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, 10 bp deletion in exon 2 and 1 bp insertion in exon 2 and 22 bp deletion in exon 2,
Antibiotic resistance:Puromycin 1µg/mL,
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-BBC3, 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.
PUMA also known as BBC3 (Bcl-2-binding component-3) is a pro-apoptotic protein that plays important mechanical roles in promoting apoptosis. It has a mass of approximately 23 kDa. PUMA is expressed widely in various tissues including the lung liver and heart. The protein works mechanically by interacting with anti-apoptotic Bcl-2 family members releasing pro-apoptotic factors like Bax and Bak which engage mitochondria to trigger cell death.
Biological function summary
PUMA functions as a pivotal mediator of apoptosis in response to diverse stimuli such as DNA damage and oncogenic stress. As part of the Bcl-2 family PUMA does not typically form a complex with other proteins but functions directly by binding and neutralizing anti-apoptotic Bcl-2 family proteins. This action results in the release of caspase-activating factors from mitochondria essential for programmed cell death.
Pathways
Several cellular pathways incorporate PUMA to regulate apoptosis. PUMA is notably included in the p53 pathway where p53 transcriptionally activates PUMA following cellular stress or DNA damage. The presence of related proteins like Bax and Bim in the mitochondrial apoptotic pathway links these signals to the mitochondrial death machinery facilitating apoptosis.
PUMA plays significant roles in cancer and neurodegenerative conditions. PUMA overexpression induces excessive cell death relevant in the pathology of neurodegenerative diseases. In cancer PUMA's interactions with proteins like p53 highlight its involvement in tumor suppression suggesting that dysregulation of PUMA expression can contribute to tumorigenesis when anti-apoptotic signals predominate potentially leading to chemoresistance.
