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Anti-CHRNB1 Antibody

品牌：Antibodies

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Anti-CHRNB1 Antibody

商品詳情參考文獻(xiàn) 相關(guān)資料

Overview

Name:	Anti-CHRNB1 Antibody See all CHRNB1 primary antibodies
Description:	Rabbit polyclonal antibody to CHRNB1
Specificity:	CHRNB1 pAb detects endogenous levels of CHRNB1 protein.
Applications:	WB, IHC
Reactivity:	Human, Mouse, Rat
Immunogen:	Recombinant full length Human CHRNB1.
Host:	Rabbit
Clonality:	Polyclonal
Conjugate:	Unconjugated
Molecular Weight:	~57 kDa
Purity:	The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen and the purity is > 95% (by SDS-PAGE).
Product Form:	1mg/ml in PBS?with?0.1%?Sodium?Azide,?50%?Glycerol.

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:	Myasthenic syndrome, congenital, 2A, slow-channel: 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: 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.
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 Location:	Cell junction > Synapse > Postsynaptic cell membrane. Cell membrane.
Database Links:	Entrez Gene: 1140?Human Entrez Gene: 11443?Mouse Entrez Gene: 24261?Rat GenBank: NP_000738.2?Human Omim: 100710?Human SwissProt: P11230?Human SwissProt: P09690?Mouse SwissProt: P25109?Rat Unigene: 330386?Human Unigene: 86425?Mouse Unigene: 44611?Rat
Synonyms:	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 Antibody Chrnb 1 Antibody chrnb1 Antibody CMS1D Antibody CMS2A Antibody Nicotinic Acetylcholine Receptor beta Antibody Nicotinic acetylcholine receptor beta subunit precursor Antibody SCCMS Antibody
Information:	Target information shown above is from the UniProt Consortium.