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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 results of the present study demonstrated that the frequency of MTHFR C677T (67%) and A1298C (77%) polymorphisms is dramatically high among deep vein thrombosis patients in Central Iranian populations.
Inheritance of variant alleles of A1298C and C677T polymorphisms of MTHFR may boost the risk of NHL. Presence of the variant (T) allele of C677T polymorphism was significantly associated with non-Hodgkin lymphoma risk, and the risk seemed to be more pronounced when at least one variant allele was present in each polymorphic site.
Findings suggested no association between MTHFR gene polymorphisms and susceptibility to hemorrhagic strokes in Moroccan patients. Further investigations should be conducted to elucidate the roles of other gene variants in the pathogenesis of this condition.
study describes 3 cases of severe methotrexate myelopathy associated with the MTHFR C677T polymorphism
MTHFR 1298 A>C polymorphism and, altered homocysteine and vitamin B12 (zeige NDUFB3 Proteine) levels might play a vital role in the precipitation of vitiligo (zeige MITF Proteine).
Significant association between MTHFR C677T polymorphism and number of losses in couples with unexplained recurrent pregnancy loss.
The MTHFR gene C677T C/T+T/T genotypes and T allele increases the risk of Large-artery atherosclerosis and Small-artery occlusion subtypes of ischemic stroke.
Suggest that MTHFR 677 variant confers risk for diabetic neuropathy among Iranian patients with type 2 diabetes.
that in MTHFR polymorphisms, the prevalence of 677CT genotype and T allele in C667T SNP influences susceptibility to migraine with aura (zeige AURKA Proteine) but not to without aura (zeige AURKA Proteine)
MTHFR SNPs are associated with susceptibility to osteoporosis and osteoporotic vertebral compression fractures in postmenopausal 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