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USF2 inhibits C/EBP-mediated transcriptional regulation of the RIIβ subunit of cAMP-dependent protein kinase

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Publisher
BioMed Central
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PMC
Keywords
  • Research Article
Disciplines
  • Biology
  • Chemistry

Abstract

1471-2199-3-10.fm ral BioMed CentBMC Molecular Biology BMC Molecular Biology 2002, 3 xResearch article USF2 inhibits C/EBP-mediated transcriptional regulation of the RIIβ subunit of cAMP-dependent protein kinase Maria Krudtaa Dahle, Kjetil Taskén and Kristin Austlid Taskén* Address: Department of Medical Biochemistry, Institute of Basic Medical Sciences, University of Oslo, N-0317 Oslo, Norway E-mail: Maria Dahle - [email protected]; Kjetil Taskén - [email protected]; Kristin Taskén* - [email protected] *Corresponding author Abstract Background: Cyclic AMP-dependent protein kinase (PKA) plays a central role in regulation of energy metabolism. Upon stimulation of testicular Sertoli cells by follicle stimulating hormone (FSH), glycolysis is activated to increase the production of nutrients for the germ cells, and a new regulatory subunit of cAMP-dependent protein kinase, RIIβ, is induced. We have previously shown that production of the transcription factor C/EBPβ is rapidly increased by FSH and cAMP in primary Sertoli cell cultures, and that C/EBPβ induces the RIIβ promoter. Results: In this work we show that USF1, USF2 and truncated USF isoforms bind to a conserved E-box in the RIIβ gene. Interestingly, overexpression of USF2, but not USF1, led to inhibition of both cAMP- and C/EBPβ-mediated induction of RIIβ. Furthermore, Western blots show that a novel USF1 isoform is induced by cAMP in Sertoli cells. Conclusions: These results indicate that the expression of various USF isoforms may be regulated by cAMP, and that the interplay between USF and C/EBPβ is important for cAMP-mediated regulation of RIIβ expression. The counteracting effects of USF2 and C/EBPβ observed on the RIIβ promoter is in accordance with the hypothesis that C/EBP and USF play opposite roles in regulation of glucose metabolism. Background Follicle stimulating hormone (FSH) regulates sperma- togenesis through the somatic Sertoli cells of the testis [1]. Sertoli cells act as "nur

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