METH rabbit pAb

METH rabbit pAb

AO-06-ES14961-50

METH rabbit pAb 50μL

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Antibody Product Overview

ELK.NoES14961
Product nameMETH rabbit pAb
ReactivityHuman; Mouse;Rat
ApplicationsWB
Other name
Size50μL
Unit price ($)148
Human gene ID4548
Human Swiss-ProtQ99707
SourceRabbit
IsotypeIgG
TargetMETH
Fields>>Cysteine and methionine metabolism;>>Selenocompound metabolism;>>One carbon pool by folate;>>Metabolic pathways;>>Biosynthesis of amino acids
Gene nameMTR
Protein nameMETH
Human gene linkView Human Gene
Human Swiss linkView Human Swiss-Prot
Mouse gene ID238505
Mouse gene linkView Mouse Gene
Mouse Swiss-ProtA6H5Y3
Mouse Swiss linkView Mouse Swiss-Prot
Rat gene ID81522
Rat gene linkView Rat Gene
Rat Swiss-ProtQ9Z2Q4
Rat Swiss linkView Rat Swiss-Prot
ImmunogenSynthesized peptide derived from human METH AA range: 1110-1160
SpecificityThis antibody detects endogenous levels of METH at Human/Mouse/Rat
FormulationLiquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
ClonalityPolyclonal
DilutionWB 1:500-2000
PurificationThe antibody was affinity-purified from rabbit serum by affinity-chromatography using specific immunogen.
Concentration1 mg/ml
Storage stability-20°C/1 year
Molecular Weight (Da)139kD
Observed band (KD)
BackgroundThis gene encodes the 5-methyltetrahydrofolate-homocysteine methyltransferase. This enzyme, also known as cobalamin-dependent methionine synthase, catalyzes the final step in methionine biosynthesis. Mutations in MTR have been identified as the underlying cause of methylcobalamin deficiency complementation group G. Alternatively spliced transcript variants encoding distinct isoforms have been found for this gene. [provided by RefSeq, May 2014],
Functioncatalytic activity:5-methyltetrahydrofolate + L-homocysteine = tetrahydrofolate + L-methionine.,cofactor:Binds 1 zinc ion per subunit.,cofactor:Methylcobalamin (MeCBL).,disease:Defects in MTR are the cause of methylcobalamin deficiency type G (cblG) [MIM:250940]; also known as homocystinuria-megaloblastic anemia complementation type G. It is an autosomal recessive inherited disease that causes mental retardation, macrocytic anemia, and homocystinuria. Mild deficiency in MS activity could be associated with mild hyperhomocysteinemia, a risk factor for cardiovascular disease and possibly neural tube defects. MS mutations could also be involved in tumorigenesis.,disease:Defects in MTR may be a cause of susceptibility to folate-sensitive neural tube defects (folate-sensitive NTD) [MIM:601634]. The most common NTDs are open spina bifida (myelomeningocele) and anencephaly. Genetic defects in M
Subcellular locationCytoplasm .
ExpressionWidely expressed. Expressed at the highest levels in pancreas, heart, brain, skeletal muscle and placenta (PubMed:8968737, PubMed:8968735). Expressed at lower levels in lung, liver and kidney (PubMed:8968737, PubMed:8968735).

Additional Images

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Western blot analysis of lysates from 293T cells, primary antibody was diluted at 1:1000, 4°over night
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: AO-06-ES14961-50
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Hurry! only 10 items left in stock.

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