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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 95 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.
Findings indicate that the homozygous mutant for 677TT of methylenetetrahydrofolate reductase (MTHFR) gene is associated with the risk of hypertension in Morocco.
Both parameters indicate a better tumor prognosis when the MTHFR 677T variant is present
combination of FVL (show F5 Antibodies) and MTHFR mutation related to the risk of recurrent fetal death and habitual abortion
The most marked loss of DNA methylation (show HELLS Antibodies) was found in sperm from patients homozygous for the methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism
A meta-analysis of 38 studies showed that the carriers of the MTHFR 677C-->T variation were more likely to increase the risk of ischemic stroke susceptibility in all-over pooled population, including Asian and European, but not in African populations.
MTHFR C677T polymorphism is associated with rheumatic heart disease in patients with mitral valve lesions, perhaps via an homocysteine-mediated cytokine effect.
Our results suggest that the MTHFR A1298C polymorphism might be related to increased risk of HCC (show FAM126A Antibodies) in Asians.
the results of our study indicated that the MTHFR C677T gene polymorphism could play a role in the development of breast cancer.
The C677 T polymorphism of the MTHFR did not associate with acquired-risk factors so it can be suppose that it is an independent risk factor.
Our meta-analysis showed that the MTHFR C677T mutation was a risk factor for male infertility in both azoospermia and oligoasthenoteratozoospermia patients, especially in Asian population
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