CDKN2B KO cell line available to order. Free of charge wild type control provided. Knockout achieved by using CRISPR/Cas9, Homozygous: 11 bp deletion in exon 1.
CDK inhibitory protein, CDK4B Inhibitor, CDN2B_HUMAN, Cdkn2b, Cyclin Dependent Kinase Inhibitor 2B, Cyclin dependent kinase inhibitor 2B p15 inhibits CDK4, Cyclin dependent kinases 4 and 6 binding protein, Cyclin-dependent kinase 4 inhibitor B, INK4B, MTS-2, Multiple Tumor Supressor 2, Multiple tumor suppressor 2, OTTHUMP00000021154, OTTHUMP00000021155, P15, TP 15, p14 CDK inhibitor, p14-INK4b, p15 CDK inhibitor, p15 inhibits CDK4, p15-INK4b
CDKN2B KO cell line available to order. Free of charge wild type control provided. Knockout achieved by using CRISPR/Cas9, Homozygous: 11 bp deletion in exon 1.
Upon arrival, the vial should be stored in liquid nitrogen vapor phase and not at -80°C. Storage at -80°C may result in loss of viability.
1. Thaw the vial in 37°C water bath for approximately 1-2 minutes.
2. Transfer the cell suspension (0.8 mL) to a 15 mL/50 mL conical sterile polypropylene centrifuge tube containing 8.4 mL pre-warmed culture medium, wash vial with an additional 0.8 mL culture medium (total volume 10 mL) to collect remaining cells, and centrifuge at 201 x g (rcf) for 5 minutes at room temperature. 10 mL represents minimum recommended dilution. 20 mL represents maximum recommended dilution.
3. Resuspend the cell pellet in 5 mL pre-warmed culture medium and count using a haemocytometer or alternative cell counting method seed all remaining cells into a T25.
4. Incubate the culture at 37°C incubator with 5% CO2. Check the culture one day after revival and continue to check until 80% confluent. Media change can be given if needed.
5. Once confluent passage into an appropriate flask at a density of 2x104 cells/cm2. Seeding density is given as a guide only and should be scaled to align with individual lab schedules. Cultures should be monitored daily.
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 and patent pages.
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.
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.
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.
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Homozygous: 11 bp deletion in exon 1.
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