Description
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, Homozygous: 11 bp deletion in exon 1,
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 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-CDKN2B, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Zygosity-Homozygous, 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 p15 INK4b protein also known as CDKN2B is an inhibitor of cyclin-dependent kinases (CDKs) specifically CDK4 and CDK6. Mechanically p15 INK4b acts by binding to these CDKs and preventing their interaction with cyclin D therefore halting the cell cycle progression at the G1 phase. This protein is small with a molecular weight of around 15 kDa. Expressed mainly in tissues with high rates of cell division such as those found in the hematopoietic system it serves as an important regulator of cell cycle progression.
Biological function summary
P15 INK4b plays a significant role in controlling cell proliferation by modulating the transition from the G1 to S phase in the cell cycle. It does not function as part of a complex but works independently to inhibit CDKs. The protein ensures that cells do not divide uncontrollably thereby acting as a tumor suppressor. Its activity is required for proper response to various growth-inhibitory signals and maintaining cellular homeostasis.
Pathways
The regulation and inhibition of the cell cycle by p15 INK4b take place within the broader framework of the retinoblastoma (RB) tumor suppressor pathway and the TGF-beta signaling pathway. This protein is closely related to other CDK inhibitors like p16 INK4a (CDKN2A) and p18 INK4c and it functions in concert with these inhibitors to maintain control over cell division. Through these pathways p15 INK4b ensures that cell growth is checked under normal physiological conditions.
Mutations or deletions in the p15 INK4b gene can lead to its inactivation contributing to the development of various cancers notably acute lymphoblastic leukemia and melanoma. Its interactions with other CDK inhibitors such as p16 INK4a often compound disease pathogenesis. Restoration of p15 INK4b function is being explored as a potential therapeutic strategy for these cancers due to its established role as a tumor suppressor.
