Predicted to enable NADPH-hemoprotein reductase activity; [methionine synthase] reductase (NADPH) activity; and nucleotide binding activity. Predicted to be involved in several processes, including folic acid metabolic process; negative regulation of cystathionine beta-synthase activity; and sulfur amino acid metabolic process. Predicted to be located in intermediate filament cytoskeleton and nucleoplasm. Predicted to be active in cytosol. Human ortholog(s) of this gene implicated in several diseases, including abdominal aortic aneurysm; endocrine gland cancer (multiple); heart disease (multiple); hematologic cancer (multiple); and homocystinuria. Orthologous to human MTRR (5-methyltetrahydrofolate-homocysteine methyltransferase reductase); PARTICIPATES IN altered folate cycle metabolic pathway; folate cycle metabolic pathway; folate mediated one-carbon metabolic pathway; INTERACTS WITH 2,3,7,8-tetrachlorodibenzodioxine; 2,6-dinitrotoluene; bisphenol A.
[Choline deficiency co-treated with Folic Acid deficiency] affects the expression of MTRR mRNA and Folic Acid inhibits the reaction [Methotrexate results in decreased expression of MTRR mRNA]
DHFR protein inhibits the reaction [Methotrexate results in decreased expression of MTRR mRNA] and Folic Acid inhibits the reaction [Methotrexate results in decreased expression of MTRR mRNA]
Common gene polymorphisms in the metabolic folate and methylation pathway and the risk of acute lymphoblastic leukemia and non-Hodgkin's lymphoma in adults.
Methylenetetrahydrofolate reductase (MTHFR) and methionine synthase reductase (MTRR) gene polymorphisms as risk factors for hepatocellular carcinoma in a Korean population.
Roles of genetic polymorphisms in the folate pathway in childhood acute lymphoblastic leukemia evaluated by Bayesian relevance and effect size analysis.
Methylenetetrahydrofolate reductase and methionine synthase reductase gene polymorphisms and protection from microvascular complications in adolescents with type 1 diabetes.
Functional variant in methionine synthase reductase intron-1 significantly increases the risk of congenital heart disease in the Han Chinese population.