| 1. |
- Miller, S J, et al.
(författare)
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A novel type of regulatory element is required for promoter-specific activity of the PDGF-B intronic enhancer region.
- 1998
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Ingår i: Growth Factors. - 0897-7194 .- 1029-2292. ; 16:2, s. 137-51
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Tidskriftsartikel (refereegranskat)abstract
- We have previously described a non-classical, promoter-specific enhancer for the human Platelet-Derived Growth Factor B (PDGF-B) gene. In JEG-3 choriocarcinoma cells the activity of the enhancer depends upon co-operation with a sequence (the Enhancer-Dependent cis Co-activator "EDC" element) within the promoter. The PDGF-B enhancer fails to activate heterologous promoters, indicating that promoter-specificity depends on an element within the enhancer that can recognise a target sequence within the promoter. Here we identify a sequence within the enhancer of the PDGF-B gene which directs activation of the PDGF-B promoter by distal cis-acting elements. This specifies the wild-type PDGF-B promoter as the target for the enhancer and has been designated the EDC specificity element (EDCse). The cell-type specific nature of this interaction is extended by the observation that the EDCse is also dispensable for enhancer activity in breast-cancer cells (ZR-75). Concomitant to this observation, JEG-3 and ZR-75 cells differ in the binding of nuclear factors to the EDCse. We discuss the relevance of the EDC/EDCse system in regulation of gene expression.
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| 2. |
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| 3. |
- Franklin, Gary C., et al.
(författare)
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An Inr-containing sequence flanking the TATA box of the human c-sis (PDGF-B) proto-oncogene promoter functions in cis as a co-activator for its intronic enhancer
- 1995
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Ingår i: Oncogene. - 0950-9232 .- 1476-5594. ; 11:9, s. 1873-1884
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- High-level activity of the human PDGF-B promoter in choriocarcinoma cell lines depends upon an atypical, intronic enhancer-like element which does not function with heterologous promoters tested. An extensive series of mutant PDGF-B promoter-driven constructs identified a sequence flanking the TATA box which is required specifically for enhancer-mediated transcription in human choriocarcinoma cell lines. This element, which we here term an enhancer-dependent cis co-activator (EDC) contains an Inr (initiator) consensus sequence upstream of the TATA box which is required, but not sufficient for its function. Requirement for the EDC is cell type-specific, since it was dispensable for enhancer-mediated transcription in a human breast cancer cell line. Although it lies within the region defined, the TATA box itself is not required for EDC function, or for basal promoter function which may derive from a second Inr-like sequence situated at the transcriptional start site. These observations indicate that interactions between some promoter and enhancer elements may be more complex than that generally described for 'classical' enhancer systems and may suggest an additional function for the initiator motif.
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| 4. |
- Johansson, Tord, et al.
(författare)
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Results from PS185.
- 1999
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Ingår i: NUCLEAR PHYSICS A. - : ELSEVIER SCIENCE BV. ; , s. 173C-178C
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Konferensbidrag (refereegranskat)abstract
- The PS185 experiment at LEAR/CERN has studied strangeness production in antiproton-proton collisions. Exclusive final states of antihyperon-hyperon pairs have been measured in order to investigate strange-quark production dynamics. A comprehensive data se
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| 5. |
- Ohlsson, R, et al.
(författare)
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PDGFB regulates the development of the labyrinthine layer of the mouse fetal placenta.
- 1999
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Ingår i: Dev Biol. - : Elsevier BV. - 0012-1606. ; 212:1, s. 124-36
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Tidskriftsartikel (refereegranskat)abstract
- PDGFB is a growth factor which is vital for the completion of normal prenatal development. In this study, we report the phenotypic analysis of placentas from mouse conceptuses that lack a functional PDGFB or PDGFRbeta gene. Placentas of both types of mutant exhibit changes in the labyrinthine layer, including dilated embryonic blood vessels and reduced numbers of both pericytes and trophoblasts. These changes are seen from embryonic day (E) 13.5, which coincides with the upregulation of PDGFB mRNA levels in normal placentas. By E17, modifications in shape, size, and number of the fetal blood vessels in the mutant placentas cause an abnormal ratio of the surface areas between the fetal and the maternal blood vessels in the labyrinthine layer. Our data suggest that PDGFB acts locally to contribute to the development of the labyrinthine layer of the fetal placenta and the formation of a proper nutrient-waste exchange system during fetal development. We point out that the roles of PDGFB/Rbeta signaling in the placenta may be analogous to those in the developing kidney, by controlling pericytes in the labyrinthine layer and mesangial cells in the kidney.
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