Acetylcholine, ELISA Kit

For Research Use Only. Not for use in diagnostic procedures.

Store all reagents at 2-8 degree C

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Small volumes of ACH elisa kit vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

MBS030036 is a ready-to-use microwell, strip-or-full plate ELISA (enzyme-linked immunosorbent assay) Kit for analyzing the presence of the Acetylcholine (ACH) ELISA Kit target analytes in biological samples. The concentration gradients of the kit standards or positive controls render a theoretical kit detection range in biological research samples containing ACH. The ELISA analytical biochemical technique of the MBS030036 kit is based on ACH antibody-ACH antigen interactions (immunosorbency) and an HRP colorimetric detection system to detect ACH antigen targets in samples. The ELISA Kit is designed to detect native, not recombinant, ACH. Appropriate sample types may include undiluted body fluids and/or tissue homogenates, secretions. Quality control assays assessing reproducibility identified the intra-assay CV (%) and inter-assay CV(%).

54,546 Da

cholinergic receptor, nicotinic, alpha 1 (muscle)

acetylcholine receptor subunit alpha; nicotinic cholinergic receptor alpha 1; muscle nicotinic acetylcholine receptor; nicotinic acetylcholine receptor alpha subunit; acetylcholine receptor, nicotinic, alpha 1 (muscle); cholinergic receptor, nicotinic, alpha polypeptide 1 (muscle)

Acetylcholine receptor subunit alpha

ACHRA; CHNRA  [Similar Products]

ACHA_HUMAN

The muscle acetylcholine receptor consiststs of 5 subunits of 4 different types: 2 alpha subunits and 1 each of the beta, gamma, and delta subunits. This gene encodes an alpha subunit that plays a role in acetlycholine binding/channel gating. Alternatively spliced transcript variants encoding different isoforms have been identified. [provided by RefSeq, Nov 2012]

nAChRA1: After binding acetylcholine, the AChR responds by an extensive change in conformation that affects all subunits and leads to opening of an ion-conducting channel across the plasma membrane. Defects in CHRNA1 are a cause of multiple pterygium syndrome lethal type (MUPSL). Multiple pterygia are found infrequently in children with arthrogryposis and in fetuses with fetal akinesia syndrome. In lethal multiple pterygium syndrome there is intrauterine growth retardation, multiple pterygia, and flexion contractures causing severe arthrogryposis and fetal akinesia. Subcutaneous edema can be severe, causing fetal hydrops with cystic hygroma and lung hypoplasia. Oligohydramnios and facial anomalies are frequent. The alpha subunit is the main focus for antibody binding in myasthenia gravis. Myasthenia gravis is characterized by sporadic muscular fatigability and weakness, occurring chiefly in muscles innervated by cranial nerves, and characteristically improved by cholinesterase-inhibiting drugs. Defects in CHRNA1 are a cause of congenital myasthenic syndrome slow-channel type (SCCMS). SCCMS is the most common congenital myasthenic syndrome. Congenital myasthenic syndromes are characterized by muscle weakness affecting the axial and limb muscles (with hypotonia in early-onset forms), the ocular muscles (leading to ptosis and ophthalmoplegia), and the facial and bulbar musculature (affecting sucking and swallowing, and leading to dysphonia). The symptoms fluctuate and worsen with physical effort. SCCMS is caused by kinetic abnormalities of the AChR, resulting in prolonged endplate currents and prolonged AChR channel opening episodes. Defects in CHRNA1 are a cause of congenital myasthenic syndrome fast-channel type (FCCMS). FCCMS is a congenital myasthenic syndrome characterized by kinetic abnormalities of the AChR. In most cases, FCCMS is due to mutations that decrease activity of the AChR by slowing the rate of opening of the receptor channel, speeding the rate of closure of the channel, or decreasing the number of openings of the channel during ACh occupancy. The result is failure to achieve threshold depolarization of the endplate and consequent failure to fire an action potential. Belongs to the ligand-gated ion channel (TC 1.A.9) family. Acetylcholine receptor (TC 1.A.9.1) subfamily. Alpha- 1/CHRNA1 sub-subfamily. 2 isoforms of the human protein are produced by alternative splicing.

Protein type: Receptor, misc.; Channel, cation; Membrane protein, multi-pass; Channel, ligand-gated; Membrane protein, integral

Chromosomal Location of Human Ortholog: 2q31.1

Cellular Component: nicotinic acetylcholine-gated receptor-channel complex; postsynaptic membrane; cell surface; plasma membrane; neuromuscular junction; cell junction

Molecular Function: acetylcholine receptor activity; ion channel activity; nicotinic acetylcholine-activated cation-selective channel activity; acetylcholine binding

Biological Process: skeletal muscle contraction; muscle maintenance; synaptic transmission; regulation of membrane potential; transport; neuromuscular process; generation of action potential; neuromuscular synaptic transmission; skeletal muscle growth; signal transduction; musculoskeletal movement; neuromuscular junction development

Disease: Myasthenic Syndrome, Congenital, Fast-channel; Myasthenic Syndrome, Congenital, Slow-channel; Multiple Pterygium Syndrome, Lethal Type

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