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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 (17) and MTHFR Proteins (5) and many more products for this protein.
Showing 10 out of 105 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
Mouse (Murine) Polyclonal MTHFR Primary Antibody for ELISA, WB - ABIN4335975
Fletcher, Kessling: MTHFR association with arteriosclerotic vascular disease? in Human genetics 1998
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.
we examined the association between methylenetetrahydrofolate reductase (MTHFR C677T, rs1801133) and methionine synthase (MTR (show MTR Antibodies) A2756G, rs1805087) polymorphisms and risk for thyroid and breast cancer. We found an association between MTHFR C677T polymorphism and risks to both thyroid (OR = 2.50; 95%CI = 1.15-5.46; P = 0.02) and breast cancer (OR = 2.53; 95%CI = 1.08-5.93; P = 0.03).
Significant interactions were observed among the methylenetetrahydrofolate reductase (MTHFR; C677T; A1298C) and cystathionine-beta-synthase (CBS (show CBS Antibodies); T833C/844ins68, G919A) polymorphisms in the results for homocysteine (Hcy) levels, where heterozygous had higher values.
Among Chinese hypertensive patients without cardiovascular comorbidities, elevated total homocysteine was a significant risk marker for death from all causes, and the association was subject to effect modification by MTHFR genotypes. If confirmed that total homocysteine and MTHFR genotypes may serve as useful biomarkers for mortality risk assessment and targeted intervention
C677T MTHFR gene polymorphism is associated with rheumatoid arthritis (RA) in Egyptians. MTHFR 677TT carriers had higher concentrations of serum homocysteine than did subjects harboring the CC and CT genotypes; presence of 677T allele increases the risk of atherosclerosis in patients with RA, probably due to hyperhomocysteinemia.
The study suggests that the MTHFR C677T and A1298C polymorphisms may have contributed to the risk of polycystic ovary syndrome in the Chinese women investigated
Authors determined whether a polymorphism at the miR (show MLXIP Antibodies)-214 binding site in the 3'-untranslated region (3'-UTR (show UTS2R Antibodies)) of the methylenetetrahydrofolate reductase gene (MTHFR) is associated with susceptibility to esophageal squamous cell carcinoma (ESCC). Data demonstrate that a polymorphism at the miR (show MLXIP Antibodies)-214 binding site in the 3'-UTR (show UTS2R Antibodies) of MTHFR is an ESCC susceptibility SNP in the Chinese population.
both tHcy and the MTHFR C677T gene polymorphism may be important determinants of the incidence of dyslipidemia in Chinese patients with essential hypertension
MDR1 (show TBC1D9 Antibodies) rs1045642 and MTHFR rs1801133 should be considered as diagnostic candidates for the identification of pediatric patients with a high risk of suffering adverse events during Acute Lymphoblastic Leukemia treatment.
meta-analysis: evaluated associations between methylenetetrahydrofolate reductase (MTHFR) gene C677T polymorphism and acute lymphoblastic leukaemia using a more comprehensive updated meta-analysis
Results identified MTHFR variant in a large family with an unknown equinus deformity that is different from variants associated with clubfoot. Bioinformatic analysis showed that this mutation could alter the protein binding region.
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