p16INK4a (encoded by CDKN2A) is a cyclin-dependent kinase inhibitor that blocks CDK4/6-mediated phosphorylation of Rb, enforcing G1 cell cycle arrest. It is one of the most frequently inactivated tumor suppressors in human cancers — deleted, mutated, or silenced by promoter methylation across melanoma, pancreatic cancer, glioblastoma, NSCLC, and many other malignancies. Simultaneously, p16INK4a accumulation is the most widely accepted biomarker of cellular senescence.
abinScience offers anti-p16INK4a antibodies for both human and mouse targets, including a VHH nanobody format, along with recombinant p16 proteins for assay development and positive controls.
Why abinScience?
✓ Human & mouse coverage — Polyclonal antibodies targeting human and mouse CDKN2A/p16INK4a separately
✓ VHH nanobody available — Recombinant nanobody (SAA2259) for enhanced tissue penetration in IHC and super-resolution imaging
✓ Recombinant proteins — His-tagged and GST-tagged human and mouse p16 proteins for controls and standards
Available Products
Anti-p16INK4a / CDKN2A Antibodies
Polyclonal and nanobody formats targeting CDKN2A/p16INK4a.
CDKN2A / p16INK4a Recombinant Proteins
Purified recombinant p16 proteins for western blot positive controls, ELISA standards, and in vitro CDK inhibition assays.
About the Target
Gene: CDKN2A (also: p16, p16INK4a, MTS1, CDK4I)
UniProt: P42771 (Human)
Molecular weight: ~16.5 kDa
Chromosomal location: 9p21.3
The CDKN2A locus is remarkable in encoding two distinct tumor suppressors through alternative reading frames: p16INK4a (exons 1α, 2, 3) and p14ARF (exons 1β, 2, 3). p16INK4a directly inhibits CDK4 and CDK6, preventing Rb phosphorylation and maintaining G1 arrest. Loss of p16 function — through homozygous deletion (especially at 9p21.3), point mutation, or CpG island methylation — is among the most common genetic alterations in cancer and a hallmark of the CDKN2A/Rb pathway disruption.
Frequently Asked Questions
What is p16INK4a used as a biomarker for?
p16INK4a serves as a biomarker in two major contexts. In oncology, loss of p16 expression (by IHC) indicates CDKN2A deletion or silencing in tumors. In cervical pathology, p16 overexpression is a surrogate marker for high-risk HPV E7 oncoprotein activity and is used clinically in CINtec Histology for cervical cancer screening. Additionally, p16 accumulation is the most widely accepted marker of cellular senescence in aging research.
What is the difference between p16INK4a and p14ARF?
Both are encoded by the CDKN2A locus but use different first exons and reading frames. p16INK4a inhibits CDK4/6 in the Rb pathway, while p14ARF stabilizes p53 by sequestering MDM2. They are functionally distinct tumor suppressors that share exons 2 and 3 but produce completely different proteins.
Why use a nanobody for p16 detection?
The VHH nanobody format (~15 kDa) offers superior tissue penetration compared to conventional IgG (~150 kDa). This is particularly useful for p16 IHC in FFPE tissues where antigen accessibility can be challenging due to cross-linking. Nanobodies also provide reduced background and more uniform staining in dense tissue sections.
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All products are for research use only (RUO). Not intended for diagnostic or therapeutic use. Product availability and specifications are subject to change. Visit individual product pages for the most current information.
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