMLH1 protein expression does not necessarily precede the development of cytological dysplasia in sessile serrated lesion (SSL).
Overexpression of MutL homolog 1 and MutS homolog 2 (show MSH2 ELISA Kits) proteins have reversed prognostic implications for stage I-II colon cancer
MLH1, a key protein involved in mismatch repair (MMR (show MRC1 ELISA Kits)), suppresses telomeric sequence insertion (TSI) at intra-chromosomal regions. The frequency of TSI can be elevated by double-strand break (DSB) inducer and abolished by ATM (show ATM ELISA Kits)/ATR (show ANTXR1 ELISA Kits) inhibition. Suppression of TSI requires MLH1 recruitment to DSBs, indicating that MLH1's role in DSB response/repair is important for suppressing TSI.
MLH1 mutations contribute to colorectal cancer susceptibility in Algerian families with suspected Lynch syndrome.
MLH1 methylation analysis defines a subset of tumors that have worse prognostic features including higher tumor volume and lymph node involvement.
High MLH1 expression is associated with the development of genetic instability and is linked to tumor aggressiveness and early PSA recurrence in prostate cancer.
MLH1 methylation is a frequent molecular event in colorectal cancer and lung cancer patients
Both the mTOR (show FRAP1 ELISA Kits)/p-mTOR (show FRAP1 ELISA Kits) and BNIP3 (show BNIP3 ELISA Kits)/Beclin-1 (show BECN1 ELISA Kits) signaling pathways were found to be related to HRS, but only mTOR (show FRAP1 ELISA Kits)/p-mTOR (show FRAP1 ELISA Kits) is involved in the regulation of HRS via MLH1 and autophagy.
Meiosis progression and female age affect expression profile of DNA repair MLH1 gene in bovine oocytes.
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.
MutL protein homolog 1
, DNA mismatch repair protein Mlh1
, mutL-like protein 1
, mutL homolog 1, colon cancer, nonpolyposis type 2 (E. coli)
, DNA mismatch repair protein Mlh1-like
, colon cancer, nonpolyposis type 2
, mutL protein homolog 1
, mismatch repair protein 1