Description

  • Product name

    Recombinant Human Nicotinic Acetylcholine Receptor alpha 1/CHRNA1 protein (Tagged)
    See all Nicotinic Acetylcholine Receptor alpha 1/CHRNA1 proteins and peptides
  • Purity

    > 90 % SDS-PAGE.

  • Expression system

    Escherichia coli
  • Accession

  • Protein length

    Protein fragment
  • Animal free

    No
  • Nature

    Recombinant
    • Species

      Human
    • Sequence

      SEHETRLVAKLFKDYSSVVRPVEDHRQVVEVTVGLQLIQLINVDEVNQIV TTNVRLKQGDMVDLPRPSCVTLGVPLFSHLQNEQWVDYNLKWNPDDYGGV KKIHIPSEKIWRPDLVLYNNADGDFAIVKFTKVLLQYTGHITWTPPAIFK SYCEIIVTHFPFDEQNCSMKLGTWTYDGSVVAINPESDQPDLSNFMESGE WVIKESRGWKHSVTYSCCPDTPYLDITYHFVMQRL
    • Predicted molecular weight

      44 kDa including tags
    • Amino acids

      21 to 255
    • Tags

      His tag N-Terminus
    • Additional sequence information

      N-terminal 6xHis-Trx-tagged. Extracellular domain.

Specifications

Our Abpromise guarantee covers the use of ab235737 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

  • Applications

    SDS-PAGE

  • Form

    Liquid
  • Additional notes

     This product was previously labelled as Nicotinic Acetylcholine Receptor alpha 1

     

  • Concentration information loading...

Preparation and Storage

  • Stability and Storage

    Shipped at 4°C. Store at -20°C or -80°C. Avoid freeze / thaw cycle.

    Constituents: Tris buffer, 50% Glycerol

General Info

  • Alternative names

    • Acetylcholine receptor subunit alpha
    • ACHA_HUMAN
    • AChR
    • ACHRA
    • ACHRD
    • CHNRA
    • Cholinergic receptor nicotinic alpha 1 subunit
    • Cholinergic receptor nicotinic alpha polypeptide 1
    • Cholinergic receptor, nicotinic, alpha polypeptide 1 (muscle)
    • Chrna1
    • CMS1A
    • CMS1B
    • CMS2A
    • FCCMS
    • Nicotinic cholinergic receptor alpha 1
    • SCCMS
    • Schizophrenia neurophysiologic defect candidate
    see all
  • Function

    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.
  • Tissue specificity

    Isoform 1 is only expressed in skeletal muscle. Isoform 2 is constitutively expressed in skeletal muscle, brain, heart, kidney, liver, lung and thymus.
  • Involvement in disease

    Defects 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 similarities

    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.
  • Cellular localization

    Cell junction > synapse > postsynaptic cell membrane. Cell membrane.
  • Information by UniProt

Images

  • (Tris-Glycine gel) Discontinuous SDS-PAGE (reduced) with 5% enrichment gel and 15% separation gel analysis of ab235737.

References

ab235737 has not yet been referenced specifically in any publications.

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