Description
Key facts
Cell type:HeLa,
Species or organism:Human,
Tissue:Cervix,
Form:LiquidSee storage information,
Knockout validation:Sanger Sequencing,Western blot,
Mutation description:Knockout achieved by using CRISPR/Cas9, 1 bp deletion in exon 2 and 2 bp deletion in exon 2 and Insertion of the selection cassette 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-BAK1, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Western blot, 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 Bak protein also known as Bcl-2 homologous antagonist killer plays a mechanical role in the mitochondrial apoptosis pathway. It often functions as a pro-apoptotic member of the Bcl-2 protein family. Bak is expressed widely in the body being present in tissues such as the brain and heart. The molecular weight of Bak is approximately 23 kilodaltons. Bak interacts with other mitochondrial proteins to trigger cell death processes.
Biological function summary
Bak engages in promoting apoptosis by disrupting the mitochondrial outer membrane potential. It is part of the Bcl-2 family complex which balances cell survival and cell death. Bak collaborates with Bax protein to form pores in the mitochondrial membrane releasing cytochrome c and other apoptotic factors. This process initiates the cascade of caspases leading to programmed cell death.
Pathways
Bak is a critical component of the intrinsic apoptotic pathway. It directly interacts with pro-apoptotic proteins like Bax and anti-apoptotic proteins such as Bcl-2 and Bcl-xL. Bak's action in the apoptotic pathway involves a delicate balance between survival and death signals affecting cellular homeostasis. In addition Bak's interaction with the p53 pathway emphasizes its role in response to DNA damage ensuring damaged cells do not proliferate uncontrollably.
Malfunction or dysregulation of Bak can lead to cancer and neurodegenerative disorders. In cancer reduced Bak activity may allow cells to evade apoptosis promoting tumor survival and growth. Conversely in diseases like Parkinson's excessive Bak activity may result in enhanced neuronal apoptosis. Bak's interaction with proteins such as Bcl-2 also makes it a potential target for therapies aimed at restoring apoptotic balance in affected cells.
