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AB257267

Human CDKN2B (p15 INK4b) knockout HeLa cell lysate

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CDKN2B KO cell lysate available now. KO validated. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, Homozygous: 11 bp deletion in exon 1.

View Alternative Names

p15INK4B, p14-INK4b, Multiple tumor suppressor 2, MTS-2, Cyclin-dependent kinase 4 inhibitor B, MTS2, p15-INK4b, CDKN2B

1 Images
Sanger Sequencing - Human CDKN2B (p15 INK4b) knockout HeLa cell lysate (AB257267)
  • Sanger seq

Unknown

Sanger Sequencing - Human CDKN2B (p15 INK4b) knockout HeLa cell lysate (AB257267)

Homozygous : 11 bp deletion in exon 1

Key facts

Cell type

HeLa

Species or organism

Human

Tissue

Cervix

Knockout validation

Sanger Sequencing

Mutation description

Knockout achieved by using CRISPR/Cas9, Homozygous: 11 bp deletion in exon 1.

Disease

Adenocarcinoma

Reactivity data

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Product details

Knockout cell lysate achieved by CRISPR/Cas9.

REACH authorisation
Abcam has not and does not intend to apply for the REACH Authorisation of customers' uses of products that contain European Authorisation list (Annex XIV) substances.
It is the responsibility of our customers to check the necessity of application of REACH Authorisation, and any other relevant authorisations, for their intended uses.

Lysate preparation: Our lysates are made using RIPA buffer to which we add a protease inhibitor cocktail and phosphatase inhibitor cocktail (ratio: 300:100:10). This means that the protein of interest is denatured. If you require a native form of the protein please use the live cell version. Please refer to our lysis protocol for further details on how our lysates are prepared.

User storage instructions: Lyophilizate may be stored at 4°C. After reconstitution, store at -20°C for short-term storage or -80°C for long-term storage.

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.

What's included?

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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
Ambient - Can Ship with Ice
Appropriate short-term storage conditions
-20°C
Appropriate long-term storage conditions
-20°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.

Quality control

STR analysis

CSF1PO, D13S317, D7S820, D5S818, TH01, D16S539, TPOX

Cell culture

Biosafety level

EU: 2 US: 2

Adherent/suspension

Adherent

Gender

Female

Product protocols

Product promise

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