Abcam, ab266066, Human VDAC3 knockout HEK-293T cell line

Size: 2 x 1000000Cells / vial / 1000000Cells / vial
VDAC3 KO cell line available to order. KO validated by. Free of charge wild type control available. Knockout achieved by using CRISPR/Cas9, 16 bp deletion in exon 6 and 1 bp insertion in exon 6. 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:HEK-293T,
Species or organism:Human,
Tissue:Kidney,
Form:LiquidSee storage information,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, 16 bp deletion in exon 6 and 1 bp insertion in exon 6

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-VDAC3, 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.
Voltage-dependent anion channel 3 (VDAC3) also known as porin 3 has a molecular mass of approximately 32 kDa. It is a part of the voltage-dependent anion channel family located in the outer mitochondrial membrane. VDAC3 plays a role in regulating the passage of ions and metabolites across the mitochondrial membrane. This channel shares a similar structure with other VDAC isoforms and is expressed in several tissues with high levels found in the heart and skeletal muscle.
Biological function summary
VDAC3 contributes to cellular energy homeostasis and the exchange of ions and small metabolites between mitochondria and cytoplasm. VDAC3 may participate in a complex with other mitochondrial proteins affecting the mitochondrial permeability transition pore (mPTP). The precise regulation of VDAC3 ensures normal mitochondrial function which is critical for maintaining cellular metabolism and programming cell death including apoptotic pathways.
Pathways
VDAC3 is involved in apoptotic regulation and energy metabolism. Its activity impacts the intrinsic pathway of apoptosis where it interacts with Bcl-2 family proteins such as Bax and Bak influencing cytochrome c release. VDAC3's role in these pathways connects it to overall cellular stress responses and energy balance. Additionally VDAC3 coordinates with other VDAC isoforms to ensure mitochondrial integrity under variable physiological conditions.
VDAC3's malfunction links to neurodegenerative diseases and cardiac disorders. Dysfunction in VDAC3 has associations with diseases like Alzheimer's due to its involvement in mitochondrial dysfunction. Additionally its influence on apoptotic pathways implicates VDAC3 in heart diseases where improper apoptosis can lead to cardiac tissue damage. In these contexts VDAC3 interacts with the protein amyloid-beta in Alzheimer's and with caspases in cardiac conditions suggesting its importance in disease mechanisms.