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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 Kits (16) and MTHFR Proteins (4) and many more products for this protein.
Showing 10 out of 100 products:
Human Polyclonal MTHFR Primary Antibody for WB - ABIN1881559
Singh, Singh, Raman: MTHFR A1298C polymorphism and idiopathic male infertility. in Journal of postgraduate medicine 2010
Show all 5 references for ABIN1881559
Human Monoclonal MTHFR Primary Antibody for IF, ELISA - ABIN561866
Forges, Chery, Audonnet, Feillet, Gueant: Life-threatening methylenetetrahydrofolate reductase (MTHFR) deficiency with extremely early onset: characterization of two novel mutations in compound heterozygous patients. in Molecular genetics and metabolism 2010
Show all 3 references for ABIN561866
Human Monoclonal MTHFR Primary Antibody for IHC, ELISA - ABIN969297
Sarecka-Hujar, Zak, Krauze: Carrier-state of two or three polymorphic variants of MTHFR, IL-6 and ICAM1 genes increases the risk of coronary artery disease. in Kardiologia polska 2009
Show all 2 references for ABIN969297
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 Antibodies), and mild vasculopathy by 24 weeks.
DNA methylation (show HELLS Antibodies) 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 Antibodies) uncoupling and downregulation of SIRT1 (show SIRT1 Antibodies).
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.
In Asian populations, a decreased risk of NSCL (show NHLH1 Antibodies)/P was observed in patients presenting the C677T variant at MTHFR gene.
The association between the MTHFR A1298C CC genotype and prostate cancer risk may vary within different populations. (Meta-analysis)
Elite hurdlers, having an unfavorable MTHFR genotype are exposed to increased cardiovascular risk, dependent on alterations of homocysteine and AOPP plasma levels
The MTHFR mutation c.677C>T was present in 17.3% of 400 ischemic stroke patients in Sri (show SRI Antibodies) Lanka. It is the predominant mutation and the only mutation that had patients with the homozygous mutant genotype.
The MTHFR 677 T allele codes a thermolabile and less active enzyme, which is associated with decreased folate and increased homocysteine levels.
The present data showed that FVL (show F5 Antibodies), MTHFR polymorphisms also combined with thrombophilic gene mutations have a strong association with recurrent pregnancy loss.
Mutations in the MTHFR gene were not found to be significantly more frequent in JIA patients intolerant to MTX (show MTX1 Antibodies).
meta-analysis is consistent with MTHFR C677T and MTHFR A1298C polymorphisms not being significantly associated with an increased risk of endometrial cancer
No significant association was found between the MTHFR C677T polymorphism and colorectal cancer.
MTHFR C667T loci polymorphism may affect atherosclerosis by regulating genome methylation level.
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