antibody

Anti-P16 (Mouse and Human) Mouse mAb

MBS475739

0.1 mL

335 USD

monoclonal

mouse

nonconjugated

[4G5-5A10-3G6]

human, mouse, rat

western blot, immunohistochemistry

Antibody

Anti-P16 (Mouse and Human) Mouse mAb

[P16]

[P16]

[p16, partial; Cyclin-dependent kinase inhibitor 2A; cyclin-dependent kinase inhibitor 2A; cyclin dependent kinase inhibitor 2A; Cyclin-dependent kinase 4 inhibitor A; CDK4I; Multiple tumor suppressor 1; MTS-1; p16-INK4a; p16-INK4; p16INK4A]

[P16]

[P16]

[CDKN2A; CDKN2A; ARF; MLM; P14; P16; P19; CMM2; INK4; MTS1; TP16; CDK4I; CDKN2; INK4A; MTS-1; P14ARF; P19ARF; P16INK4; P16INK4A; P16-INK4A; CDK4I; MTS-1; p16-INK4; p16INK4A]

Monoclonal

Mouse IgG1

[4G5-5A10-3G6]

Mouse

Human, Rat, Mouse

Ascitic fluid

Ascitic fluid containing 0.03% sodium azide.

Store at +4°C short term. store at -20°c long term.Avoid freeze/thaw cycle

Western Blot (WB), Immunohistochemistry (IHC)

WB:1/500-1/2000. IHC:1/200-1/1000. Elisa:1/10000

Western Blot (WB)

Immunohistochemistry (IHC)

Antibody type: Primary antibody. Conjugation: Unconjugated. Modification: unmodified. Subcellular location: Mitochondrion,Nucleus

Immunogen: Purified recombinant fragment of P16 expressed in E Coli.

The progression of cells through the cell cycle is regulated by a family of protein kinases known as 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. The cyclins function as differentially expressed positive regulators of Cdks. Negative regulators of the cycle include the p53-inducible 21 kDa WAF1/Cip1 protein designated p21, Kip1 p27 and p16. The complexes formed by Cdk4 and the D-type cyclins have been strongly implicated in the control of cell proliferation during the G1 phase. It has recently been shown that p16 binds to Cdk4 and inhibits the catalytic activity of the Cdk4/cyclin D complex. Moreover, the gene encoding p16 exhibits a high frequency of homozygous deletions and point mutations in established human tumor cell lines.

89355819

ABD72255.1

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: 9p21.3. Cellular Component: cytoplasm; cytosol; nucleus. Molecular Function: cyclin-dependent protein kinase inhibitor activity; NF-kappaB binding; protein binding; protein kinase 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

0.1 mL

335 USD