Use your antibodies-online credentials, if available.
Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
Afficher tous les synonymes
Sélectionnez vos espèces d'intérêt
Reduction of the Mlh1 protein level leads to defective oocytes that fail to complete embryogenesis after fertilization thereby reducing female fertility.
Results suggest that Xenopus MBD4/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 genes, mlh1, msh2, and msh6, in zebrafish that develop tumors at low frequencies.
Cancer preceding changes are already seen in histologically normal colon mucosa and that decreased expressions of Mlh1.
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 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 partner PMS2
Down-regulation of MLH1 is associated with initiation and growth of neuroblastoma 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 deficiency and a cancer predisposition phenotype similar to Mlh1-/- mice.
Ablation of Mlh1 did not appreciably influence the developmental phenotypes conferred by the absence of Rad51d.
Role for mismatch repair proteins Msh2, Mlh1, and Pms2 in immunoglobulin class switching shown by sequence analysis of recombination junctions.
In this study, we investigated whether failure to develop foci of MLH1 protein on chromosomes in prophase would lead to elimination of prophase spermatocytes.Thus, spermatocytes are not eliminated in direct response to the initial meiotic defect
We found that MLH1 and PMS2 have functional nuclear localization signals (NLS) and nuclear export sequences, yet nuclear import depended on their C-terminal dimerization to form MutLalpha
Mlh1 can function in antibody class switch recombination independently of Msh2.
Mlh1 deficiency accelerates myeloid leukemogenesis in neurofibromatosis 1 (Nf1) heterozygous mice.These results suggest that MMR deficiency can accelerate myeloid leukemogenesis in Nf1+/- mice, presumably by inactivating Nf1 gene expression.
The cellular content of MLH1 protein seems to be critical for determining if damaged cells enter into either a death or mutation-inducing pathway.
Mlh1 modulates error-prone nonhomologous end-joining by inhibiting the annealing of DNA ends containing noncomplementary base pairs or by promoting the annealing of microhomologies.
Repression of MLH1 is associated with precancerous conditions in hyperplastic mucosa adjacent to colon cancer
A novel heterozygous germline mutation (c.3G>T, p.Met1Ile) in MLH1 gene was discovered by next generation sequencing.
Mutational analysis of the MLH1/MSH2 genes was carried out. Analysis was extended to the family members and the general population. This led to the identification of a heterozygous frameshift duplication in the MLH1 gene at position 910 (c.910dupG). Three siblings had inherited the mutation from their mother, two of whom were asymptomatic at the time of diagnosis.
Lynch syndrome associated MLH1 c.2059C>T mutation is a Swedish founder mutation with a probable origin in a single founder individual in the north of Sweden, whose descendants have migrated southwards in Sweden as well as across the border to Finland.
Inconsistent with previous meta-analyses, this meta-analysis shows that the hMLH1 655A>G and 1151T>A polymorphisms might be risk factors for colorectal cancer. Moreover, the -93G>A polymorphism is associated with the susceptibility of colorectal cancer in Asian population.
Hypomethylation of MLH1 gene is associated with chemotolerance of breast carcinoma.
Low MLH1 expression is associated with Colonic Adenoma and Adenocarcinoma.
Single-Nucleotide Polymorphisms of the MLH1 is associated with Basal Cell Carcinoma.
this meta-analysis suggested that hMLH1 methylation was associated with an increased CRC risk.
The DNA mismatch repair gene (MMR) plays an important role in anti-carcinogenesis and MMR gene deficiency.
Study investigated the counteraction of oxidative stress by vitamin E in the colorectal cancer cell line Caco-2 under normal and high glucose cell culture condition. Gene expression and promoter methylation of the DNA repair gene MutL homolog 1 (MLH1) and the DNA methyltransferase 1 (DNMT1) were investigated. Induction of MLH1 and DNMT1 gene expression was noticed, accompanied by an increase in global methylation.
the results identified for the first time a MLH1 missense mutation (NM_000249.3:p.Tyr379Ser/c.1136A>C) in a Chinese family with Gardner syndrome (GS), thus broadening the range of mutated genes associated with GS.
This study demonstrated that Aberrant methylation of mutL homolog 1 is associated with increased risk of non-small cell lung cancer
MLH1's ATPase domain has a crucial role in preventing the aberrant formation of telomeric sequences at the intra-chromosomal regions and preserving genome stability.
provide evidence that four of the alterations in MLH1 are causative for Lynch syndrome, four are likely neutral and one shows compromised activity which can currently not be classified with respect to its pathogenic potential
This pilot study indicates oligozoospermic patients have more methylation of MLH1 than normozoospermic patients.
MLH1 and PMS2 can be imported to the nucleus by a classical nuclear import pathway
The MLH1-93 AA genotype is significantly associated with promoter hypermethylation and MLH1 loss in the context of Sessile serrated adenoma of dysplasia. BRAF mutant microsatellite stable colorectal cancers with the AA genotype most likely arise in traditional serrated adenomas since the A allele does not predispose to methylation in this context.
Cancer developed more often in mutation carriers, with no consistent difference between MLH1 and MSH2 carriers. More polyps (mostly adenomas) were detected in MLH1 carriers. The majority (13 of 21) of malignant tumours occurred in organs for which there is no recommended surveillance, and were lethal in three patients.
Data suggest that the concurrent mutations of the adenomatous polyposis coli protein (APC) and mutL protein homolog 1 (MLH1) genes probably underline the familial adenomatous polyposis (FAP) in the pedigree.
Among 13 gastric tumors showing no hMLH1 or hMSH2 expression, 8 MSI-H (high) and 5 MSI-L (low) were identified.
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