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Hypomorphic Mtrrgt/gt mutation in mice results in late-onset and sex-specific blood defects, including macrocytic anemia.
MTTR-deficient mouse strain exhibits short-term memory impairment and disturbances in brain choline metabolism.
The Mtrr genotype of either maternal grandparent dictates the developmental potential of their wild-type grandprogeny. These effects are associated with altered DNA methylation patterns and two distinct phenotypes: intrauterine growth defects and congenital malformations that are separable through embryo transfer experiments.
Mtrr deficiency adversely impacts reproductive outcomes and cardiac development in mice.
The analysis of MTHFR C677T and MTRR A66G polymorphisms with neural tube defects has demonstrated a significant difference in vitamin B12 levels between recessive and dominant genotypes in case mothers of Tunisian patients.
the rs1801394 SNP in MTRR fulfilled the high association standards. Its minor allele was associated with less improvement than the major allele according to DeltaDAS28 (p = 0.0016), and EULAR response (p = 0.004), with independence of sex, age, baseline DAS28, smoking, seropositivity, concomitant corticosteroid use or previous treatments.
The MTRR A66G polymorphism was only associated with the risk of cervical cancer but not cervical intraepithelial neoplasia.
Analysis of MTR and MTRR Gene Polymorphisms in Chinese Patients With Ventricular Septal Defect.
The methionine synthase reductase (MTRR), TAF4B protein, PIWI protein (PIWIL1) four single nucleotide polymorphisms (SNPs) are not shown to be significantly related with non-obstructive azoospermia (NOA).
There were no differences in distribution of genotypes for the MTR AG and MTR AC polymorphisms between patients with multiple sclerosis and controls
We conclude that abnormal MTRR mRNA expression and the methylation of the MTRR promoter can be used to classify the risk of acute lymphoblastic leukemia (ALL)in children.
These findings indicated that MTRR rs1532268, MTHFR rs1801131 and MTHFR rs1801133 polymorphisms may affect the risk of congenital heart disease in Asians and Caucasians, while the MTRR rs1801394 polymorphism may only affect in risk of congenital heart disease in Asians.
This study verified three SNPs in the MTRR were associated with neural tube defects risk in an independent Chinese population
rs1532268 in MTRR with a minor allele T was significantly associated with increased risk of gastric cancer in Chinese Han population.
combined genotypes of MTHFR 677 CT with MTR 2756 AA and MTHFR 677 CT with MTRR AG added to the potential risk in Chinese Down syndrome mothers
These data show that the processing of cobalamin in cytoplasm occurs in a multiprotein complex composed of at least methionine synthase, methionine synthase reductase, MMACHC and MMADHC.
This meta-analysis indicates that MTHFR C677T, A1298C, and MTRR A66G polymorphisms are the risk factors with susceptibility to male infertility in Asians.
study indicated that SNPs of MTRR have relatively limited or no roles in the genesis of cachexia in patients with gastrointestinal cancers
It can be inferred from the data obtained that folate system genetic variants and mild hyperhomocysteimenia may affect ADHD associated traits by attenuating folate metabolism.
12 articles were included in this study. The pooled results did not reveal a significant association of the MTRR A66G polymorphism (G vs. A: OR = 0.99, 95% CI = 0.82-1.18, p = 0.72) with Nonsyndromic Cleft Lip With or Without Cleft Palate risk
The gene polymorphism of MTRR A66G may not be an independent genetic risk factor in deep venous thrombosis in China.
Genotypes of transcobalamin 2 (TCN2) rs1801198, methionine synthase (MTR) rs1805087, methionine synthase reductase (MTRR) rs1801394, and methylene tetrahydrofolate reductase (MTHFR) rs1801133 were examined in 201 children with Autism Spectrum Disorder and 200 healthy controls from the Han Chinese population. Our results showed no association of all examined SNPs with childhood ASD and its severity.
The genotypes of three women having spina bifida fetuses from two unrelated Chinese families were screened in candidate alleles. A trinucleotide deletion (c.4_6delAGG) was found in the first exon of MTRR only in the affected women, but not in their siblings with healthy babies or in controls. The Arg2del variant's subcellular localization and catalysis was unchanged, but it failed to efficiently activate MTR.
The risk factors noted for congenital heart disease in children were presence of MTHFR C677-->T among children and their mothers and MTRR A66-->G among mothers.
Methionine is an essential amino acid required for protein synthesis and one-carbon metabolism. Its synthesis is catalyzed by the enzyme methionine synthase. Methionine synthase eventually becomes inactive due to the oxidation of its cob(I)alamin cofactor. The protein encoded by this gene regenerates a functional methionine synthase via reductive methylation. It is a member of the ferredoxin-NADP(+) reductase (FNR) family of electron transferases. Patients of the cbl-E complementation group of disorders of folate/cobalamin metabolism are defective in reductive activation of methionine synthase. Alternative splicing of this gene results in multiple transcript variants encoding distinct isoforms.
methionine synthase reductase
, [methionine synthase]-cobalamin methyltransferase (cob(II)alamin reducing)
, methionine synthase reductase, mitochondrial
, 5-methyltetrahydrofolate-homocysteine methyltransferase reductase