Abcam, ab265346, Human SCNN1D knockout HeLa cell line

Size: 2 x 1000000Cells / vial / 1000000Cells / vial
SCNN1D KO cell line available to order. KO validated by. Free of charge wild type control available. Knockout achieved by using CRISPR/Cas9, 1 bp deletion in exon 8 and 2 bp deletion in exon 8. 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, 1 bp deletion in exon 8 and 2 bp deletion in exon 8,
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 and ERS Genomics Limited, and is developed with patented technology. For full details of the limited use licenses and relevant patents please refer to our
limited use license
patent pages

Properties and Storage Information:
Gene name-SCNN1D, 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.
The SCNN1D gene encodes the delta subunit of the epithelial sodium channel often referred to as ENaC-delta. This subunit forms a part of the multisubunit complex that regulates sodium balance at the epithelial surface. It resides on the cell membrane and plays a mechanical role in facilitating sodium ion transport across epithelial cells. SCNN1D is about 74 kDa in size and is expressed predominantly in renal epithelium and respiratory tissues contributing to sodium homeostasis and fluid balance.
Biological function summary
SCNN1D plays an important role in sodium reabsorption as part of the epithelial sodium channel complex which includes alpha beta and gamma subunits. Together these subunits form a channel responsible for the movement of sodium ions into the cells critical for maintaining electrolyte balance and blood pressure. Its specific contribution enhances the channel's sensitivity and responsiveness to hormonal regulation particularly by aldosterone which modulates electrolyte transport further influencing fluid accumulations in tissues.
Pathways
SCNN1D acts within the aldosterone-regulated sodium reabsorption pathway and the renin-angiotensin-aldosterone system (RAAS). These pathways are essential in regulating blood pressure and fluid balance. SCNN1D works closely with other proteins like the mineralocorticoid receptor which influences ENaC activity by regulating its transcription under the stimulus of aldosterone ensuring facilitating rapid sodium uptake in epithelial cells.
SCNN1D involvement becomes significant in hypertension and cystic fibrosis. Mutations or dysregulation of SCNN1D or its associated pathways can lead to altered blood pressure control due to improper sodium retention. Moreover its role in sodium reabsorption associates this subunit with cystic fibrosis where the balance of ions and fluids in the lungs impacts disease severity. The protein is also linked with cystic fibrosis transmembrane conductance regulator (CFTR) which co-regulates ion transport and channel activity across epithelial surfaces.