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In genotypic combination analysis considering PEMT (show PEMT Proteins) -744GG/CHDH (show CHDH Proteins) +432GG/BHMT +742GG as the reference combination, PEMT (show PEMT Proteins) -744GC/CHDH (show CHDH Proteins) +432GG/BHMT +742GG genotypic combination was significantly higher in mothers of a down syndrome child compared with that in control mothers with an odds ratio of 2.061 (95% CI: 1.10-3.86, P=0.0342).
It was concluded that during pregnancy, the BHMT pathway is affected by folate status and by the variant BHMT c.716A allele.
low BHMT expression is correlated with aggressive malignant phenotype of HCC (show FAM126A Proteins). Our data indicate that BHMT may serve as a novel prognostic marker for HCC (show FAM126A Proteins).
The faster evolutionary rate of BHMT2 (show BHMT2 Proteins) overall suggests that selective constraints were reduced relative to BHMT.
Multiple SNPs in BHMT and BHMT2 (show BHMT2 Proteins) were identified to be associated with the occurrence of infant obstructive heart defects and interaction effects with maternal use of folic acid supplements.
Data suggest BHMT is activated by binding of potassium ions; role of potassium ions in BHMT appears to be structural; potassium ions facilitate specific binding of substrate homocysteine (rather than substrate betaine) to active site of the enzyme.
Study suggests BHMT holds considerable potential as a blood biomarker for acute liver injury.
Women harboring the single nucleotide polymorphism BHMT 742G>A have a decreased risk of a Down Syndrome pregnancy.
Known common single-nucleotide polymorphisms in MTRR (show MTRR Proteins) and BHMT genes may not be significant risk factors for cororonary artery disease.
Our study suggests that the polymorphism BHMT G742A may modulate the Down syndrome risk in Brazilian mothers.
These findings indicate that greater synthesis of phosphatidylcholine (show SGMS1 Proteins) and antioxidants contribute to the better performance and immuno-metabolic status in methionine-supplemented cows.
BHMT expression is robustly regulated by taurine.
It was concluded that the BHMT pathway is a major route for the elimination of Hcy in mice and that the methionine synthase (show MTR Proteins) pathway has little excess capacity to methylate the Hcy that accumulates when the BHMT pathway is blocked.
mouse blastocysts are unusual in being able to generate AdoMet (show MAT1A Proteins) not only by the ubiquitous folate-dependent mechanism but also from betaine metabolized by BHMT
a role for BHMT in energy homeostasis.
BHMT has an important role in Hcy, choline, and one-carbon homeostasis
The BHMT/betaine system directly protects hepatocytes from homocysteine-induced injury but not tunicamycin-induced injury, including an endoplasmic reticulum stress response, lipid accumulation, and cell death.
function for Bhmt involving modulation of Shh (show SHH Proteins) signaling to control beta-cell development.
This gene encodes a cytosolic enzyme that catalyzes the conversion of betaine and homocysteine to dimethylglycine and methionine, respectively. Defects in this gene could lead to hyperhomocyst(e)inemia, but such a defect has not yet been observed.
betaine--homocysteine S-methyltransferase 1
, betaine-homocysteine methyltransferase