Reactive species
Human; Mouse;Rat
Antibody type
Polyclonal Antibody
Immunogen
Synthesized peptide derived from human METH AA range: 1110-1160
Specificity
This antibody detects endogenous levels of METH at Human/Mouse/Rat
Constitute
Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
Source
Polyclonal, Rabbit,IgG
Dilution rate
WB 1：500-2000
Purification process
The antibody was affinity-purified from rabbit serum by affinity-chromatography using specific immunogen.
Background
This 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],
Function
catalytic 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
