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Ganglion cell loss and vasculopathy observed in Mthfr+/- and Cbs (zeige CBS Proteine)+/- 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 (zeige NEFL Proteine), and mild vasculopathy by 24 weeks.
DNA methylation (zeige HELLS Proteine) 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 (zeige NOS3 Proteine) uncoupling and downregulation of SIRT1 (zeige SIRT1 Proteine).
The MTHFR gene polymorphism could be an important genetic determinant of baseline DBP (zeige GC Proteine) levels in Chinese essential hypertensive patients.
compared with wild-type genotype CC, patients with CT/TT genotypes had higher incidence of leukopenia, neutropenia, nausea, and fatigue among the non-squamous Non-Small Cell Lung Cancer patients. Therefore, MTHFR C677T polymorphism could be a predictive factor for leukopenia, neutropenia, nausea, and fatigue in non-squamous Non-Small Cell Lung Cancer patients receiving single-agent PEM treatment
The risk factors noted for congenital heart disease in children were presence of MTHFR C677-->T among children and their mothers and MTRR (zeige MTRR Proteine) A66-->G among mothers.
findings suggest that the T-allele-carrying MTHFR C677T genotype or haplotype may reduce the risk of PMODs
Our study did not confirm an association between the MTHFR C677T gene polymorphism and the development of Metabolic Syndrome in polycystic ovary syndrome.
Methylene tetrahydrofolate reductase (MTHFR) C677T, 5-methyltetrahydrofolate homocysteine methyltransferase (MTR (zeige MTR Proteine)) A2756G and 5- methyltetrahydrofolate homocysteine methyltransferase reductase (MTRR (zeige MTRR Proteine)) A66G were shown to be positively associatiated with homocysteine, while nonvegetarian diet, serine hydroxymethyltransferase 1 (SHMT1 (zeige SHMT1 Proteine)) C1420T and TYMS (zeige TYMS Proteine) 5'-UTR 28 bp tandem repeat exhibited negative association with homocysteine.
MTHFR 677 gene polymorphism may be a risk factor for the development of the lichen planus, and to predispose these patients to higher risk of cardiovascular disease.
Treatment with low-dose aspirin, enoxaparin and folic acid was the most effective therapy in women with recurrent miscarriages who carried a C677T MTHFR mutation.
In ALL and NHL patients treated with methotrexate, treatment toxicities and outcome were evaluated. Multivariate analysis showed that DHFR (zeige DHFR Proteine)-1610G/T (OR=0.107, p=0.018) and MTHFR677T alleles (OR=0.12, p=0.026) had a strong protective effect against hematologic toxicity, while DHFR (zeige DHFR Proteine)-1610CC genotype increased this toxicity (OR=9, p=0.045).
we were not able to confirm the association between the polymorphisms of f5, f2, and mthfr and pregnancy loss in Bosnian women
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