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Literature summary for 1.16.1.8 extracted from

  • Han, D.; Shen, C.; Meng, X.; Bai, J.; Chen, F.; Yu, Y.; Jin, Y.; Fu, S.
    Methionine synthase reductase A66G polymorphism contributes to tumor susceptibility: evidence from 35 case-control studies (2012), Mol. Biol. Rep., 39, 805-816.
    View publication on PubMed

Application

Application Comment Organism
diagnostics the MTRR A66G polymorphism is a potential biomarker for cancer risk Homo sapiens

Cloned(Commentary)

Cloned (Comment) Organism
gene MTRR, genotyping for the A66G polymorphism and analysis of the association with cancer risk, overview. The G allele and GG variant genotypes are associated with a significantly increased cancer risk Homo sapiens

Protein Variants

Protein Variants Comment Organism
A66G naturally occuring mutation, the MTRR polymorphism leads to a lower affinity for substrate methionine synthase compared to the wild-type enzyme Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
-
-

Synonyms

Synonyms Comment Organism
Methionine synthase reductase
-
Homo sapiens
MTRR
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Homo sapiens

General Information

General Information Comment Organism
metabolism the MTRR gene is involved in tumorigenesis by regulating DNA methylation through activation of methionine synthase Homo sapiens
additional information genotyping for the A66G polymorphism and analysis of the association with cancer risk reveals that the G allele and GG variant genotypes are associated with a significantly increased cancer risk Homo sapiens