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, Homozygous: 217 bp deletion in exon 1,
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-CDKN1C, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Western blot, 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 protein p57^Kip2 also known as CDKN1C plays an important role as a cyclin-dependent kinase inhibitor aligning closely with proteins like p21 and p27. It weighs approximately 57 kiloDaltons. P57^Kip2's expression occurs in various tissues including the placenta muscle brain and kidney. This widespread expression suggests a multitiered function in different tissues. Researchers use p57 immunostain techniques to confirm its presence in tissues.
Biological function summary
P57^Kip2 acts as a regulator of cell cycle progression. It binds directly to cyclin-CDK complexes stopping cell cycle transition from G1 to S phase. This action prevents unregulated cell division and contributes to cellular differentiation. p57^Kip2 forms part of larger protein complexes further influencing various cellular processes. Its activity is important for embryonic development where it controls cell proliferation rates.
Pathways
P57^Kip2 integrates into pathways controlling cell cycle checkpoints and apoptosis. It interacts with proteins like cyclin D and E and the retinoblastoma protein (Rb) within the cell cycle regulation pathway. Additionally its presence in growth signaling pathways intersects with TGF-beta signaling. These pathways hold significant influence over development and cellular responses to DNA damage.
Abnormal expression of p57^Kip2 connects with cancers and growth disorders. Loss of function or downregulation often links to overgrowth syndromes like Beckwith-Wiedemann syndrome. Conversely reduced expression levels associate with cancer proliferation particularly in cases such as Wilms' tumor. This association intertwines with mutations in genes like IGF2 and H19 which are critical in these conditions.
