antibody

p16 (C20) Antibody

MBS440018

0.2 mg

240 USD

polyclonal

rabbit

nonconjugated

western blot, immunohistochemistry, immunoprecipitation

Antibody

p16 (C20) Antibody

p16

p16, partial; P16; cyclin-dependent kinase inhibitor 2A; CDK4 inhibitor p16-INK4; CDKN2A; alternative reading frame; cell cycle negative regulator beta; cyclin-dependent kinase 4 inhibitor A; cyclin-dependent kinase inhibitor 2A (melanoma, p16, inhibits CDK4); multiple tumor suppressor 1; cyclin-dependent kinase inhibitor 2A; P16

p16

CDKN2A; CDKN2A; ARF; MLM; P14; P16; P19; CMM2; INK4; MTS1; TP16; CDK4I; CDKN2; INK4A; MTS-1; P14ARF; P19ARF; P16INK4; P16INK4A; P16-INK4A

Q208B5_HUMAN

Polyclonal

Rabbit

Human

67

p16(C20) reacts with p16 of human origin by Western Blotting, Immunoprecipitation, and Immunohistochemistry. Western Blotting starting dilution: 1:200.

200 ug/ml of affinity purified rabbit IgG, p16 (C20) DB018, in 1ml PBS containing 0.1 % sodium azide and 0.2% gelatin.

Store this product at 4 degree C, do not freeze. The product is stable for one year from the date of shipment.

Western Blot (WB), Immunoprecipitation (IP), Immunohistochemistry (IHC)

p16(C20) DB018 reacts with p16 of human origin by western blotting, immunoprecipitation, and immunohistochemistry. Western blotting starting dilution: 1:200.

Origin: p16 (C20) is provided as an affinity purified rabbit polyclonal antibody, raised against a peptide mapping to the carboxy terminus of human p16. Product Details: Each vial contains 200ug/ml of affinity purified rabbit IgG, p16 (C20), in 1 ml PBS containing 0.1% sodium azide and 0.2% gelatin.

Immunogen: Synthetic peptide mapping to the carboxy terminus of human p16. Competition Studies: A blocking peptide is also available MBS443018 for use in competititon studies. Each vial containing 100 ug of peptide in 0.5ml PBS with 0.1% sodium azide and 100 ug BSA.

The progression through the cell cycle is regulated by cyclins and their cognate Cdks by promoting cell cycle transitions (1,2,3). This orderly progression can be inhibited by a family of proteins known as CDK inhibitors (CDIs) that bind to cyclin/Cdk complexes and halt cell division (3). p21 (also designated WAF1/Cip1) is one has been shown to inhibit the activity of each member of the cyclin/Cdk family and over expression of this protein inhibits the proliferation of mammalian cells (5). The expression of p21 is inducible by a wide range of stress stimuli and its transcription can be enhanced by p53 (6). Another member of the CDIs is p27 (also known as Kip1), which also sees up regulation in response to antimitogenic stimuli (7). The increased protein expression of p27 results in cellular arrest by binding to cyclin/Cdk complexes, like cyclin D1/Cdk4 (4,8). An additional CDI has been found to bind Cdk4 and Cdk6, p16 (INK4A), and when such complexes are formed, the progression of the cell cycle is halted (9). It has become increasingly clear that p16 is a very important tumor suppressor gene whose frequent loss occurs early in many human cancers. p16 is a major target in carcinogenesis that is rivaled in frequency only by p53 (10).

1.) Bihani T, Mason DX, Jackson TJ, Chen SC, Boettner B, Lin AW. 2004. Differential oncogenic Ras signaling and senescence in tumor cells. Cell Cycle 3(9):1201-7. 2.) Weebadda WK, Jackson TJ, Lin AW. 2005. Expression of p16(INK4A) variants in senescent human fibroblasts independent of protein phosphorylation. J Cell Biochem. Apr 15;94(6):1135-47.3.) Mason DX, Jackson TJ, Lin AW. Molecular signature of oncogenic ras-induced senescence. Oncogene. 2004 Dec 9;23(57):9238-46.4.) Bihani T, Chicas A, Lo CP, Lin AW. 2007. Dissecting the senescence-like program in tumor cells activated by Ras signaling. J Biol Chem. Jan 26;282(4):2666-75.5.) Achour M, Jacq X, Rondé P, Alhosin M, Charlot C, Chataigneau T, Jeanblanc M, Macaluso M, Giordano A, Hughes AD, Schini-Kerth VB, Bronner C. 2007. The interaction of the SRA domain of ICBP90 with a novel domain of DNMT1 is involved in the regulation of VEGF gene expression. Oncogene. Oct 15. 1. Harper JW, Adami GR, Wei N, Keyomarsi K, Elledge SJ. 1993. The p21 Cdk-interacting protein Cip1 is a potent inhibitor of G1 cyclin-dependent kinases. Cell 75(4):805-816.2. Gartel AL, Serfas MS, Tyner AL. 1996. p21 - -negative regulator of the cell cycle. Proc Soc Exp Biol Med 213(2):138-149.3. Moller MB. 2000. p27 in cell cycle control and cancer. Leuk Lymphoma 39(1-2):19-27.4. Sgambato A, Cittadini A, Faraglia B, Weinstein IB. 2000. Multiple functions of p27(Kip1) and its alterations in tumor cells: a review. J Cell Physiol 183(1):18-27.5. Xiong Y, Hannon GJ, Zhang H, Casso D, Kobayashi R, Beach D. 1993. p21 is a universal inhibitor of cyclin kinases. Nature 366(6456):634.6. Gorospe M, Wang X, Holbrook NJ. 1999. Functional role of p21 during the cellular response to stress. Gene Expr 7(4-6):377-385.7. Slingerland J, Pagano M. 2000. Regulation of the cdk inhibitor p27 and its deregulation in cancer. J Cell Physiol 183(1):10-17.8. Toyoshima H, Hunter T. 1994. p27, a novel inhibitor of G1 cyclin-Cdk protein kinase activity, is related to p21. Cell 78(1):67-74.9. Shapiro GI, Edwards CD, Rollins BJ. 2000. The physiology of p16(INK4A)-mediated G1 proliferative arrest. Cell Biochem Biophys 33(2):189-197.10. Liggett WH Jr, Sidransky D. 1998. Role of the p16 tumor suppressor gene in cancer. J Clin Oncol 16(3):1197-1206.

89355819

ABD72255.1

Q208B5

6,862 Da

Apoptosis Pathway (198797); Apoptosis Modulation And Signaling Pathway (198822); Bladder Cancer Pathway (83115); Bladder Cancer Pathway (527); Cell Cycle Pathway (530733); Cell Cycle, Mitotic Pathway (105765); Cell Cycle Pathway (198811); Cell Cycle Pathway (83054); Cell Cycle Pathway (463); Cellular Senescence Pathway (905991)

This gene generates several transcript variants which differ in their first exons. At least three alternatively spliced variants encoding distinct proteins have been reported, two of which encode structurally related isoforms known to function as inhibitors of CDK4 kinase. The remaining transcript includes an alternate first exon located 20 Kb upstream of the remainder of the gene; this transcript contains an alternate open reading frame (ARF) that specifies a protein which is structurally unrelated to the products of the other variants. This ARF product functions as a stabilizer of the tumor suppressor protein p53 as it can interact with, and sequester, the E3 ubiquitin-protein ligase MDM2, a protein responsible for the degradation of p53. In spite of the structural and functional differences, the CDK inhibitor isoforms and the ARF product encoded by this gene, through the regulatory roles of CDK4 and p53 in cell cycle G1 progression, share a common functionality in cell cycle G1 control. This gene is frequently mutated or deleted in a wide variety of tumors, and is known to be an important tumor suppressor gene. [provided by RefSeq, Sep 2012]

p16-INK4A: a cell-cycle regulatory protein that interacts with CDK4 and CDK6, inhibiting their ability to interact with cyclins D. Inhibits the phosphorylation of the retinoblastoma protein by CDK4 or CDK6, and entry into the S phase of the cell cycle. The p16INK4A and p14ARF proteins are encoded by CDKN2A, a known tumour suppressor gene in multiple cancers. CDKN2A is inactivated in 72% of cases of lung squamous cell carcinoma: 21% by epigenetic silencing by methylation, 18% inactivating mutation, 4% by exon 1b skipping, and 29% by homozygous deletion. Defects in CDKN2A are the cause of familial atypical multiple mole melanoma-pancreatic carcinoma syndrome, Li-Fraumeni syndrome, and the melanoma-astrocytoma syndrome. The melanoma-astrocytoma syndrome is characterized by a dual predisposition to melanoma and neural system tumors, commonly astrocytoma. Four alternatively spliced p16 isoforms have been reported. Two alternatively spliced isoforms of ARF have been reported. Protein type: Cell cycle regulation; Nucleolus; Tumor suppressor. Chromosomal Location of Human Ortholog: 9p21. Cellular Component: nucleoplasm; nuclear body; protein complex; mitochondrion; cytoplasm; nucleolus; nucleus; cytosol. Molecular Function: cyclin-dependent protein kinase inhibitor activity; NF-kappaB binding; protein binding; DNA binding; p53 binding; ubiquitin-protein ligase inhibitor activity; transcription factor binding; protein kinase binding. Biological Process: protein polyubiquitination; positive regulation of apoptosis; positive regulation of transcription, DNA-dependent; regulation of protein stability; negative regulation of B cell proliferation; regulation of protein export from nucleus; negative regulation of cell proliferation; apoptotic mitochondrial changes; regulation of G2/M transition of mitotic cell cycle; somatic stem cell division; cell cycle arrest; caspase activation; negative regulation of immature T cell proliferation in the thymus; protein destabilization; transcription, DNA-dependent; protein stabilization; negative regulation of cyclin-dependent protein kinase activity; negative regulation of cell-matrix adhesion; positive regulation of protein sumoylation; inhibition of NF-kappaB transcription factor; Ras protein signal transduction; negative regulation of ubiquitin-protein ligase activity; negative regulation of phosphorylation; negative regulation of protein kinase activity; positive regulation of transcription from RNA polymerase II promoter; positive regulation of DNA damage response, signal transduction by p53 class mediator; mitotic cell cycle; negative regulation of cell growth; negative regulation of transcription, DNA-dependent; rRNA processing; G1/S transition of mitotic cell cycle. Disease: Melanoma-astrocytoma Syndrome; Melanoma, Cutaneous Malignant, Susceptibility To, 2; Melanoma-pancreatic Cancer Syndrome

0.2 mg

240 USD