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2 common and functional MTHFD1 polymorphisms (rs2236225 and rs1076991) modulate the risk associations of plasma serine and glycine with acute myocardial infarction in patients with stable angina pectoris.
MTHFD1 1958AA genotype is linked to a significantly reduced cancer risk. The 1958GG genotype is associated to PBMCs DNA hypomethylation as compared to the A allele carriership that may exert a protective effect for cancer risk by preserving from DNA hypomethylation
Results propose that MTHFD1 synthetase deficiency does not contribute to tumor initiation in the normal colon, but it limits tumor growth by reducing purine pools and altering expression of genes involved in cell proliferation and inflammation.
B vitamin treatments modify the risk of myocardial infarction associated with a MTHFD1 polymorphism in patients with stable angina pectoris.
Paternal, rather than a maternal, transmission bias of MTHFD1 G1958A variant for neural tube defects susceptibility in the offspring.
impairments in MTHFD1 activity compromise both homocysteine remethylation and de novo thymidylate biosynthesis, and provide evidence that MTHFD1-associated disruptions in de novo thymidylate biosynthesis lead to genome instability that may underlie folate-associated immunodeficiency and birth defects
G1958A (MTHFD1) polymorphisms showed no association with ischemic heart disease in patients from Yucatan, Mexico
polymorphism of SNP loci rs1956545 and rs56811449 as well as a haplotype in MTHFD1 gene could have a role in the occurrence of neural tube defects in the Chinese population
MTHFD1 1958G > A is significantly associated with the susceptibility of neural tube defects in a Chinese population.
Data suggest impaired folate metabolism down-regulates placenta trophoblast proliferation, viability, invasive capacity, and progesterone secretion; silencing MTHFD1 gene down-regulates cell proliferation but does not alter progesterone secretion.
Data suggest that upregulation of 10-formyltetrahydrofolate dehydrogenase (FDH (show ALDH1L1 ELISA Kits)) involving CEBPalpha helps relieve embryonic oxidative stress induced (show SQSTM1 ELISA Kits) by ethanol exposure.
Study evaluated cognitive function in Mthfd1(gt/+) male and female mice using a behavioral battery composed of eight different tests, found that these mice display impaired cue-conditioned learning, while other behaviors remain intact.
Study observed decreased tumor growth in mice with reduced MTHFD1-synthetase activity, a model for the decreased metabolic activity of the human R653Q variant. These results propose that synthetase deficiency does not contribute to tumor initiation in the normal colon, but it limits tumor growth by reducing purine pools and altering expression of genes involved in cell proliferation and inflammation.
Moderately higher folate intake and MTHFD1-synthetase deficiency in pregnant mice result in a lower methylation potential in maternal liver and embryos and a greater incidence of defects in embryos.
Deficiency of the MTHFD1 10-formyltetrahydrofolate synthetase activity in embryos is associated with increased incidence of congenital heart defects
methylenetetrahydrofolate dehydrogenase 1 (MTHFD1), an enzyme that generates methylenetetrahydrofolate from formate, ATP, and NADPH (show FDXR ELISA Kits), functions in the nucleus to support de novo thymidylate biosynthesis.
Mthfd1gt/+ mice exhibited attentional dysfunction and a blunted affective response to committing an error. They also showed decreased expression levels for genes encoding choline dehydrogenase (show CHDH ELISA Kits) and the alpha 7 nicotinic cholinergic receptor (show CHRFAM7A ELISA Kits).
Data suggest that decreased MTHFD1 activity (here, insertional mutant heterozygotes) has greater impact on one-carbon metabolism compared with folate-deficient diet; no interaction was observed between MTHFD1 genotype and folate deficiency.
Data suggest that heterozygosity in a lethal Mthfd1 mutation impairs folate status in pregnant mice (i.e., impairs fetal growth) but does not significantly affect homocysteine metabolism (i.e., does not cause neural tube defects).
Mthfd1 is a modifier of chemically induced intestinal carcinogenesis.
MTHFD1 has a role in production of monofunctional 10-formyltetrahydrofolate synthetase in mammalian mitochondria
This gene encodes a protein that possesses three distinct enzymatic activities, 5,10-methylenetetrahydrofolate dehydrogenase, 5,10-methenyltetrahydrofolate cyclohydrolase and 10-formyltetrahydrofolate synthetase. Each of these activities catalyzes one of three sequential reactions in the interconversion of 1-carbon derivatives of tetrahydrofolate, which are substrates for methionine, thymidylate, and de novo purine syntheses. The trifunctional enzymatic activities are conferred by two major domains, an aminoterminal portion containing the dehydrogenase and cyclohydrolase activities and a larger synthetase domain.
, C-1-tetrahydrofolate synthase, cytoplasmic
, c-1-tetrahydrofolate synthase, cytoplasmic
, C1-THF synthase
, methylenetetrahydrofolate dehydrogenase 1
, mthfd1 protein
, methylenetetrahydrofolate dehydrogenase (NADP+ dependent) 1, methenyltetrahydrofolate cyclohydrolase, formyltetrahydrofolate synthetase
, c-1-tetrahydrofolate synthase, cytoplasmic-like
, 5,10-methylenetetrahydrofolate dehydrogenase, 5,10-methylenetetrahydrofolate cyclohydrolase, 10-formyltetrahydrofolate synthetase
, cytoplasmic C-1-tetrahydrofolate synthase
, C1-tetrahydrofolate synthase
, methylenetetrahydrofolate dehydrogenase (NADP+ dependent), methenyltetrahydrofolate cyclohydrolase, formyltetrahydrofolate synthase
, formyltetrahydrofolate synthetase
, methenyltetrahydrofolate cyclohydrolase
, methylenetetrahydrofolate dehydrogenase (NADP+ dependent), methenyltetrahydrofolate cyclohydrolase, formyltetrahydrofolate synthetase