Human P16 Antibody - #BF0580

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Product: Human P16 Antibody
Catalog: BF0580
Description: Mouse monoclonal antibody to Human P16
Application: WB IHC IF/ICC ELISA
Reactivity: Human
Mol.Wt.: 40kDa; 17kD(Calculated).
Uniprot: P42771
RRID: AB_2833600

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Lead Time: Same day delivery

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Related Downloads
MSDS
Data Sheet
COA
Protocols
WB Handbook
IHC Protocol
IF/ICC Protocol

Product Info

Source:
Mouse
Application:
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.
*Tips:

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.

Reactivity:
Human
Clonality:
Monoclonal [AFB1575]
Specificity:
Human P16 antibody detects endogenous levels of total Human P16.
RRID:
AB_2833600
Cite Format: Affinity Biosciences Cat# BF0580, RRID:AB_2833600.
Conjugate:
Unconjugated.
Purification:
Affinity-chromatography.
Storage:
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.
Alias:

Fold/Unfold

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;

Immunogens

Immunogen:

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

Uniprot:

P42771(CDN2A_HUMAN) >>Visit HPA database.

Gene(ID):
CDKN2A(1029)
Expression:
P42771 CDN2A_HUMAN:

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

Description:
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.
Sequence:
MEPAAGSSMEPSADWLATAAARGRVEEVRALLEAGALPNAPNSYGRRPIQVMMMGSARVAELLLLHGAEPNCADPATLTRPVHDAAREGFLDTLVVLHRAGARLDVRDAWGRLPVDLAEELGHRDVARYLRAAAGGTRGSNHARIDAAEGPSDIPD

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

Function:

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.

PTMs:

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.

Family&Domains:

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)

References

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

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