CUPRIC ION BLOCKS NF-KAPPA-B ACTIVATION THROUGH INHIBITING THE SIGNAL-INDUCED PHOSPHORYLATION OF I-KAPPA-B-ALPHA
CUPRIC ION BLOCKS NF-KAPPA-B ACTIVATION THROUGH INHIBITING THE SIGNAL-INDUCED PHOSPHORYLATION OF I-KAPPA-B-ALPHA
复制标题
DOI：
10.1006/bbrc.1995.2660
复制
发表时间：
1995-11-13
影响因子：
3.1
通讯作者：
INOUE, J
中科院分区：
文献类型：
--
作者：
SATAKE, H;SUZUKI, K;INOUE, J
转录因子NF kappa B作为抑制蛋白I kappa B的复合体存在于细胞质中，调控参与免疫应答的多种细胞基因和包括HIV在内的病毒基因的表达。多种细胞外信号诱导I kappa B α的磷酸化和快速降解，从而释放出NF kappa B。在Cu2+的存在下，对tnf - α刺激的细胞制备的细胞质提取物进行脱氧胆酸处理，导致NF κ B从I κ B α中释放出来，这表明Cu2+干扰了NF κ B-I κ B复合物的解离。在Cu2+的存在下，tnf - α刺激未观察到I κ B α的磷酸化或降解。这些结果表明Cu2+通过阻断导致I κ B α磷酸化的信号来抑制NF κ B的释放。(C) 1995学术出版社，Inc。
A transcription factor NF kappa B, which regulates expression of various cellular genes involved in immune responses and viral genes including HIV, is sequestered in the cytoplasm as a complex with an inhibitory protein I kappa B. Various extracellular signals induce phosphorylation and rapid degradation of I kappa B alpha to release NF kappa B. Cu2+ was found to inhibit the activation of NF kappa B induced by TNF-alpha, TPA, or H2O2. Deoxycholate treatment of the cytoplasmic extract prepared from cells stimulated by TNF-alpha in the presence of Cu2+ resulted in the release of NF kappa B from I kappa B alpha, indicating that Cu2+ interferes with the dissociation of the NF kappa B-I kappa B complex. Neither phosphorylation nor degradation of I kappa B alpha was observed upon TNF-alpha stimulation in the presence of Cu2+. These results indicate that Cu2+ inhibits the release of NF kappa B by blockade of a signal leading to the phosphorylation of I kappa B alpha. (C) 1995 Academic Press, Inc.