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P19INK4D and Cell Death
Luz E. Tavera-Mendoza, Tian-Tian Wang and John H. White
volume 5 | issue 6
16 march 2006Pages: 596 - 598
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INK4 proteins are members of a family of cyclin-dependent kinase (CDK) inhibitors that function in G1 to block the activity of CDKs 4 and 6. While they share clear structural similarities, numerous studies have shown that INK4 proteins differ in their expression patterns during development and in the adult, and have differing roles in tumor suppression. A recent study from our laboratory showed that expression of the gene encoding p19INK4D is induced by the hormonal form of vitamin D3 and by retinoids, both of which signal through related nuclear receptor transcription factors. Although vitamin D3 and retinoids have distinct developmental and physiological functions, both regulate the cell cycle and have been shown to have chemopreventive effects in a range of studies. Induction of p19INK4D expression contributed to cell cycle arrest by both ligands. However, knockdown of p19INK4D rendered cells sensitive to autophagic cell death, a remarkable phenotype given the hyperproliferative responses to loss of other INK4 proteins. We discuss the relevance of our studies and recent findings of others to the cell death observed in p19INK4D-deficient animals and to a possible role for p19INK4D induction in chemoprevention.
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.