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Ganglion cell loss and vasculopathy observed in Mthfr+/- and Cbs (show CBS ELISA Kits)+/- 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 ELISA Kits), and mild vasculopathy by 24 weeks.
DNA methylation (show HELLS ELISA Kits) 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 ELISA Kits) uncoupling and downregulation of SIRT1 (show SIRT1 ELISA Kits).
Mutations in the genes involved in the folate pathway had an important role in the etiology of birth defects. MTHFR C677T polymorphism is associated with Secundum Atrial Septal Defects.
Nominally significant parental genetic effects were found between the SNPs rs11191548 (CYP17A1 (show CYP17A1 ELISA Kits)) (paternal, beta = 2.78+/-1.49, P = 6.1x10-2 for SBP (show SHBG ELISA Kits) and beta = 3.60+/-1.24, P = 3.7x10-3 for DBP (show GC ELISA Kits)), rs17367504 (MTHFR) (paternal, beta = 2.42+/-0.93, P = 9.3x10-3 for SBP (show SHBG ELISA Kits) and beta = 1.89+/-0.80, P = 1.8x10-2 for DBP (show GC ELISA Kits) and maternal, beta = -1.32+/-0.60, P = 2.9x10-2 and beta = -1.97+/-0.77, P = 1.0x10-2, for SBP (show SHBG ELISA Kits) and DBP (show GC ELISA Kits) respecti...
We identified 16 studies reporting Methotrexate efficacy in 2373 RA cases, and 25 studies reporting Methotrexate toxicity in 4063 Rheumatoid Arthritis cases. The pooled data analysis indicated that the MTHFR C677T polymorphism was associated with increased toxicity, but not efficacy, of Methotrexate in Rheumatoid Arthritis patients.
Studied methylenetetrahydrofolate reductase (MTHFR) polymorphisms on susceptibility to human papilloma virus infection and cervical cancer; results suggest that heterozygous 677CT genotypes and homozygous mutant 677TT in MTHFR polymorphisms are associated with reducing the risk of cervical cancer. .
Results suggest that the combination of the ADORA2A (show ADORA2A ELISA Kits) rs2298383TT and MTHFR 1298AC-677CT genotypes might lead to a low risk of nodule formation in patients treated with methotrexate.
The TT genotype and T allele of MTHFR C677Tmay confer a protective effect on disease progression to hepatocellular carcinoma in hepatitis B-infected individuals, especially among male patients, in a population with a high prevalence of this genetic marker.
meta-analysis confirms that there is a conclusive association between maternal MTHFR C677T polymorphism and preterm birth (PTB (show PTBP1 ELISA Kits)) as well as low birth weight (LBW) risk and indicates null significant association between neonatal MTHFR C677T polymorphism with PTB (show PTBP1 ELISA Kits) or LBW
The results did not indicate any correlation between global DNA methylation (show HELLS ELISA Kits) and MTHFR A1298C, C677T polymorphisms.
results demonstrated that the offspring and maternal genotypes for MTHFR c.677C>T variant are strongly associated with non-syndromic cleft lip with or without cleft palate in this Chilean population
This is the first study associating the minor (G) allele of the rs17367504 SNP within the MTHFR gene with a protective effect on preeclampsia, and in doing so identifying a possible pleiotropic protective effect on preeclampsia and hypertension.
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