Results 141 to 150 of about 5,812 (165)

DNA Methylation in Gastric Cancer and Preneoplastic Lesions: Emerging Insights and Future Directions. [PDF]

open access: yesCancers (Basel)
Ceccon C   +9 more
europepmc   +1 more source

Enhanced transcriptomic profiling of esophageal tissue through optimized PAXgene fixation protocols. [PDF]

open access: yesGenes Dis
Charara F   +9 more
europepmc   +1 more source

Expression of human MutS homolog 2 (hMSH2) protein in resting and proliferating cells. [PDF]

open access: yesOncogene, 1996
The hMSH2 protein plays an important role in the DNA mismatch repair system. Since this system is involved in the correction of errors that occur during DNA replication, we studied the expression of hMSH2 protein in resting and DNA-replicating cells, as well as through the cell cycle in cell types with different growth characteristics.
Marra, Giancarlo   +5 more
core   +7 more sources

Cadmium(Cd)-induced oxidative stress down-regulates the gene expression of DNA mismatch recognition proteins MutS homolog 2 (MSH2) and MSH6 in zebrafish (Danio rerio) embryos

Aquatic Toxicology, 2013
DNA mismatch repair (MMR) of simple base mismatches and small insertion-deletion loops in eukaryotes is initiated by the binding of the MutS homolog 2 (MSH2)-MSH6 heterodimer to mismatched DNA. Cadmium (Cd) is a genotoxic heavy metal that has been recognized as a human carcinogen.
Todd Hsu
exaly   +3 more sources

[Abnormal expression of fragile histidine triad (FHIT) and Mut S homolog 2 (MSH2) proteins in human sporadic colorectal carcinoma and their clinical significance].

Ai zheng = Aizheng = Chinese journal of cancer, 2004
Frequent loss of fragile histidine triad (FHIT) expression in human gastrointestinal tract carcinomas has been reported; however, there were divergent opinions regarding FHIT expression in colorectal carcinoma. Recent studies have suggested that FHIT inactivation can be a consequence of defects in mismatch repair proteins, particularly mut S homolog 2 (
Cheng-Cai, Yao   +2 more
openaire   +1 more source

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