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Qureshi HY Sylvester J El Mabrouk M Zafarullah M 《Journal of cellular physiology》2005,203(2):345-352
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Chadjichristos C Ghayor C Herrouin JF Ala-Kokko L Suske G Pujol JP Galéra P 《The Journal of biological chemistry》2002,277(46):43903-43917
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Bontemps Y Vuillermoz B Antonicelli F Perreau C Danan JL Maquart FX Wegrowski Y 《The Journal of biological chemistry》2003,278(24):21566-21575
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Transcription factor Sp1 binds to and activates a human hsp70 gene promoter. 总被引:7,自引:6,他引:1
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W D Morgan 《Molecular and cellular biology》1989,9(9):4099-4104
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We have previously demonstrated that activation of the Ras/Mapk pathways is required for transforming growth factor beta (TGF-beta) induction of TGF-beta(1) expression. Here we examined the role of the Ras/Mapk pathways in TGF-beta induction of urokinase-type plasminogen activator receptor (uPAR) expression in untransformed intestinal epithelial cells (IECs). TGF-beta activated the stress-activated protein kinases (Sapk)/c-Jun N-terminal kinases (JNKs) within 5-10 min, an effect that preceeded TGF-beta induction of uPAR expression in these cells. TGF-beta induction of both JNK1 activity and JunD phosphorylation was blocked by expression of a dominant-negative mutant of the type II TGF-beta receptor (DN TbetaRII), a dominant-negative mutant of MKK4 (DN MKK4), or a dominant-negative mutant of Ras (RasN17), or by the addition of the JNK inhibitor SP600125. TGF-beta also induced AP-1 complex formation at the distal AP-1 site (-184 to -178) of the uPAR promoter within 2 h of TGF-beta addition, consistent with the time-dependent up-regulation of uPAR expression. The primary components present in the TGF-beta-stimulated AP-1 complex bound to the uPAR promoter were Jun D and Fra-2. Moreover, addition of SP600125, or expression of DN MKK4 or DN TbetaRII, blocked TGF-beta up-regulation of uPAR in IECs. Accordingly, our results indicate that TGF-beta activates the Ras/MKK4/JNK1 signaling cascade, leading to induction of AP-1 activity, which, in turn, up-regulates uPAR expression. Our results also indicate that the type II TGF-beta receptor (RII) is required for TGF-beta activation of JNK1 and the resulting up-regulation of uPAR expression. 相似文献
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S J Kim F Denhez K Y Kim J T Holt M B Sporn A B Roberts 《The Journal of biological chemistry》1989,264(32):19373-19378
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