Role of ERp57 in the signaling and transcriptional activity of STAT3 in a melanoma cell line
Role of ERp57 in the signaling and transcriptional activity of STAT3 in a melanoma cell line
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DOI：
10.1016/j.abb.2009.12.004
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发表时间：
2010-02-15
影响因子：
3.9
通讯作者：
Eufemi, Margherita
中科院分区：
文献类型：
--
作者：
Chichiarelli, Silvia;Gaucci, Elisa;Eufemi, Margherita
M14黑色素瘤细胞中的染色质免疫沉淀显示，蛋白ERp 57（内质网蛋白57）在STAT 3调节基因的子集中与STAT 3附近的DNA结合。在相同的细胞中，IL-6诱导这些基因之一，即CRP的表达显著增加。通过RNA干扰消除ERp 57后。STAT 3在酪氨酸705上的磷酸化水平降低。IL-6诱导的CRP表达激活被完全抑制。体外实验表明，ERp 57也是STAT 3与其DNA上的共有序列结合所必需的。因此，ERp 57，以前显示与STAT 3在胞质溶胶和核STAT 3的增强体，是一个必要的辅因子的至少一个子集的STAT 3依赖性基因的调节，可能干预在网站的STAT 3磷酸化和在核水平。(C)2009 Elsevier Inc. All rights reserved.
Chromatin immunoprecipitation in M14 melanoma cells showed that the protein ERp57 (endoplasmic reticulum protein 57) binds to DNA in the proximity of STAT3 in a subset of STAT3-regulated genes. In the same cells, IL-6 induced a significant increase of the expression of one of these genes, i.e. CRP. Upon depletion of ERp57 by RNA interference. the phosphorylation of STAT3 on tyrosine 705 was decreased. and the IL-6-induced activation of CRP expression was completely suppressed. In vitro experiments showed that ERp57 is also required for the binding of STAT3 to its consensus sequence on DNA. Thus ERp57, previously shown to associate with STAT3 in the cytosol and in the nuclear STAT3-containing enhanceosome, is a necessary cofactor for the regulation of at least a subset of STAT3-dependent genes, probably intervening both at the site of STAT3 phosphorylation and at the nuclear level. (C) 2009 Elsevier Inc. All rights reserved.