Moser, M and Pscherer, A and Roth, C and Becker, J and Mucher, G and Zerres, K and Dixkens, C and Weis, J and GuayWoodford, L and Buettner, R and Fassler, R (1997) Enhanced apoptotic cell death of renal epithelial cells in mice lacking transcription factor AP-2 beta. GENES & DEVELOPMENT, 11 (15). pp. 1938-1948. ISSN 0890-9369,
Full text not available from this repository.Abstract
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.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | POLYCYSTIC KIDNEY-DISEASE; FACTOR AP-2; DNA-BINDING; C-MYC; ACTIVATION; CLONING; INSITU; AP-2 beta; gene targeting; apoptosis; c-myc; ARPKD |
| Depositing User: | Dr. Gernot Deinzer |
| Last Modified: | 19 Oct 2022 08:31 |
| URI: | https://pred.uni-regensburg.de/id/eprint/50668 |
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