کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10904848 | 1086702 | 2005 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Elevation of cyclic AMP in Jurkat T-cells provokes distinct transcriptional responses through the protein kinase A (PKA) and exchange protein activated by cyclic AMP (EPAC) pathways
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کلمات کلیدی
pKaEMSACPT-cAMPDulbecco's modified Eagles' mediumPhorbol 12-myristate-13-acetateH-89P27kip1GEFcyclic AMP-response element binding proteinEpacCREBPAGEGSTIBMXDMEMORFp53PMA - LDC هاCyclic adenosine monophosphate - آدنوزین مونوفسفات CyclicElectrophoretic mobility shift assay - آزمون تحرک تحرک الکتروفورزpolyacrylamide gel electrophoresis - الکتروفورز ژل پلی آکریل آمیدisobutylmethylxanthine - ایزوبویل methylxanthinec-Jun - جون ژوئنguanine nucleotide exchange factor - فاکتور تبادل نوکلئوتید گوانینopen reading frame - قاب خواندن بازpolymerase chain reaction - واکنش زنجیره ای پلیمرازPCR - واکنش زنجیرهٔ پلیمرازprotein kinase A - پروتئین کیناز ACell cycle - چرخه سلولیglutathione-S-transferase - گلوتاتیون S-ترانسفراز
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Elevation of cyclic AMP in Jurkat T-cells provokes distinct transcriptional responses through the protein kinase A (PKA) and exchange protein activated by cyclic AMP (EPAC) pathways Elevation of cyclic AMP in Jurkat T-cells provokes distinct transcriptional responses through the protein kinase A (PKA) and exchange protein activated by cyclic AMP (EPAC) pathways](/preview/png/10904848.png)
چکیده انگلیسی
Elevating cyclic AMP with a combination of forskolin and IBMX (Fskn/IBMX) was found as the cause of G1 growth arrest in Jurkat T-cells, concomitant with an induction of the cyclin-dependent kinase inhibitor, p27Kip1. The protein kinase inhibitor H-89, which can discriminate between EPAC and PKA pathways, blocked the inhibition in cell growth and induction of p27Kip1, indicating an involvement of PKA, but not EPAC. The EPAC-specific cyclic AMP analogue, 8-CPT-2Me-cAMP was able to activate Rap1, but failed to induce growth arrest or induction p27Kip1. These results demonstrate that PKA, and not EPAC, mediates cyclic AMP-dependent growth arrest in Jurkat T-cells. To further investigate a role for EPAC in these cells, we carried out cDNA microarray analysis of cells stimulated with 8-CPT-2Me-cAMP. We identified separate groups of genes whose expression was either induced or repressed in response to 8-CPT-2Me-cAMP. This provides the first demonstration that EPAC can regulate gene expression, although it may not be involved in cell cycle control. Finally, we identify c-Jun as a transcription factor whose activity is specifically down-regulated following EPAC activation, but not PKA. The control of gene expression by cyclic AMP in Jurkat T-cells therefore requires input from the EPAC signalling cascade.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Cell Research - Volume 309, Issue 1, 10 September 2005, Pages 161-173
Journal: Experimental Cell Research - Volume 309, Issue 1, 10 September 2005, Pages 161-173
نویسندگان
Suzanne Fuld, Gillian Borland, Stephen J. Yarwood,