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Mouse Anti-CHRNB1 Recombinant Antibody (CBYY-C3045) (CBMAB-C4488-YY)


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Published Data
CBMAB-C4488-YY-1
Mouse Anti-CHRNB1 Recombinant Antibody (CBYY-C3045) (CBMAB-C4488-YY) in WB
Western blot analysis of AChR α1, β1, δ, ϵ subunits and rapsyn. Uninfected HEK293T cells were used as the NC. ****P < 0.0001 compared with NC. ...View More
Cai, Y., Han, L., Zhu, D., Peng, J., Li, J., Ding, J., ... & Guan, Y. (2021). A stable cell line expressing clustered AChR: a novel cell-based assay for Anti-AChR antibody detection in Myasthenia Gravis. Frontiers in Immunology, 12, 666046.
Distributed under Open Access license CC BY 4.0, without modification.

Summary

Host Animal
Mouse
Specificity
Human, Mouse, Rat
Clone
CBYY-C3045
Antibody Isotype
IgG2a, κ
Application
ELISA, IF, WB, IP

Basic Information

Immunogen
Amino acids 356-456 mapping near the C-terminus of AChRβ1 of human.
Host Species
Mouse
Specificity
Human, Mouse, Rat
Antibody Isotype
IgG2a, κ
Clonality
Monoclonal Antibody
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.
ApplicationNote
WB1:100-1:1,000
IP1-2 µg per 100-500 µg of total protein (1 ml of cell lysate)
IF(ICC)1:50-1:500
ELISA1:100-1:1,000

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Buffer
PBS, 0.1% gelatin
Preservative
< 0.1% sodium azide
Concentration
0.2 mg/ml
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
Cholinergic Receptor Nicotinic Beta 1 Subunit
Entrez Gene ID
1140
UniProt ID
P11230
Alternative Names
Gap Junction Protein Gamma 1; Gap Junction Protein, Gamma 1, 45kDa; Gap Junction Alpha-7 Protein; Connexin-45; CX45; GJA7;
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.
Biological Process
Behavioral response to nicotine Source: UniProtKB
Cation transport Source: UniProtKB
Chemical synaptic transmission Source: GO_Central
Ion transmembrane transport Source: GO_Central
Muscle contraction Source: UniProtKB
Muscle fiber development Source: UniProtKB
Nervous system process Source: UniProtKB
Neuromuscular synaptic transmission Source: UniProtKB
Postsynaptic membrane organization Source: UniProtKB
Regulation of membrane potential Source: UniProtKB
Signal transduction Source: UniProtKB
Skeletal muscle contraction Source: Ensembl
Synaptic transmission, cholinergic Source: UniProtKB
Cellular Location
Postsynaptic cell membrane; Cell membrane
Involvement in disease
Myasthenic syndrome, congenital, 2A, slow-channel (CMS2A): A form of congenital myasthenic syndrome, a group of disorders characterized by failure of neuromuscular transmission, including pre-synaptic, synaptic, and post-synaptic disorders that are not of autoimmune origin. Clinical features are easy fatigability and 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. CMS2A is a slow-channel myasthenic syndrome. It is caused by kinetic abnormalities of the AChR, resulting in prolonged AChR channel opening episodes, prolonged endplate currents, and depolarization block. This is associated with calcium overload, which may contribute to subsequent degeneration of the endplate and postsynaptic membrane.
Myasthenic syndrome, congenital, 2C, associated with acetylcholine receptor deficiency (CMS2C): A form of congenital myasthenic syndrome, a group of disorders characterized by failure of neuromuscular transmission, including pre-synaptic, synaptic, and post-synaptic disorders that are not of autoimmune origin. Clinical features are easy fatigability and 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. CMS2C is an autosomal recessive disorder of postsynaptic neuromuscular transmission, due to deficiency of AChR at the endplate that results in low amplitude of the miniature endplate potential and current. CMS2C is clinically characterized by early-onset muscle weakness with variable severity.
Topology
Extracellular: 24-244
Helical: 245-269
Helical: 277-295
Helical: 311-332
Cytoplasmic: 333-469
Helical: 470-488
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For research use only. Not intended for any clinical use.

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