Sp1 is a key regulator of the PDGF β-receptor transcription View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2001-12

AUTHORS

Catrin Molander, Anders Hackzell, Mitsuhiro Ohta, Hiroto Izumi, Keiko Funa

ABSTRACT

The mouse PDGF β-receptor promoter is tightly controlled by NF-Y that binds to a CCAAT box located upstream of the initiation site [1, 2]. In this report, we show that Sp1 plays an essential role in the PDGF β-receptor transcription. Within the upstream GC rich area there are two Sp1 binding sites located in close proximity to the CCAAT box. Deletion of the GC rich region resulted in a 50% decrease of the transcriptional activity of the promoter, and a complete loss of its responsiveness to over-expression of Sp1. There was an additive effect between NF-Y and Sp1 in reporter activity when they were co-transfected together with the promoter-reporter construct. Furthermore, transfection of NF-Y failed to enhance transcriptional activity when the Sp1 binding sites were deleted from the promoter, suggesting an important role for Sp1 in this NF-Y controlled transcription. We have recently reported that c-Myc represses PDGF β-receptor transcription through its interference with the transactivation activity of NF-Y [3]. In the case of p21waf1/cip1 transcription, c-Myc was shown to repress its transcription by sequestering Sp1 [4]. However, we could not find any effect of Sp1 in the c-Myc-mediated repression on the PDGF β-receptor promoter, since the deletion of Sp1 binding sites could not attenuate the repression by c-Myc on the promoter activity. More... »

PAGES

223-233

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1023/a:1015701232589

DOI

http://dx.doi.org/10.1023/a:1015701232589

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1005218977

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/12153142


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