Product Info

ELISA 1:10000, WB 1:500-1:2000, IHC 1:200-1:1000, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Monoclonal [AFB1575]
Human P16 antibody detects endogenous levels of total Human P16.
Cite Format: Affinity Biosciences Cat# BF0580, RRID:AB_2833600.
Mouse IgG1 in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.


Cyclin-dependent kinase inhibitor 2A;Cyclin-dependent kinase 4 inhibitor A;CDK4I;Multiple tumor suppressor 1;MTS-1;p16-INK4a;p16-INK4;p16INK4A;CDKN2A;CDKN2;MTS1;



Purified recombinant fragment of human Human P16 expressed in E. Coli.


Widely expressed but not detected in brain or skeletal muscle. Isoform 3 is pancreas-specific.

p16 (cyclin-dependent kinase inhibitor 2A, INK4a) is a tumor suppressor protein. It is a specific inhibitor of Cdk 4 / Cdk 6, and a tumor suppressor involved in the pathogenesis of a variety of malignancies. Recent analyses of the p16 INK4a gene revealed homozygous deletions, nonsense, missense, or frameshift mutations in several human cancers. Although the frequency of p16 INK4a abnormalities is higher in tumor derived cell lines than in unselected primary tumors, significant subsets of clinical cases with aberrant p16 INK4a gene have been reported among melanomas, gliomas, esophageal, pancreatic, lung, and urinary bladder carcinomas, and some types of leukemia.

PTMs - P42771 As Substrate

Site PTM Type Enzyme
M1 Acetylation
S7 Phosphorylation Q13535 (ATR)
S8 Phosphorylation O14920 (IKBKB) , Q13535 (ATR)
Y44 Phosphorylation
R99 Methylation
R131 Methylation
R138 Methylation
S140 Phosphorylation Q13535 (ATR)
S152 Phosphorylation Q13535 (ATR)

Research Backgrounds


Acts as a negative regulator of the proliferation of normal cells by interacting strongly with CDK4 and CDK6. This inhibits their ability to interact with cyclins D and to phosphorylate the retinoblastoma protein.


Phosphorylation seems to increase interaction with CDK4.

Subcellular Location:

Cytoplasm. Nucleus.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Widely expressed but not detected in brain or skeletal muscle. Isoform 3 is pancreas-specific.

Subunit Structure:

Heterodimer with CDK4 or CDK6. Predominant p16 complexes contained CDK6. Interacts with CDK4 (both 'T-172'-phosphorylated and non-phosphorylated forms); the interaction inhibits cyclin D-CDK4 kinase activity. Interacts with ISCO2.


Belongs to the CDKN2 cyclin-dependent kinase inhibitor family.

Research Fields

· Cellular Processes > Cell growth and death > Cell cycle.   (View pathway)

· Cellular Processes > Cell growth and death > p53 signaling pathway.   (View pathway)

· Cellular Processes > Cell growth and death > Cellular senescence.   (View pathway)

· Human Diseases > Drug resistance: Antineoplastic > Endocrine resistance.

· Human Diseases > Drug resistance: Antineoplastic > Platinum drug resistance.

· Human Diseases > Infectious diseases: Viral > HTLV-I infection.

· Human Diseases > Cancers: Overview > Pathways in cancer.   (View pathway)

· Human Diseases > Cancers: Overview > Viral carcinogenesis.

· Human Diseases > Cancers: Overview > MicroRNAs in cancer.

· Human Diseases > Cancers: Specific types > Pancreatic cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Glioma.   (View pathway)

· Human Diseases > Cancers: Specific types > Melanoma.   (View pathway)

· Human Diseases > Cancers: Specific types > Bladder cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Chronic myeloid leukemia.   (View pathway)

· Human Diseases > Cancers: Specific types > Non-small cell lung cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Hepatocellular carcinoma.   (View pathway)


1). Characterization of immune microenvironment in patients with HPV-positive and negative head and neck cancer. Scientific data (PubMed: 37828063) [IF=9.8]

Application: IHC    Species: Human    Sample:

Fig. 6 The in vitro study reveals that FCER2+ B cells inhibit the proliferation and migration ability of HPV+ tumors. (a) Flow cytometry analysis of B cells, plasma cells, macrophages, and FCER2+ B cells from PBMCs of patients with HNSCC. (b) Representative histopathological staining and HPV-p16, as well as FCER2 immunofluorescent staining images of HNSCC samples. FCER2+ B cells are cocultured with HPV+ SCC090 cells. (c) Scratch experiment showing cell migration. (d) Transwell chamber invasion assay showing cell invasion. (e) CCK-8 experiment showing cell proliferation. Figure 6 represents three experiments that achieved similar results. *p 

2). Effects of Ginsenoside Rg1 on the Biological Behavior of Human Amnion-Derived Mesenchymal Stem/Stromal Cells (hAD-MSCs). Stem Cells International (PubMed: 36845966) [IF=4.3]

Application: WB    Species: Human    Sample: hAD-MSCs

Figure 6 Effects of ginsenoside Rg1 on the senescence of hAD-MSCs. (a) Senescent cells were detected by SA-β-Gal staining in the control, D-gal, Rg1, and Rg1+D-gal groups (×100). (b) hAD-MSC senescence rates were compared in the control, D-gal, Rg1, and Rg1+D-gal groups. (c, d) The expressions of cyclin D1, cyclin E1, CDK2, CDK4, p14ARF, p21CIP1, p53, and p16INK4a in hAD-MSCs were analyzed (c) and compared (d) by western blot in the control, D-gal, Rg1, and Rg1+D-gal groups. Representative images are shown. The red arrow indicates senescent hAD-MSCs stained with blue. Scale bars = 100 μm.

3). p16 and p53 can Serve as Prognostic Markers for Head and Neck Squamous Cell Carcinoma. International dental journal (PubMed: 38105167) [IF=3.3]

4). Yishen Xiezhuo formula ameliorates the development of cisplatin-induced acute kidney injury by attenuating renal tubular epithelial cell senescence. Annals of Translational Medicine (PubMed: 36660714)

Application: WB    Species: Human    Sample: kidney

Figure 2 Expression of senescence-related proteins of each group. **P

Restrictive clause


Affinity Biosciences tests all products strictly. Citations are provided as a resource for additional applications that have not been validated by Affinity Biosciences. Please choose the appropriate format for each application and consult Materials and Methods sections for additional details about the use of any product in these publications.

For Research Use Only.
Not for use in diagnostic or therapeutic procedures. Not for resale. Not for distribution without written consent. Affinity Biosciences will not be held responsible for patent infringement or other violations that may occur with the use of our products. Affinity Biosciences, Affinity Biosciences Logo and all other trademarks are the property of Affinity Biosciences LTD.