| First Author | Moser M | Year | 1997 |
| Journal | Genes Dev | Volume | 11 |
| Issue | 15 | Pages | 1938-48 |
| PubMed ID | 9271117 | Mgi Jnum | J:42260 |
| Mgi Id | MGI:1095454 | Doi | 10.1101/gad.11.15.1938 |
| Citation | Moser M, et al. (1997) Enhanced apoptotic cell death of renal epithelial cells in mice lacking transcription factor AP-2beta. Genes Dev 11(15):1938-48 |
| abstractText | Expression of AP-2 transcription factors has been detected previously in embryonic renal tissues. We show here that AP-2 beta -/- mice complete embryonic development and die at postnatal days 1 and 2 because of polycystic kidney disease. Analyses of kidney development revealed that induction of epithelial conversion, mesenchyme condensation, and further glomerular and tubular differentiation occur normally in AP-2 beta-deficient mice. At the end of embryonic development expression of bcl-X-L, bcl-w, and bcl-2 is down-regulated in parallel to massive apoptotic death of collecting duct and distal tubular epithelia. Addressing the molecular mechanism we show that transfection of AP-2 into cell lines in vitro strongly suppresses c-myc-induced apoptosis pointing to a function of AP-2 in programming cell survival during embryogenesis. The position of the human AP-2 beta gene was identified at chromosome 6p12-p21.1, within a region that has been mapped for autosomal recessive polycystic kidney disease (ARPKD). Sequence analyses of ARPKD patients and linkage analyses using intragenic polymorphic markers indicate that the AP-2 beta gene is located in close proximity to but distinct from the ARPKD gene. |
