βc Cytokine Receptor-Induced Stimulation of cAMP Response Element Binding Protein Phosphorylation Requires Protein Kinase C In Myeloid Cells: A Novel Cytokine Signal Transduction Cascade

奶油 蛋白激酶C 磷酸化 生物 分子生物学 信号转导 细胞生物学 蛋白激酶A 激酶 响应元素 转录因子 化学 生物化学 基因表达 发起人 基因
作者
E. Gubina,Xu Luo,Evelyn M. Kwon,Kathleen M. Sakamoto,Yufang Shi,R. Allan Mufson
出处
期刊:Journal of Immunology [The American Association of Immunologists]
卷期号:167 (8): 4303-4310 被引量:29
标识
DOI:10.4049/jimmunol.167.8.4303
摘要

Abstract We have recently shown that IL-3R occupancy activates a phosphatidylcholine-specific phospholipase C, and the sustained diacylglycerol accumulation subsequently activates protein kinase C (PKC). In human IL-3-dependent myeloid cells (TF-1), the novel PKCε isoform regulates bcl-2 expression and cell survival. The report of a PKC activatable cAMP response element (CRE) in the bcl-2 promoter and a role for PKC in bcl-2 expression in B cells led us to the hypothesis that PKC phosphorylation activates transcription factor CREB after IL-3R engagement. We found that IL-3 and GM-CSF induced phosphorylation of CREB on Ser133 in TF-1 cells, and this phosphorylation was blocked by two structurally unrelated classes of PKC inhibitors. An inhibitor of cyclic nucleotide-dependent kinases did not block this phosphorylation. IL-4, which is biologically active in these cells but does not use the β common subunit, did not phosphorylate CREB on Ser133. Inhibition of mitogen-activated protein kinase kinase activity also inhibited IL3-induced CREB phosphorylation. The PKC inhibitors, but not a cyclic nucleotide-dependent kinase inhibitor, blocked IL-3 activation of CRE-dependent transcription from an egr-1 promoter/chloramphenicol acetyltransferase (CAT) reporter construction transiently transfected into TF-1 cells. Finally, TF-1 cells stably overexpressing PKCε, but not the δ isoform of PKC, enhanced CRE-dependent CAT expression from the promoter/reporter construction. Therefore, it is likely that a PKCε kinase cascade resulting in CREB phosphorylation represents a novel signal transduction cascade for regulating cellular gene expression through the β common cytokine receptor.
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