CDKN1C KO cell lysate available now. KO validated by Western blot. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, Homozygous: 217 bp deletion in exon 1.
BWCR, BWS, Beckwith Wiedemann syndrome, CDKI, CDKN 1C, CDN1C_HUMAN, Cyclin-dependent kinase inhibitor 1C, Cyclin-dependent kinase inhibitor p57, KIP 2, WBS, p57, p57 Kip 2
CDKN1C KO cell lysate available now. KO validated by Western blot. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, Homozygous: 217 bp deletion in exon 1.
Knockout cell lysate achieved by CRISPR/Cas9.
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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.
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.
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.
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.
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All lanes: Western blot - Anti-p57 Kip2 antibody [EP2516] (Anti-p57 Kip2 antibody [EP2516] ab119989) at 1/1000 dilution
Lane 1: Wild-type HeLa Vehicle Control Dexamethasone (0 nM, 16 h) ab277359 cell lysate at 20 µg
Lane 2: Wild-type HeLa Treated Dexamethasone (50 nM, 16 h) ab287335 cell lysate at 20 µg
Lane 2: Western blot - Human CDKN1C (p57 Kip2) knockout HeLa cell line (Human CDKN1C (p57 Kip2) knockout HeLa cell line ab280061)
Lane 3: CDKN1C knockout HeLa Vehicle Control Dexamethasone (0 nM, 16 h) ab277299 cell lysate at 20 µg
Lane 4: CDKN1C knockout HeLa Treated Dexamethasone (50 nM, 16 h) ab281877 cell lysate at 20 µg
Lane 5: MCF7 cell lysate at 20 µg
Lane 6: SH-SY5Y cell lysate at 20 µg
Performed under reducing conditions.
Predicted band size: 32 kDa
Observed band size: 50 kDa
217 bp Deletion in Exon 1
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