| First Author | Cunningham JJ | Year | 2002 |
| Journal | Mol Cell Neurosci | Volume | 19 |
| Issue | 3 | Pages | 359-74 |
| PubMed ID | 11906209 | Mgi Jnum | J:75882 |
| Mgi Id | MGI:2177993 | Doi | 10.1006/mcne.2001.1090 |
| Citation | Cunningham JJ, et al. (2002) The Cyclin-Dependent Kinase Inhibitors p19(Ink4d) and p27(Kip1) Are Coexpressed in Select Retinal Cells and Act Cooperatively to Control Cell Cycle Exit. Mol Cell Neurosci 19(3):359-74 |
| abstractText | Cyclin-dependent kinase inhibitors (cdki's), including p19(Ink4d) and p27(Kip1), mediate exit from the cell cycle. To determine the function of these cdki's in regulating neurogenesis, we examined retina from wild-type, Ink4d-null, and Ink4d/Kip1-double null animals. Ink4d was expressed in progenitors and select neurons in the mature retina. Ink4d-null retina showed an extended period of proliferation, followed by apoptosis. Colabeling for p19(Ink4d) and p27(Kip1) revealed that a subpopulation of cells expressed both inhibitors. Deletion of Ink4d and Kip1 resulted in continued proliferation that was synergistic. This hyperproliferation led to an increase in number of horizontal cells and differentiated neurons reentering the cell cycle. Deletion of Ink4d and Kip1 also exacerbated the retinal dysplasia observed in Kip1-null mice, which was shown to be partly dependent on p53. These data indicate that select retinal cells express both p19(Ink4d) and p27(Kip1) and that they act cooperatively to ensure cell cycle exit. (c)2002 Elsevier Science (USA). |
