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anti-Rat (Rattus) MTRR Anticorps:
anti-Mouse (Murine) MTRR Anticorps:
anti-Human MTRR Anticorps:
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Cow (Bovine) Polyclonal MTRR Primary Antibody pour IHC, WB - ABIN2787324
Richard, Desviat, Ugarte, Pérez: Oxidative stress and apoptosis in homocystinuria patients with genetic remethylation defects. dans Journal of cellular biochemistry 2012
Human Monoclonal MTRR Primary Antibody pour ELISA, WB - ABIN561873
Guise, Abbattista, Tipparaju, Lambie, Su, Li, Wilson, Dachs, Patterson: Diflavin oxidoreductases activate the bioreductive prodrug PR-104A under hypoxia. dans Molecular pharmacology 2011
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.
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.
Methylene tetrahydrofolate reductase (MTHFR) C677T, 5-methyltetrahydrofolate homocysteine methyltransferase (MTR) A2756G and 5- methyltetrahydrofolate homocysteine methyltransferase reductase (MTRR) A66G were shown to be positively associatiated with homocysteine, while nonvegetarian diet, serine hydroxymethyltransferase 1 (SHMT1) C1420T and TYMS 5'-UTR 28 bp tandem repeat exhibited negative association with homocysteine.
Our results suggest an association between underweight and early childhood caries; in addition it is suggested that MTRR is a common genetic risk factor for early childhood caries and underweight
Results of this study showed that the MTRR rs1801394 alone or together with the MTHFR rs1801133 is not a risk factor for colorectal cancer in Iranian population.
higher frequency of 66GG genotype and 66G allele of MTRR 66A > G polymorphism observed in the women with pre-eclampsia compared to control group
In either maternal or paternal group, the MTHFR 677C>T polymorphism was independently related to fetal non-VSD, while the MTRR 66A>G polymorphism was independently related to fetal VSD.
tagSNPs in MTHFR, MTR, MTRR, and TCN2 were not associated with NSCLP in our study, but continued exploration, including allele frequency of various populations and molecular mechanism of the gene-gene interactions of the genes, may provide additional insight into NSCLP.
in this study, we did not find any significant associations between Rheumatoid Arthritis or Rheumatoid Arthritis characteristics such as activity disease and polymorphisms MTRR A66G, RFC1 G80A, and MTHFR C677T and A1298C.
Common polymorphisms in MTHFR, methionine synthase and cystathione beta lyase genes have no role in premature acute myocardial infarction in Pakistani population.
An association between the MTRR A66G polymorphism and LC ( p = 0.042) was found. In addition, this allele was observed more frequently in smokers compared to nonsmokers ( p = 0.030). In contrast, the distribution of the MTR 2756A>G and the MTRR 524 C> T allele frequencies were similar in the subject cases and controls.
Meta-analysis suggests that MTRR 66A>G polymorphism may be associated with oligoasthenozoospermia risk.
Study in Egyptian children showed that MTRR A66G and C524T polymorphisms were associated with a higher congenital heart diseases risk in the homozygote comparison of wild and mutant genotypes and also in heterozygote and mutant comparison.
Our findings suggest that individuals with the MTHFR 677TT or MTRR 66AG/GG genotypes are more susceptible to the detrimental effect of being overweight/obesity on Type 2 Diabetes Mellitus
The MTR A2756G, MTRR A66G, MTHFR C677T and MTHFR A1298C polymorphisms were assessed. MTR A2756G, MTRR A66G, and MTHFR C677T gene polymorphisms were associated with the risk of NSCL/P (all p < 0.05). Logistic regression analysis revealed that MTR A2756G, MTR RA66G, and MTHFR C667T might increase the risk of Nonsyndromic Cleft Lip/Palate
study widens the clinical, molecular, metabolic, and cytological knowledge of deficiency MTRR enzyme.
The present study suggests that the G allele of MTR A2756G polymorphism is associated with an increased risk of autism.
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