Abcam, ab264733, Human SCN1B knockout HeLa cell line

Size: 2 x 1000000Cells / vial / 1000000Cells / vial
SCN1B KO cell line available to order. KO validated by. Free of charge wild type control available. Knockout achieved by using CRISPR/Cas9, 106 bp insertion in exon 2 and 1 bp deletion in exon 2. To order both knockout and wild-type control cells: select 2 x 1000000Cells/vial. To order only knockout cells: select 1000000Cells/vial.
Key facts
Cell type:HeLa,
Species or organism:Human,
Tissue:Cervix,
Form:LiquidSee storage information,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, 106 bp insertion in exon 2 and 1 bp deletion in exon 2,
Disease:Adenocarcinoma

Product details:
We will provide viable cells that proliferate on revival.
This product is subject to limited use licenses from The Broad Institute, ERS Genomics Limited and Sigma-Aldrich Co. LLC, and is developed with patented technology. For full details of the licenses and patents please refer to our
limited use license
patent pages

Properties and Storage Information:
Gene name-SCN1B, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Shipped at conditions-Dry Ice, Appropriate short-term storage conditions--196°C, Appropriate long-term storage conditions--196°C

Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
SCN1B also known as sodium channel beta-1 subunit mechanically functions as an accessory protein to voltage-gated sodium channels. It is a protein with a mass of approximately 22 kDa. SCN1B modulates the function of these channels including their kinetics and cell surface expression. This protein is expressed predominantly in the central and peripheral nervous systems but can also be found in other tissues like the heart.
Biological function summary
The sodium channel beta-1 subunit participates in the initiation and propagation of action potentials. It forms part of the sodium channel complex contributing structural stability and influencing the gating properties of the channel. SCN1B interacts with alpha subunits of sodium channels and other beta subunits which allow it to regulate the excitability of neurons and cardiac myocytes. It plays a critical role in maintaining the electrical signaling within these cells.
Pathways
The activity of SCN1B contributes significantly to the regulation of neuronal firing and cardiac rhythm. It is involved in the voltage-gated sodium channel complex which is an important player in the excitation-contraction coupling pathway and neuronal excitability pathways. SCN1B modulates the activity of related proteins such as SCN8A the sodium channel protein type 8 subunit alpha within these pathways influencing their function in electrical signaling processes.
Mutations or dysfunctions in SCN1B can lead to diseases such as epilepsy and cardiac arrhythmias. Such conditions may result from altered sodium channel function caused by mutations in SCN1B that impact the excitability of neurons or cardiac muscles. For instance it connects to proteins like SCN1A another sodium channel subunit which also is involved in disorders such as Dravet syndrome. These conditions highlight the importance of SCN1B in maintaining normal neurophysiological and cardiac functions.