Butyrylcholinesterase (BCHE) Antibody – Rabbit Polyclonal

This gene encodes a cholinesterase enzyme and member of the type-B carboxylesterase/lipase family of proteins. The encoded enzyme exhibits broad substrate specificity and is involved in the detoxification of poisons including organophosphate nerve agents and pesticides, and the metabolism of drugs including cocaine, heroin and aspirin. Humans homozygous for certain mutations in this gene exhibit prolonged apnea after administration of the muscle relaxant succinylcholine. [provided by RefSeq, Jul 2016]

BCHE: Esterase with broad substrate specificity. Contributes to the inactivation of the neurotransmitter acetylcholine. Can degrade neurotoxic organophosphate esters. Defects in BCHE are the cause of butyrylcholinesterase deficiency (BChE deficiency). BChE deficiency is a metabolic disorder characterized by prolonged apnoea after the use of certain anesthetic drugs, including the muscle relaxants succinylcholine or mivacurium and other ester local anesthetics. The duration of the prolonged apnoea varies significantly depending on the extent of the enzyme deficiency. BChE deficiency is a multifactorial disorder. The hereditary condition is transmitted as an autosomal recessive trait. Belongs to the type-B carboxylesterase/lipase family.

Protein type: EC 3.1.1.8; Hydrolase; Nuclear envelope; Secreted; Secreted, signal peptide

Chromosomal Location of Human Ortholog: 3q26.1

Cellular Component: endoplasmic reticulum lumen; extracellular region; membrane; nuclear envelope lumen

Molecular Function: acetylcholinesterase activity; amyloid-beta binding; catalytic activity; choline binding; cholinesterase activity; enzyme binding; hydrolase activity, acting on ester bonds; identical protein binding

Biological Process: choline metabolic process; cocaine metabolic process; learning; negative regulation of cell proliferation; negative regulation of synaptic transmission; neuroblast differentiation; response to alkaloid; response to drug; response to folic acid; response to glucocorticoid stimulus