Browse our MLH1 Proteins (MLH1)

Fruit Fly (Drosophila melanogaster) MutL Homolog 1, Colon Cancer, Nonpolyposis Type 2 (E. Coli) (MLH1) interaction partners

1. Reduction of the Mlh1 protein level leads to defective oocytes that fail to complete embryogenesis after fertilization thereby reducing female fertility.

Xenopus laevis MutL Homolog 1, Colon Cancer, Nonpolyposis Type 2 (E. Coli) (MLH1) interaction partners

1. 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.

Zebrafish MutL Homolog 1, Colon Cancer, Nonpolyposis Type 2 (E. Coli) (MLH1) interaction partners

1. 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.

2. 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.

3. 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.

Mouse (Murine) MutL Homolog 1, Colon Cancer, Nonpolyposis Type 2 (E. Coli) (MLH1) interaction partners

1. 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.

2. 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

3. radiation exposure could further increase the risk of colorectal carcinogenesis induced by inflammation under the conditions of Mlh1 deficiency.

4. 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

5. Data indicate that Mlh1 showed only modest methylation was still expressed in both Mlh1(+/-) and Mlh1(+/+) mice.

6. 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.

7. 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)

8. Down-regulation of MLH1 is associated with initiation and growth of neuroblastoma (show ARHGEF16 Proteins) and brain tumour multicellular spheroids.

9. 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.

10. 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.

Human MutL Homolog 1, Colon Cancer, Nonpolyposis Type 2 (E. Coli) (MLH1) interaction partners

1. MLH1 and PMS2 (show PMS2 Proteins) can be imported to the nucleus by a classical nuclear import pathway

2. The MLH1-93 AA genotype is significantly associated with promoter hypermethylation and MLH1 loss in the context of Sessile serrated adenoma of dysplasia. BRAF (show BRAF Proteins) 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.

3. Cancer developed more often in mutation carriers, with no consistent difference between MLH1 and MSH2 (show MSH2 Proteins) 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.

4. Data suggest that the concurrent mutations of the adenomatous polyposis coli protein (APC (show APC Proteins)) and mutL protein homolog 1 (MLH1) genes probably underline the familial adenomatous polyposis (FAP) in the pedigree.

5. Among 13 gastric tumors showing no hMLH1 or hMSH2 (show MSH2 Proteins) expression, 8 MSI (show MSI1 Proteins)-H (high) and 5 MSI (show MSI1 Proteins)-L (low) were identified.

6. Results show that folate concentrations >45.3 nmol/L increased the risk of methylation in specific CpG sites of MLH1.

7. In contrast to colorectal carcinoma, sporadic MLH1 deficiency is not seen in small bowel adenocarcinoma

8. MLH1 methylation is associated with colorectal cancer.

9. 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.

10. The results of this meta-analysis show a significant association between hMLH1 hypermethylation and colorectal cancer risk.

Cow (Bovine) MutL Homolog 1, Colon Cancer, Nonpolyposis Type 2 (E. Coli) (MLH1) interaction partners

1. Meiosis progression and female age affect expression profile of DNA repair MLH1 gene in bovine oocytes.