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SHARPIN 负向关联 TRAF2 介导的 NFκB 激活。

SHARPIN negatively associates with TRAF2-mediated NFκB activation.

机构信息

Department of Dermatology, Yale University School of Medicine, New Haven, Connecticut, United States of America.

出版信息

PLoS One. 2011;6(7):e21696. doi: 10.1371/journal.pone.0021696. Epub 2011 Jul 29.

Abstract

NFκB is an inducible transcriptional factor controlled by two principal signaling cascades and plays pivotal roles in diverse physiological processes including inflammation, apoptosis, oncogenesis, immunity, and development. Activation of NFκB signaling was detected in skin of SHAPRIN-deficient mice and can be diminished by an NFκB inhibitor. However, in vitro studies demonstrated that SHARPIN activates NFκB signaling by forming a linear ubiquitin chain assembly complex with RNF31 (HOIP) and RBCK1 (HOIL1). The inconsistency between in vivo and in vitro findings about SHARPIN's function on NFκB activation could be partially due to SHARPIN's potential interactions with downstream molecules of NFκB pathway. In this study, 17 anti-flag immunoprecipitated proteins, including TRAF2, were identified by mass spectrum analysis among Sharpin-Flag transfected mouse fibroblasts, B lymphocytes, and BALB/c LN stroma 12 cells suggesting their interaction with SHARPIN. Interaction between SHARPIN and TRAF2 confirmed previous yeast two hybridization reports that SHARPIN was one TRAF2's partners. Furthermore, luciferase-based NFκB reporter assays demonstrated that SHARPIN negatively associates with NFκB activation, which can be partly compensated by over-expression of TRAF2. These data suggested that other than activating NFκB signaling by forming ubiquitin ligase complex with RNF31 and RBCK1, SHARPIN may also negatively associate with NFκB activation via interactions with other NFκB members, such as TRAF2.

摘要

NFκB 是一种可诱导的转录因子,受两条主要信号通路控制,在多种生理过程中发挥关键作用,包括炎症、细胞凋亡、肿瘤发生、免疫和发育。在 SHAPRIN 缺陷型小鼠的皮肤中检测到 NFκB 信号的激活,并且可以通过 NFκB 抑制剂来减弱。然而,体外研究表明,SHARPIN 通过与 RNF31(HOIP)和 RBCK1(HOIL1)形成线性泛素链组装复合物来激活 NFκB 信号。SHAPRIN 在 NFκB 激活中的功能的体内和体外研究结果之间的不一致可能部分归因于 SHAPRIN 与 NFκB 途径下游分子的潜在相互作用。在这项研究中,通过质谱分析鉴定了在 Sharpin-Flag 转染的小鼠成纤维细胞、B 淋巴细胞和 BALB/cLN 基质 12 细胞中 17 种抗 flag 免疫沉淀的蛋白质,包括 TRAF2,表明它们与 SHARPIN 相互作用。SHARPIN 和 TRAF2 之间的相互作用证实了先前的酵母双杂交报告,即 SHARPIN 是 TRAF2 的一个伙伴。此外,基于荧光素酶的 NFκB 报告基因测定表明,SHARPIN 负调控 NFκB 激活,而过表达 TRAF2 可部分补偿 NFκB 激活。这些数据表明,SHARPIN 除了通过与 RNF31 和 RBCK1 形成泛素连接酶复合物来激活 NFκB 信号外,还可能通过与其他 NFκB 成员(如 TRAF2)相互作用来负调控 NFκB 激活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2399/3146465/8c0c09088391/pone.0021696.g001.jpg

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