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Ganglion cell loss and vasculopathy observed in Mthfr+/- and Cbs (show CBS Proteins)+/- mouse retinas may be milder than expected, not because of compensatory increases of enzymes in remethylation/transsulfuration pathways, but because downstream transsulfuration pathway products GSH, taurine, and H2S are maintained at robust levels.
In summary, high folate intake during pregnancy leads to pseudo-MTHFR deficiency, disturbed choline/methyl metabolism, embryonic growth delay and memory impairment in offspring. These findings highlight the unintended negative consequences of supplemental folic acid.
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).
A possible association was detected betweengermline MTHFR 677 C>T and 1298 A>C genotypes and psoriasis risk in a Turkish population.
T allele of MTHFR C677T is accompanied by the highest susceptibility to infertility and increased serum total homocysteine levels. Sufficient consumption of vitamins B9 and B12 (show NDUFB3 Proteins) influences sperm parameters of men with different MTHFR polymorphisms, especially genotypes with T allele.
Results showed that among type 2 diabetic patients, the combined effect of MTHFR TT and EPHX2 (show EPHX2 Proteins) GG or GA + AA genotype has a higher risk of ischemic stroke compared with the control group.
Data suggested that the polymorphism in miR (show MLXIP Proteins)-149 played an important role in the development of NAFLD via altering the expression of miR (show MLXIP Proteins)-149 as well as its target, MTHFR.
tagSNPs in MTHFR, MTR (show MTR Proteins), MTRR (show MTRR Proteins), and TCN2 (show TCN2 Proteins) were not associated with NSCLP in our study, but continued exploration, including allele frequency of various populations and molecular mechanism of the gene-gene interactions of the genes, may provide additional insight into NSCLP.
This study is the first to show that the C677T variant in methylene-tetrahydrofolate reductase modulates associations between blood-based and CSF (show CSF2 Proteins) biomarkers of neurodegeneration.
both rs1801133 and rs1801131 within MTHFR gene were associated with ALL risk in Chinese children, we also found a significant gene-gene interaction between MTHFR C677T and A1298C polymorphisms, and participants with rs1801133 - CT or TT and rs1801131 - AC or CC genotype have the lowest ALL risk, but we did not find significant haplotype combination in the haplotype analysis.
present meta-analysis strongly suggested a significant association of the MTHFR C677T polymorphism with autism.
our study demonstrates a sex difference in Hcy concentrations among Brazilian young adults regarding MTHFR C677T-lifestyle interactions that are worsened under conditions of low blood folate. Identification of potentially modifiable factors related to an increase in homocysteine in young adults, especially in those who are genetically susceptible, is important to prevent negative health consequences in the future.
Heterozygous FV Leiden, homozygous PAI-1 4G/4G, heterozygous MTHFR C677T, homozygous MTHFR A1298C, as much as the combined thrombophilic genotypes MTHFR 677T + ACE Iota/D, MTHFR 677T/1298C + ACE D/D, ACE I/D + b-fibrinogen -455 G/A, FV HR2 + b-fibrinogen -455 G/A showed a correlation as risk factors for Recurrent pregnancy loss.
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