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Results suggest that Xenopus MBD4 (show MBD4 Proteins)/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 Proteins) genes, mlh1, msh2 (show MSH2 Proteins), and msh6 (show MSH6 Proteins), 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 Proteins) 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 activity of MLH1 beyond the activation of the endonuclease functions of its MMR (show MRC1 Proteins) partner PMS2 (show PMS2 Proteins)
Down-regulation of MLH1 is associated with initiation and growth of neuroblastoma (show ARHGEF16 Proteins) 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 Proteins) deficiency and a cancer predisposition phenotype similar to Mlh1-/- mice.
In contrast to colorectal carcinoma, sporadic MLH1 deficiency is not seen in small bowel adenocarcinoma
MLH1 methylation is associated with colorectal cancer.
We found no correlation between the DLEC1, TUSC4 (show NPRL2 Proteins) and MLH1 gene expression and NSCLC patient characteristics (gender, age and smoking) or cancer histopathology. No significant differences in the gene expression among NSCLC subtypes indicate the weakness of DLEC1, TUSC4 (show NPRL2 Proteins) and MLH1 expression analysis as potential differentiating markers of NSCLC subtypes in the Polish population.
The results of this meta-analysis show a significant association between hMLH1 hypermethylation and colorectal cancer risk.
study to estimate frequency of point mutations and chromosomal rearrangements in 3 mismatch repair (MMR (show MRC1 Proteins)) genes MLH1, MSH2 (show MSH2 Proteins), and MSH6 (show MSH6 Proteins) among unselected patients with ovarian cancer; estimate that approximately 0.6% of unselected ovarian cancer patients have mutations in the MMR (show MRC1 Proteins) genes
CpG island methylator phenotype (CIMP)+/MLH1-unmethylated (MLH1-U) tumors exhibit aggressive features and are associated with poor clinical outcomes.
Analysis of expression Quantitative Trait Loci (eQTLs) provides modest support for altered regulation of MLH1 and LRRFIP2 (show LRRFIP2 Proteins), raising the possibility that the modifier affects regulation of both genes.
MLH1 deficiency had an impact on the evolution of the tumor after surgical resection in a murine xenograft model.
Results indicate that the normal tissue types tested (colorectum and PBMC) experience dynamic genotype-associated epigenetic alterations at the MLH1 shore, whereas cancer tumor DNA incurs aberrant hypermethylation compared to normal DNA. These results reveal that the epigenetic landscape of MLH1 is dynamically regulated at least in part by the static genetic sequence.
MLH1-methylated CpG island methylator phenotype is associated with serrated adenoma in colorectal carcinoma.
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