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Mouse (Murine) Monoclonal CHRNA1 Primary Antibody for IF, WB - ABIN968298
Garchon, Djabiri, Viard, Gajdos, Bach: Involvement of human muscle acetylcholine receptor alpha-subunit gene (CHRNA) in susceptibility to myasthenia gravis. in Proceedings of the National Academy of Sciences of the United States of America 1994
Show all 5 Pubmed References
Mouse (Murine) Monoclonal CHRNA1 Primary Antibody for IF, WB - ABIN968299
Kincer, Uittenbogaard, Dressman, Guerin, Febbraio, Guo, Smart: Hypercholesterolemia promotes a CD36-dependent and endothelial nitric-oxide synthase-mediated vascular dysfunction. in The Journal of biological chemistry 2002
Show all 5 Pubmed References
This study shown that the genetic analysis revealed that the very early onset JMG had a more prominent genetic predisposition in an autoantigen gene (CHRNA1).
Data suggest that the mutations made the cholinergic receptor nicotinic alpha 1 subunit channel (CHRNA1) resistant to the antagonists, not by impairing antagonist binding, but rather by producing a gain-of-function phenotype, e.g. increased agonist sensitivity.
Study indicated that nicotinic acetylcholine receptor alpha 1-subunit peptides may act as receptor decoy molecules and inhibit the binding of virus to the native host cell receptors and hence may reduce viral infection.
ChRnA1 gene variants did not affect the pharmacodynamics of rocuronium.
Cholesterol and CAV-1 (show CAV1 Antibodies) modulate the function and dynamics of the slow channel congenital myasthenia syndrome alphaC418W nicotinic acetylcholine receptor mutation.
nicotine contributes to the progression and erlotinib-resistance of the NSCLC xenograft model via the cooperation between nAChR (show CHRNA4 Antibodies) and EGFR (show EGFR Antibodies).
show that AON complementary to the 5' splice site of the exon was the most effective at exon skipping of the minigene with causative mutations, as well as endogenous wild-type CHRNA1
The CHRNA1 extracellular domain is an improved protein for use in antigen-specific Myasthenia Gravis therapeutic strategies.
HnRNP L (show HNRNPL Antibodies) and hnRNP (show HNRNPC Antibodies) LL antagonistically modulate PTB (show PTBP1 Antibodies)-mediated splicing suppression of CHRNA1 pre-mRNA.
High expression of CHRNA1 is associated with lung adenocarcinoma after complete resection.
The results indicate that in the absence of the alpha1-nAChR (show CHRNA4 Antibodies) subunit, clusters of nAChRs coupled to SK2 (show PAPSS2 Antibodies) potassium channels as well as functional efferent synapses did form, showing that alpha1 is not necessary for these processes to take place.
This study demonstrates that genes coding for CHRNA1 subunits may contain variants associated with statin-induced ADRs.
Chrna1 was co-purified with nicotinic acetylcholine receptor (AChR) in C2C12 myotubes. In addition, Stau1 (show STAU1 Antibodies) was found to interact with Chrna1 mRNA, and knocking down of Stau1 (show STAU1 Antibodies) by RNAi resulted in defective AChR clustering.
These results suggest that in skeletal muscle cells, neural activity reduces the molar ratio of YB-1 (show YBX1 Antibodies) relative to its binding AChR alpha mRNA, leading to an increase of ribosome binding to the mRNA, and thus activating translation.
Chrna1 could be the first transcriptional target of atonal homolog 1 in the inner ear
These data identify caveolin-3 (show CAV3 Antibodies) as a critical component of the signaling machinery that drives nicotinic acetylcholine receptor clustering and controls neuromuscular junction function.
HDAC4 (show HDAC5 Antibodies) is a neural activity-regulated deacetylase and a key signaling component that relays neural activity to the muscle transcriptional machinery through Dach2 (show DACH2 Antibodies), myogenin (show MYOG Antibodies), and nAChR (show CHRNA4 Antibodies)
In S269I, mutant the peak-current amplitude decreases along trains of nearly saturating ACh (show FGFR3 Antibodies) pulses delivered at physiologically relevant frequencies, consistent with enhanced entry into desensitization in congenital myasthenic syndrome.
In this mouse experiemntal myasthenia gravis study demonstrated that Acetylcholine receptor (show CHRNB1 Antibodies)-alpha1 subunit expression was increase with varying disease severity.
The muscle acetylcholine receptor consiststs of 5 subunits of 4 different types: 2 alpha subunits and 1 each of the beta, gamma, and delta subunits. This gene encodes an alpha subunit that plays a role in acetlycholine binding/channel gating. Alternatively spliced transcript variants encoding different isoforms have been identified.
acetylcholine receptor subunit alpha
, acetylcholine receptor, nicotinic, alpha 1 (muscle)
, cholinergic receptor, nicotinic, alpha polypeptide 1 (muscle)
, muscle nicotinic acetylcholine receptor
, nicotinic acetylcholine receptor alpha subunit
, nicotinic cholinergic receptor alpha 1
, muscle nicotinic acetylcholine receptor alpha-su exon P4
, nachr alpha-subunit
, nicotinic acetylcholine recepter alpha-subunit
, cholinergic receptor nicotinic alpha polypeptide 1
, alpha-1 subunit, nicotinic acetylcholine receptor
, nicotinic cholinergic receptor alpha polypeptide 1