Mouse Acetylcholinesterase (AchE) ELISA Kit-Sandwich

Acetylcholinesterase swiftly terminates signal transduction at the neuromuscular junction by hydrolyzing acetylcholine released into the synaptic cleft. In mice, acetylcholinesterase serves a broad array of critical functions, including the regulation of neuromuscular junctions, nervous system development, effects in disease models, regulation of the blood system, and use in toxicity studies. AChE is instrumental in the neuromuscular junction (NMJ), regulating neural signal transmission by breaking down acetylcholine (ACh) to end synaptic transmission. AChE binds in an asymmetric form to collagen Q (ColQ) and is anchored to the synaptic cleft's basement membrane. This structure is vital for AChE's normal function, as the absence of ColQ results in a total loss of AChE in the skeletal muscle and heart, causing congenital myasthenic syndrome. Additionally, the tetrameric form of AChE is the primary structural form under physiological conditions, with its active center characteristics enabling efficient acetylcholine hydrolysis.