Acetylcholinesterase (AChE) Antibody

Product specifications

Primary Antibodies

Target: Acetylcholinesterase (AChE)
Immunogen: abx269634 - C-Terminus: QFDHYSKQDRCSDL

Goat

Human

Concentration: 0.5 mg/ml

P-ELISA: 1/32000, WB: 0.3-1 µg/ml, IF/ICC: 10 µg/ml, FCM: 10 µg/ml. Optimal dilutions/concentrations should be determined by the end user.

Polyclonal

Unconjugated

IgG

Purified from goat serum by ammonium sulphate precipitation followed by antigen affinity chromatography using the immunizing peptide.

200 µl

Liquid

P-ELISA, WB, IF/ICC, FCM

Tris saline, pH 7.3, containing 0.02% sodium azide and 0.5% bovine serum albumin.

Shipped within 5-10 working days.

Aliquot and store at -20°C. Avoid repeated freeze/thaw cycles.

No

43

NP_000656.1, NP_001269378.1

YT,ACEE,ARACHE,N-ACHE

Antibody anti-AChE

RUO

THIS PRODUCT IS FOR RESEARCH USE ONLY. NOT FOR USE IN DIAGNOSTIC, THERAPEUTIC OR COSMETIC PROCEDURES. NOT FOR HUMAN OR ANIMAL CONSUMPTION.

Descripción

Acetylcholinesterase (AChE) is an enzyme that plays a critical role in the nervous system by breaking down the neurotransmitter acetylcholine. AChE is a globular protein, typically found as a tetramer composed of four subunits. Each subunit contains a catalytic site responsible for the enzymatic breakdown of acetylcholine. Acetylcholine is involved in transmitting signals across synapses, which are the gaps between nerve cells. After acetylcholine has transmitted its signal, AChE rapidly breaks it down into its constituent parts: choline and acetate. This breakdown process is crucial for terminating the signal transmission and allowing the nerve cell to return to its resting state . AChE is found primarily at cholinergic synapses, where acetylcholine is released as a neurotransmitter. These synapses are abundant in the central nervous system (CNS) and the peripheral nervous system (PNS). At neuromuscular junctions, AChE is particularly important for allowing muscles to relax after contraction. When a motor neuron releases acetylcholine to signal muscle contraction, AChE quickly degrades the acetylcholine, allowing the muscle to relax. AChE activity can be regulated through various mechanisms, including gene expression, post-translational modifications, and interactions with other proteins. Dysregulation of AChE activity has been implicated in various neurological disorders, including Alzheimer's disease and myasthenia gravis.

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