Increased expression of polypyrimidine tract binding protein results in higher insulin mRNA levels.
The aim of this study was to further elucidate the role of the polypyrimidine tract binding protein (PTB) in the control of insulin mRNA stability. We observed that the glucose- or interleukin-1beta-induced increase in insulin mRNA was paralleled by an increase in PTB mRNA. To further test the hypothesis that PTB controls insulin gene expression, betaTC-6 cells were treated with a PTB-specific siRNA to modify the beta-cell content of PTB. Surprisingly, we observed an increase in PTB mRNA and PTB protein levels in response to the siRNA treatment. In addition, the PTB-siRNA treatment also increased insulin mRNA. We conclude that expression of the PTB gene controls insulin production.
Fred
Rikard G
RG
Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
Welsh
Nils
N
D000818:Animals; D002460:Cell Line; D004305:Dose-Response Relationship, Drug; D005786:Gene Expression Regulation / Q000187:drug effects / Q000502:physiology*; D005947:Glucose / Q000494:pharmacology; D007328:Insulin / Q000235:genetics / Q000378:metabolism*; D007375:Interleukin-1 / Q000494:pharmacology; D007515:Islets of Langerhans / Q000187:drug effects / Q000378:metabolism*; D051379:Mice; D038941:Polypyrimidine Tract-Binding Protein / Q000235:genetics / Q000378:metabolism*; D015202:Protein Engineering / Q000379:methods; D012333:RNA, Messenger / Q000378:metabolism*; D011994:Recombinant Proteins / Q000378:metabolism
D007328:Insulin; D007375:Interleukin-1; D012333:RNA, Messenger; D011994:Recombinant Proteins; D038941:Polypyrimidine Tract-Binding Protein; D005947:Glucose