ELISA/assay

Rat Acetylcholine ELISA Kit

MBS043949

48-Strip-Wells

435 USD

ELISA Kit

Rat Acetylcholine ELISA Kit

Acetylcholine

acetylcholine receptor subunit alpha isoform a; Acetylcholine receptor subunit alpha; 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); cholinergic receptor, nicotinic, alpha 1 (muscle)

ACH

CHRNA1; CHRNA1; ACHRA; ACHRD; CHRNA; CMS2A; FCCMS; SCCMS; ACHRA; CHNRA

ACHA_HUMAN

Rat

482

No significant cross-reactivity or interference between Rat ACH and analogues was observed.

Store all reagents at 2-8 degree C

Samples: Serum, Plasma, Tissue Homogenate, Feces and Urine. Assay Type: Sandwich. Detection Range: 31.2 nmol/L - 1000 nmol/L. Sensitivity: 5.0 nmol/L.

Intra-assay Precision: Intra-assay CV (%) is less than 15%. Inter-assay Precision: Inter-assay CV (%) is less than 15%. [CV(%) = SD/mean ×100].

Intended Uses: This Quantitative Sandwich ELISA kit is only for in vitro research use only, not for drug, household, therapeutic or diagnostic applications! It is intended to be determinated ACH concentrations in Rat serum, plasma and other body fluids. Using Purified Rat ACH antibody to coat Microelisa Stripplate wells to make solid-phase antibody, then add ACH and ACH antibody which has been labeled with HRP to wells, then the reactants become antibody-antigen-antibody-enzyme complex, after washing completely, add TMB substrate solution, TMB substrate becomes blue color under HRP enzyme-catalyzed, reaction is terminated by the addition of a sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450 nm. The concentration of ACH in the samples is then determined by comparing the O.D. of the samples to the standard curve.

87567783

NP_001034612.1

NM_001039523.2

P02708

54,546 Da

Acetylcholine Binding And Downstream Events Pathway (106535); Activation Of Nicotinic Acetylcholine Receptors Pathway (161027); Effects Of Botulinum Toxin Pathway (138028); ErbB2/ErbB3 Signaling Events Pathway (137955); Highly Calcium Permeable Nicotinic Acetylcholine Receptors Pathway (161029); Highly Calcium Permeable Postsynaptic Nicotinic Acetylcholine Receptors Pathway (161032); Neuroactive Ligand-receptor Interaction Pathway (83053); Neuroactive Ligand-receptor Interaction Pathway (462); Neuronal System Pathway (106513); Neurotransmitter Receptor Binding And Downstream Transmission In The Postsynaptic Cell Pathway (106534)

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: Membrane protein, multi-pass; Receptor, misc.; Channel, cation; Membrane protein, integral; Channel, ligand-gated. Chromosomal Location of Human Ortholog: 2q31.1. Cellular Component: nicotinic acetylcholine-gated receptor-channel complex; postsynaptic membrane; cell surface; plasma membrane; cell junction; neuromuscular junction. Molecular Function: acetylcholine receptor activity; ion channel activity; acetylcholine binding; nicotinic acetylcholine-activated cation-selective channel activity. Biological Process: muscle maintenance; skeletal muscle contraction; synaptic transmission; regulation of membrane potential; transport; neuromuscular process; generation of action potential; neuromuscular synaptic transmission; skeletal muscle growth; musculoskeletal movement; signal transduction; neuromuscular junction development. Disease: Myasthenic Syndrome, Congenital, Fast-channel; Myasthenic Syndrome, Congenital, Slow-channel; Multiple Pterygium Syndrome, Lethal Type

48-Strip-Wells

435 USD

96-Strip-Wells

600