Role in Regeneration Knockdown of CDKN1B stimulates regeneration of cochlear hair cells in mice. Since CDKN1B prevents cells from entering the cell cycle, inhibition of the protein could cause re-entry and subsequent division. In mammals where regeneration of cochlear hair cells normally does not occur, this inhibition could help regrow damaged cells who are otherwise incapable of proliferation. In fact, when the CDKN1B gene is disrupted in adult mice, hair cells of the organ of Corti proliferate, while those in control mice do not. Lack of CDKN1B expression appears to release the hair cells from natural cell-cycle arrest. Because hair cell death in the human cochlea is a major cause of hearing loss, the CDKN1B protein could be an important factor in the clinical treatment of deafness. Interactions CDKN1B has been shown to interact with: AKT1, CKS1B, Cyclin D3, Cyclin E1, Cyclin-dependent kinase 2, Cyclin-dependent kinase 4, Grb2, NUP50 SKP2, SPDYA, and XPO1. See also Sic1 (homologue in Saccharomyces cerevisiae) P21waf-1 (another CDK inhibitor) Hyaluronic acid synthase Hyaluronidase References Further reading External links Cell cycle regulators Tumor suppressor genes