Key features and details
- Rabbit polyclonal to Nicotinic Acetylcholine Receptor alpha 1/CHRNA1
- Suitable for: ICC/IF
- Reacts with: Human
- Isotype: IgG
Product nameAnti-Nicotinic Acetylcholine Receptor alpha 1/CHRNA1 antibody
See all Nicotinic Acetylcholine Receptor alpha 1/CHRNA1 primary antibodies
DescriptionRabbit polyclonal to Nicotinic Acetylcholine Receptor alpha 1/CHRNA1
Tested applicationsSuitable for: ICC/IFmore details
Species reactivityReacts with: Human
Predicted to work with: Mouse, Rat, Cow, Cat
- ICC/IF: RH-30 cells.
This product was previously labelled as Nicotinic Acetylcholine Receptor alpha 1
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Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle.
Storage bufferpH: 7.20
Preservative: 0.02% Sodium azide
Constituents: 40% Glycerol (glycerin, glycerine), PBS
Concentration information loading...
PurityImmunogen affinity purified
Our Abpromise guarantee covers the use of ab221868 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|ICC/IF||Use a concentration of 0.25 - 2 µg/ml.
Fixation/Permeabilization: PFA/Triton X-100.
FunctionAfter 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.
Tissue specificityIsoform 1 is only expressed in skeletal muscle. Isoform 2 is constitutively expressed in skeletal muscle, brain, heart, kidney, liver, lung and thymus.
Involvement in diseaseDefects in CHRNA1 are a cause of multiple pterygium syndrome lethal type (MUPSL) [MIM:253290]. 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.
Note=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) [MIM:601462]. 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) [MIM:608930]. 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.
Sequence similaritiesBelongs to the ligand-gated ion channel (TC 1.A.9) family. Acetylcholine receptor (TC 1.A.9.1) subfamily. Alpha-1/CHRNA1 sub-subfamily.
Cellular localizationCell junction > synapse > postsynaptic cell membrane. Cell membrane.
- Information by UniProt
- Acetylcholine receptor subunit alpha antibody
- ACHA_HUMAN antibody
- AChR antibody
ab221868 has not yet been referenced specifically in any publications.