ELISA/assay

Cholinergic Receptor, Nicotinic, Alpha 1 (CHRNa1) ELISA Kit

MBS2023548

48-Strip-Wells

515 USD

ELISA Kit

Cholinergic Receptor, Nicotinic, Alpha 1 (CHRNa1) ELISA Kit

Cholinergic Receptor, Nicotinic, Alpha 1 (CHRNa1)

CHR-NA1; N-AChRA1; NAChRA1; ACHRA; ACHRD; CMS2A; FCCMS; SCCMS; Acetylcholine receptor subunit alpha; N-AChR-A1; Neuronal Acetylcholine Receptor Alpha 1,Muscle

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

CHRNa1

CHRNA1; CHRNA1; ACHRA; ACHRD; CHRNA; CMS1A; CMS1B; CMS2A; FCCMS; SCCMS; ACHRA; CHNRA

ACHA_HUMAN

Human

457

This assay has high sensitivity and excellent specificity for detection of Cholinergic Receptor, Nicotinic, Alpha 1 (CHRNa1). No significant cross-reactivity or interference between Cholinergic Receptor, Nicotinic, Alpha 1 (CHRNa1) and analogues was observed.

For unopened kit: All the reagents should be kept according to the labels on vials. The Standard, Detection Reagent A, Detection Reagent B and the 96-well strip plate should be stored at -20 degree C upon receipt while the others should be at 4 degree C. For opened kit: When the kit is opened, the remaining reagents still need to be stored according to the above storage condition. Besides, please return the unused wells to the foil pouch containing the desiccant pack, and reseal along entire edge of zip-seal. The stability of kit is determined by the loss rate of activity. The loss rate of this kit is less than 5% within the expiration date under appropriate storage condition. To minimize extra influence on the performance, operation procedures and lab conditions, especially room temperature, air humidity, incubator temperature should be strictly controlled. It is also strongly suggested that the whole assay is performed by the same operator from the beginning to the end.

Samples: Tissue homogenates, Cell lysates and other biological fluids. Assay Type: Sandwich. Detection Range: 0.781-50ng/mL. Sensitivity: Typically less than 0.29ng/mL.

Precision: Intra-assay Precision (Precision within an assay): 3 samples with low, middle and high level Cholinergic Receptor, Nicotinic, Alpha 1 (CHRNa1) were tested 20 times on one plate, respectively. Inter-assay Precision (Precision between assays): 3 samples with low, middle and high level Cholinergic Receptor, Nicotinic, Alpha 1 (CHRNa1) were tested on 3 different plates, 8 replicates in each plate. CV(%) = SD/meanX100 . Intra-Assay: CV<10% . Inter-Assay: CV<12% . Assay Procedure Summary: 1. Prepare all reagents, samples and standards;. 2. Add 100uL standard or sample to each well. Incubate 2 hours at 37 degree C;. 3. Aspirate and add 100uL prepared Detection Reagent A. Incubate 1 hour at 37 degree C;. 4. Aspirate and wash 3 times;. 5. Add 100uL prepared Detection Reagent B. Incubate 30 minutes at 37 degree C;. 6. Aspirate and wash 5 times;. 7. Add 90uL Substrate Solution. Incubate 15-25 minutes at 37 degree C;. 8. Add 50uL Stop Solution. Read at 450nm immediately.

Principle of the Assay: The test principle applied in this kit is Sandwich enzyme immunoassay. The microtiter plate provided in this kit has been pre-coated with an antibody specific to Cholinergic Receptor, Nicotinic, Alpha 1 (CHRNa1). Standards or samples are then added to the appropriate microtiter plate wells with a biotin-conjugated antibody specific to Cholinergic Receptor, Nicotinic, Alpha 1 (CHRNa1). Next, Avidin conjugated to Horseradish Peroxidase (HRP) is added to each microplate well and incubated. After TMB substrate solution is added, only those wells that contain Cholinergic Receptor, Nicotinic, Alpha 1 (CHRNa1), biotin-conjugated antibody and enzyme-conjugated Avidin will exhibit a change in color. The enzyme-substrate reaction is terminated by the addition of sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450nm 10nm. The concentration of Cholinergic Receptor, Nicotinic, Alpha 1 (CHRNa1) in the samples is then determined by comparing the O.D. of the samples to the standard curve.

119631533

EAX11128.1

P02708

51,839 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.; Membrane protein, integral; Channel, ligand-gated; Channel, cation. 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: 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; Multiple Pterygium Syndrome, Lethal Type; Myasthenic Syndrome, Congenital, Slow-channel

48-Strip-Wells

515 USD

96-Strip-Wells

695

5x96-Strip-Wells

2685

10x96-Strip-Wells

4850