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anti-Rat (Rattus) MTRR Antikörper:
anti-Mouse (Murine) MTRR Antikörper:
anti-Human MTRR Antikörper:
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Human Monoclonal MTRR Primary Antibody für ELISA, WB - ABIN561873
Guise, Abbattista, Tipparaju, Lambie, Su, Li, Wilson, Dachs, Patterson: Diflavin oxidoreductases activate the bioreductive prodrug PR-104A under hypoxia. in Molecular pharmacology 2011
Cow (Bovine) Polyclonal MTRR Primary Antibody für IHC, WB - ABIN2787324
Richard, Desviat, Ugarte, Pérez: Oxidative stress and apoptosis in homocystinuria patients with genetic remethylation defects. in Journal of cellular biochemistry 2012
The Mtrr genotype of either maternal grandparent dictates the developmental potential of their wild-type grandprogeny. These effects are associated with altered DNA methylation (zeige HELLS Antikörper) 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.
Genotypes of transcobalamin 2 (TCN2 (zeige TCN2 Antikörper)) rs1801198, methionine synthase (MTR (zeige MTR Antikörper)) rs1805087, methionine synthase reductase (MTRR) rs1801394, and methylene tetrahydrofolate reductase (MTHFR (zeige MTHFR Antikörper)) 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 (zeige ARSD Antikörper) 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 (zeige MTR Antikörper).
The risk factors noted for congenital heart disease in children were presence of MTHFR (zeige MTHFR Antikörper) C677-->T among children and their mothers and MTRR A66-->G among mothers.
Methylene tetrahydrofolate reductase (MTHFR (zeige MTHFR Antikörper)) C677T, 5-methyltetrahydrofolate homocysteine methyltransferase (MTR (zeige MTR Antikörper)) A2756G and 5- methyltetrahydrofolate homocysteine methyltransferase reductase (MTRR) A66G were shown to be positively associatiated with homocysteine, while nonvegetarian diet, serine hydroxymethyltransferase 1 (SHMT1 (zeige SHMT1 Antikörper)) C1420T and TYMS (zeige TYMS Antikörper) 5'-UTR (zeige UTS2R Antikörper) 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 (zeige MTHFR Antikörper) 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 (zeige MTHFR Antikörper) 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 (zeige MTHFR Antikörper), MTR (zeige MTR Antikörper), MTRR, and TCN2 (zeige TCN2 Antikörper) 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 (zeige RFC1 Antikörper) G80A, and MTHFR (zeige MTHFR Antikörper) C677T and A1298C.
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.
, 5-methyltetrahydrofolate-homocysteine methyltransferase
, methionine synthase reductase
, [methionine synthase]-cobalamin methyltransferase (cob(II)alamin reducing)
, methionine synthase reductase, mitochondrial
, 5-methyltetrahydrofolate-homocysteine methyltransferase reductase
, 5-methyltetrahydrofolate--homocysteine methyltransferase