Title : Cyclic AMP inhibition of thrombin-induced growth in vascular smooth muscle cells correlates with decreased JNK1 activity and c-Jun expression.

Pub. Date : 1996 Aug 23

PMID : 8702835






4 Functional Relationships(s)
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1 This report examines the role of ERKs and Jun N-terminal kinase 1 (JNK1) groups of mitogen-activated protein kinases in thrombin-induced DNA synthesis in VSMCs using agents such as forskolin and dibutyrylcyclic AMP that increase intracellular cAMP levels. Colforsin coagulation factor II, thrombin Homo sapiens
2 In contrast to ERKs and c-Fos, thrombin-induced JNK1 activation and c-Jun expression were sensitive to inhibition by forskolin, suggesting an association of these events with thrombin-stimulated growth in these cells. Colforsin coagulation factor II, thrombin Homo sapiens
3 In contrast to ERKs and c-Fos, thrombin-induced JNK1 activation and c-Jun expression were sensitive to inhibition by forskolin, suggesting an association of these events with thrombin-stimulated growth in these cells. Colforsin coagulation factor II, thrombin Homo sapiens
4 Thrombin also increased AP-1 activity, and this response was significantly blunted by forskolin. Colforsin coagulation factor II, thrombin Homo sapiens