Overview

  • Product name

    Anti-Nicotinic Acetylcholine Receptor beta/CHRNB1 antibody
    See all Nicotinic Acetylcholine Receptor beta/CHRNB1 primary antibodies
  • Description

    Rabbit polyclonal to Nicotinic Acetylcholine Receptor beta/CHRNB1
  • Host species

    Rabbit
  • Tested applications

    Suitable for: WB, IHC-Pmore details
  • Species reactivity

    Reacts with: Human
    Predicted to work with: Mouse, Rat, Cow
  • Immunogen

    Recombinant fragment corresponding to Human Nicotinic Acetylcholine Receptor beta/CHRNB1 aa 274-466.
    Database link: P11230

  • Positive control

    • NT2D1, IMR32, MCF7 and U-87 MG whole cell lysates; H661 xenograft tissue.
  • General notes

     This product was previously labelled as Nicotinic Acetylcholine Receptor beta

     

Properties

  • Form

    Liquid
  • Storage instructions

    Shipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles.
  • Storage buffer

    pH: 7.00
    Preservative: 0.01% Thimerosal (merthiolate)
    Constituents: 1.21% Tris, 0.75% Glycine, 20% Glycerol
  • Concentration information loading...
  • Purity

    Immunogen affinity purified
  • Clonality

    Polyclonal
  • Isotype

    IgG
  • Research areas

Applications

Our Abpromise guarantee covers the use of ab126234 in the following tested applications.

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

Application Abreviews Notes
WB 1/500 - 1/3000. Predicted molecular weight: 57 kDa.
IHC-P 1/100 - 1/500. Perform heat mediated antigen retrieval with citrate buffer pH 6 before commencing with IHC staining protocol.

Target

  • 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.
  • Involvement in disease

    Defects in CHRNB1 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 CHRNB1 are a cause of congenital myasthenic syndrome with acetylcholine receptor deficiency (ACHRDCMS) [MIM:608931]. ACHRDCMS is a post-synaptic congenital myasthenic syndrome. Mutations underlying AChR deficiency cause a 'loss of function' and show recessive inheritance.
  • Sequence similarities

    Belongs to the ligand-gated ion channel (TC 1.A.9) family. Acetylcholine receptor (TC 1.A.9.1) subfamily. Beta-1/CHRNB1 sub-subfamily.
  • Cellular localization

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

  • Alternative names

    • Acetylcholine receptor protein beta chain precursor antibody
    • Acetylcholine receptor subunit beta antibody
    • ACHB_HUMAN antibody
    • AChR antibody
    • ACHRB antibody
    • Cholinergic receptor nicotinic beta polypeptide 1 (muscle) antibody
    • Chrnb 1 antibody
    • CHRNB antibody
    • chrnb1 antibody
    • CMS1D antibody
    • CMS2A antibody
    • Nicotinic acetylcholine receptor beta subunit precursor antibody
    • SCCMS antibody
    see all

Images

  • Anti-Nicotinic Acetylcholine Receptor beta/CHRNB1 antibody (ab126234) at 1/1000 dilution + MCF7 whole cell lysate at 30 µg

    Predicted band size: 57 kDa



    7.5% SDS PAGE
  • ab126234, at a 1/250 dilution, staining Nicotinic Acetylcholine Receptor beta/CHRNB1 in paraffin-embedded H661 xenograft tissue by Immunohistochemistry.

References

ab126234 has not yet been referenced specifically in any publications.

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