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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 103 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.
The prognostic index comprising XRCC1 (show XRCC1 Antibodies) rs25487, ERCC2 (show ERCC2 Antibodies) rs13181, and rs1799793 polymorphisms may be a useful predictor of clinical outcomes in MGC treated with EOF.
The prevalence of factor V G1691A, prothrombin (show F2 Antibodies) G20210A and MTHFR C677T single nucleotide polymorphism among Syrians is 11.5%, 2.5% and 84.5%, respectively.
MTHFR C677T polymorphism, qualitatively, is not a genetic factor for the pathogenesis of psoriasis but could quantitatively reflect the severity of psoriasis to some extent. Meta-analysis.
the studied polymorphisms MTHFR C677T (rs1801133) and MTR (show MTR Antibodies) A2756G (rs1805087) do not contribute to genetic susceptibility to varicose veins in ethnical Russians.
the influence of polymorphisms in methylenetetrahydrofolate reductase (MTHFR-C677T) and apolipoprotein-E (apo-E (show APOE Antibodies)) as risk factors for ischemic stroke patients in south Indian population
Rheumatoid arthritis patients with the MTHFR 677TT genotype had the highest asymmetric dimethylarginine levels, significantly higher than either those patients carrying the MTHFR 677CT or the MTHFR 677CC genotype.
There is an association between variants of the MTHFR gene and hypertension in Cameroonian patients from the South West region.
There were no other associations between single -nucleotide polymorphisms and the efficacy of MTX (show MTX1 Antibodies) treatment. CONCLUSIONS: The MTHFR 677CC and GGH (show GGH Antibodies) 401TT and CT genotypes were associated with a reduction in the number of MTX (show MTX1 Antibodies)-related adverse events.
Frequency of MTHFR risk allele (T) in patients with maternal age <25 years is marginally significant higher than those in cases with maternal age >/=25 years (p = .069) with an OR of 2.7 (95% CI = 0.90-8.07). Conclusions: MTHFR is a common susceptibility factor for gastroschisis in Indonesia.
The association of colorectal adenomas with the rs6983267 variant at 8q24 was considered as 'highly credible', the 'less credible' associations were identified with a further four variants of four independent genes: MTHFR c.677C>T p.A222V(rs1801133), TP53 (show TP53 Antibodies) c.215C>G p.R72P (rs1042522), NQO1 (show NQO1 Antibodies) c.559C>T p.P187S (rs1800566), and NAT1 (show EIF4G2 Antibodies) alleles imputed as fast acetylator genotypes. [meta-analysis]
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