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The protein encoded by MTHFR catalyzes the conversion of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate, a co-substrate for homocysteine remethylation to methionine. Additionally we are shipping MTHFR Antibodies (95) and MTHFR Kits (16) and many more products for this protein.
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Study demonstrated that maternal MTHFR deficiency (i.e., in utero MTHFR deficiency) and early life exposure to vigabatrin separately and together alter the levels of proteins in the glutamatergic synapse
Mildly hyperhomocysteinemic Mthfr+/- mice demonstrate reduced ganglion cell function, thinner NFL (show NEFL Proteins), and mild vasculopathy by 24 weeks.
DNA methylation (show HELLS Proteins) patterns in undifferentiated spermatogonia are relatively stable in culture over time under conditions of altered methionine and MTHFR levels.
Data from Mthfr knockout mice (in homozygous/heterozygous matings) suggest that maternal genotype contributes to sensitivity to arsenic as embryotoxin (i.e., genetic predisposition to fetal resorption/congenital malformation in arsenic poisoning).
our results support an interaction between mild neonatal stress, the MTHFR genotype and sex
investigation of Mthfr regulation in an in vivo mouse model revealed temporal- and tissue-specific regulation that supports important roles for MTHFR in the developing embryo, and in postnatal brain and male reproductive tissues
A possible mechanism for the epigenetic involvement of Mthfr deficiency is proposed in the gender-dependent regulation of proteins associated with plasticity of the excitatory synapse.
These results showed that methylenetetrahydrofolate reductase deficiency impairs endothelial progenitor cell formation and increases endothelial progenitor cell senescence by endothelial nitric oxide synthase (show NOS3 Proteins) uncoupling and downregulation of SIRT1 (show SIRT1 Proteins).
Variable presentation of MTHFR deficiency in different genetic backgrounds; plasma homocysteine is not a predictor of severity.
Newborn reflex development was slightly influenced by Mthfr +/- genotype and by the combination genotype and the neonatal vigabatrin (GVG) administration, in a sex-independent manner. Females presented attenuated anxiety due to Mthfr +/- genotype and GVG.
MTHFR C667T loci polymorphism may affect atherosclerosis by regulating genome methylation level.
MTHFR C677T mutation was the most common cause of primary Budd-Chiari syndrome.
The MTHFR 1298 CC, AC and ACE (show ACE Proteins) DD genotypes were associated with diabetic retinopathy and diabetic polyneuropathy.
The combination of MTHFR, DRD3 (show DRD3 Proteins) and MDR1 polymorphisms associated with a slow ATV (show NBN Proteins) metabolizer phenotype
Review/Meta-analysis: MTHFR C677T variants may influence diabetic nephropathy risk in Chinese population.
Findings indicate that the homozygous mutant for 677TT of methylenetetrahydrofolate reductase (MTHFR) gene is associated with the risk of hypertension in Morocco.
Both parameters indicate a better tumor prognosis when the MTHFR 677T variant is present
combination of FVL (show F5 Proteins) and MTHFR mutation related to the risk of recurrent fetal death and habitual abortion
The most marked loss of DNA methylation (show HELLS Proteins) was found in sperm from patients homozygous for the methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism
A meta-analysis of 38 studies showed that the carriers of the MTHFR 677C-->T variation were more likely to increase the risk of ischemic stroke susceptibility in all-over pooled population, including Asian and European, but not in African populations.
The protein encoded by this gene catalyzes the conversion of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate, a co-substrate for homocysteine remethylation to methionine. Genetic variation in this gene influences susceptibility to occlusive vascular disease, neural tube defects, colon cancer and acute leukemia, and mutations in this gene are associated with methylenetetrahydrofolate reductase deficiency.
, 5,10-methylenetetrahydrofolate reductase (NADPH)
, methylenetetrahydrofolate reductase (NAD(P)H)
, methylenetetrahydrofolate reductase-like
, methylenetetrahydrofolate reductase