|Positive WB detected in||mouse heart tissue|
|Positive IHC detected in||mouse skeletal muscle tissue|
Note: suggested antigen retrieval with TE buffer pH 9.0; (*) Alternatively, antigen retrieval may be performed with citrate buffer pH 6.0
|Western Blot (WB)||WB : 1:500-1:1000|
|Immunohistochemistry (IHC)||IHC : 1:50-1:500|
|Sample-dependent, check data in validation data gallery|
The immunogen of 23016-1-AP is Nav1.5 Fusion Protein expressed in E. coli.
|Tested Reactivity||human, mouse|
|Host / Isotype||Rabbit / IgG|
|Immunogen||Nav1.5 fusion protein Ag19275|
|Full Name||sodium channel, voltage-gated, type V, alpha subunit|
|Calculated molecular weight||2016 aa, 227 kDa|
|Observed molecular weight||227 kDa|
|GenBank accession number||BC140813|
|Gene ID (NCBI)||6331|
|Purification Method||Antigen affinity purification|
|Storage Buffer||PBS with 0.02% sodium azide and 50% glycerol pH 7.3.|
|Storage Conditions||Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20oC storage.|
Voltage-gated sodium channels are responsible for initiation and propagation of action potentials in the membranes of neurons and most electrically excitable cells (PMID: 10798388). These channels are composed of a large alpha subunit that forms the ion conduction pore and auxiliary beta subunits (PMID: 11486343). The alpha subunits form a gene family with at least 10 members. Nav1.5, encoded by the SCN5A gene in humans, is a pore forming alpha subunit of voltage-gated sodium channels. Nav1.5 is the principal Na+ channel isoform expressed in cardiomyocytes. Mutations in SCN5A gene have been linked to many cardiac electrical disorders, including the congenital and acquired long QT syndrome, Brugada syndrome, conduction slowing, sick sinus syndrome, atrial fibrillation, and dilated cardiomyopathy (PMID: 23123192).
Scorpion Venom Analgesic Peptide, BmK AGAP Inhibits Stemness, and Epithelial-Mesenchymal Transition by Down-Regulating PTX3 in Breast Cancer.
J Biol Chem
Mechanistic insights into the interaction of the MOG1 protein with the cardiac sodium channel Nav1.5 clarify the molecular basis of Brugada syndrome.