CDKN2A; ARF; CDK4I; CDKN2; CMM2; INK4; INK4a; MLM; MTS1; TP16; p14; p14ARF; p16; p16INK4; p16INK4a; p19; ARF; CDKN2A

For Research Use Only. Not for use in diagnostic procedures.

Polyclonal

IgG

Rabbit

Store at -20 degree C. Avoid freeze/thaw cycles.

Manufactured in an ISO 9001:2015 Certified Laboratory.

Small volumes of anti-CDKN2A antibody vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

The division cycle of eukaryotic cells is regulated by a family of protein kinases known as the cyclin-dependent kinases (CDKs). The sequential activation of individual members of this family and their consequent phosphorylation of critical substrates promotes orderly progression through the cell cycle. It has been reported that CDKN2A binds to CDK4 and inhibits the catalytic activity of the CDK4/cyclin D enzymes. CDKN2A seems to act in a regulatory feedback circuit with CDK4, D-type cyclins and retinoblastoma protein (1). The INK4 (inhibitor of cyclin-dependent kinase 4) family consists of four tumor-suppressor proteins: p15(INK4B), CDKN2A(INK4A), p18(INK4C), and p19(INK4D). While their sequences and structures are highly homologous, they show appreciable differences in conformational flexibility, stability, and aggregation tendency (2). Cell cycle arrest at the G1 checkpoint allows completion of critical macromolecular events prior to S phase. Regulators of the G1 checkpoint include an inhibitor of cyclin-dependent kinase, CDKN2AINK4; two tumor-suppressor proteins, p53 and RB and cyclin D1. CDKN2AINK4 is a tumor-suppressor protein and that genetic and epigenetic abnormalities in genes controlling the G1 checkpoint can lead to both escape from senescence and cancer formation (3).

Western Blot (WB), Immunofluorescence (IF)

WB: 1:500 - 1:2000

11kDa

cyclin dependent kinase inhibitor 2A

cyclin-dependent kinase inhibitor 2A

Cyclin-dependent kinase inhibitor 2A

CDK4I; MTS-1; p16-INK4; p16INK4A??[Similar Products]

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: 9p21.3

Cellular Component: cytoplasm; cytosol; nucleus

Molecular Function: cyclin-dependent protein kinase inhibitor activity; NF-kappaB binding; protein binding; protein kinase binding; RNA binding

Biological Process: cell cycle arrest; G1/S transition of mitotic cell cycle; inhibition of NF-kappaB transcription factor; negative regulation of cell growth; negative regulation of cell proliferation; negative regulation of cell-matrix adhesion; negative regulation of cyclin-dependent protein kinase activity; negative regulation of phosphorylation; negative regulation of transcription, DNA-dependent; Ras protein signal transduction

Disease: Melanoma, Cutaneous Malignant, Susceptibility To, 2; Melanoma-astrocytoma Syndrome; Melanoma-pancreatic Cancer Syndrome

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