p16^INK4A (C-Term) Rabbit Monoclonal Antibody (Clone RM409)

p16^INK4A is a negative regulator of the cell cycle encoded by the CDKN2A gene in humans that limits cell cycle progression and promotes cellular senescence.^1,2 It induces cell cycle arrest at the G₁ phase by binding to cyclin-dependent kinase 4 (Cdk4) or Cdk6 in the cytoplasm, inhibiting formation of the cyclin D1/Cdk4/6 complex. p16^INK4A is expressed at low levels during homeostasis and is increased in response to cellular stressors, including oncogene activation and reactive oxygen species (ROS).² It is regulated by a variety of transcriptional, translational, and epigenetic mechanisms, such as chromatin modifications mediated by polycomb repressive complex 1 (PRC1) and PRC2 that inhibit CDKN2A expression.^1,2,3 Aberrant CDKN2A mRNA and p16^INK4A protein levels have been found in tumor biopsies from patients with a variety of cancers, including colon, breast, gall bladder, or head and neck cancer.² CDKN2A SNPs have been found in patients with follicular lymphoma and are associated with reduced overall survival.⁴ Cayman's p16^INK4A (C-Term) Rabbit Monoclonal Antibody (Clone RM409) can be used for immunohistochemistry (IHC) and Western blot (WB) applications.

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1. Zhao, R., Choi, B.Y., Lee, M.-H., et al. Implications of genetic and epigenetic alterations of CDKN2A (p16INK4a) in cancer. EBioMedicine 8, 30-39 (2016).

2. Inoue, K., and Fry, E.A. Aberrant expression of p16INK4a in human cancers – a new biomarker? Cancer Rep. Rev. 2(2), (2018).

3. LaPak, K.M., and Burd, C.E. The molecular balancing act of p16INK4a in cancer and aging. Mol. Cancer Res. 12(2), 167-183 (2014).

4. Alhejaily, A., Day, A.G., Feilotter, H.E., et al. Inactivation of the CDKN2A tumor-suppressor gene by deletion or methylation is common at diagnosis in follicular lymphoma and associated with poor clinical outcome. Clin. Cancer Res. 20(6), 1676-1686 (2014).