Inhibition of CREB transcriptional activity in human T lymphocytes by oxidative stress.
Inhibition of CREB transcriptional activity in human T lymphocytes by oxidative stress.
复制标题
氧化应激对人 T 淋巴细胞 CREB 转录活性的抑制。
DOI：
10.1016/j.freeradbiomed.2005.02.035
复制
发表时间：
2005
影响因子：
7.4
通讯作者：
Franklin,RichardA
中科院分区：
文献类型：
--
作者：
Rodriguez-Mora,OswaldoG;Howe,ChristopherJ;Lahair,MichelleM;McCubrey,JamesA;Franklin,RichardA
过氧化氢（HP）通过p38和MSK 1诱导Jurkat T淋巴细胞Ser 133上cAMP反应元件结合蛋白（CREB）磷酸化。虽然CREB Ser 133磷酸化，增加HP刺激CREB介导的转录是不存在的。用抗CD 3和抗CD 28刺激T淋巴细胞诱导CREB Ser 133磷酸化，以及CREB介导的转录活性。当用HP处理CD 3/CD 28刺激的淋巴细胞时，Ser 133被磷酸化，但TCR诱导的CREB介导的转录活性降低。这些数据提供了一个潜在的机制，氧化应激可以改变T细胞受体诱导的CREB激活和反应性的洞察。
Hydrogen peroxide (HP) induced the phosphorylation of cAMP response element binding protein (CREB) on Ser133 in Jurkat T lymphocytes via p38 and MSK1. Although CREB Ser133 was phosphorylated, increases in HP-stimulated CREB-mediated transcription were absent. T lymphocyte stimulation with anti-CD3 and anti-CD28 induced CREB Ser133 phosphorylation, as well as CREB-mediated transcriptional activity. When CD3/CD28-stimulated lymphocytes were treated with HP, Ser133 was phosphorylated, but TCR-induced CREB-mediated transcriptional activity was reduced. These data provide insight into a potential mechanism by which oxidative stress can alter T cell receptor-induced CREB activation and responsiveness.