About: Proteomic Profiling of the TRAF3 Interactome Network Reveals a New Role for the ER-to-Golgi Transport Compartments in Innate Immunity

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About: Proteomic Profiling of the TRAF3 Interactome Network Reveals a New Role for the ER-to-Golgi Transport Compartments in Innate Immunity Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	Proteomic Profiling of the TRAF3 Interactome Network Reveals a New Role for the ER-to-Golgi Transport Compartments in Innate Immunity
Creator	Thiel, Volker Doyon, Priscilla Dô, Florence Emery, Gregory Gingras, Anne-Claude Meloche, Sylvain St-Amant-Verret, Myriam Wissanji, Tasheen Gallen, St Hospital, Kantonal Khan, Kashif Servant, Marc Clé, Jean-François D'ambrosio, Lisa Van Zuylen, Wendy
source	Medline; PMC
abstract	Tumor Necrosis Factor receptor-associated factor-3 (TRAF3) is a central mediator important for inducing type I interferon (IFN) production in response to intracellular double-stranded RNA (dsRNA). Here, we report the identification of Sec16A and p115, two proteins of the ER-to-Golgi vesicular transport system, as novel components of the TRAF3 interactome network. Notably, in non-infected cells, TRAF3 was found associated with markers of the ER-Exit-Sites (ERES), ER-to-Golgi intermediate compartment (ERGIC) and the cis-Golgi apparatus. Upon dsRNA and dsDNA sensing however, the Golgi apparatus fragmented into cytoplasmic punctated structures containing TRAF3 allowing its colocalization and interaction with Mitochondrial AntiViral Signaling (MAVS), the essential mitochondria-bound RIG-I-like Helicase (RLH) adaptor. In contrast, retention of TRAF3 at the ER-to-Golgi vesicular transport system blunted the ability of TRAF3 to interact with MAVS upon viral infection and consequently decreased type I IFN response. Moreover, depletion of Sec16A and p115 led to a drastic disorganization of the Golgi paralleled by the relocalization of TRAF3, which under these conditions was unable to associate with MAVS. Consequently, upon dsRNA and dsDNA sensing, ablation of Sec16A and p115 was found to inhibit IRF3 activation and anti-viral gene expression. Reciprocally, mild overexpression of Sec16A or p115 in Hec1B cells increased the activation of IFNβ, ISG56 and NF-κB -dependent promoters following viral infection and ectopic expression of MAVS and Tank-binding kinase-1 (TBK1). In line with these results, TRAF3 was found enriched in immunocomplexes composed of p115, Sec16A and TBK1 upon infection. Hence, we propose a model where dsDNA and dsRNA sensing induces the formation of membrane-bound compartments originating from the Golgi, which mediate the dynamic association of TRAF3 with MAVS leading to an optimal induction of innate immune responses.
has issue date	2012-07-05(xsd:dateTime)
bibo:doi	10.1371/journal.ppat.1002747
bibo:pmid	22792062
has license	cc-by
sha1sum (hex)	f6b79474869aa89ef3a3cab01f39abac279c5132
schema:url	https://doi.org/10.1371/journal.ppat.1002747
resource representing a document's title	Proteomic Profiling of the TRAF3 Interactome Network Reveals a New Role for the ER-to-Golgi Transport Compartments in Innate Immunity
has PubMed Central identifier	PMC3390413
has PubMed identifier	22792062
schema:publication	PLoS Pathog
resource representing a document's body	covid:f6b79474869aa89ef3a3cab01f39abac279c5132#body_text
is schema:about of	named entity 'GOLGI' named entity 'REVEALS' named entity 'contrast' named entity 'led' named entity 'response' named entity 'cis-Golgi' named entity 'production' named entity 'mediator' named entity 'Golgi' named entity 'TRAF3' named entity 'NEW' named entity 'INTERACTOME' named entity 'MODEL' covid:arg/f6b79474869aa89ef3a3cab01f39abac279c5132 named entity 'COMPARTMENTS' named entity 'TANK' named entity 'RESPONSE TO' named entity 'TO INHIBIT' named entity 'INNATE IMMUNITY' named entity 'WHERE' named entity 'EXIT' named entity 'FRAGMENTED' named entity 'ASSOCIATED' named entity 'IMMUNE RESPONSES' named entity 'ECTOPIC EXPRESSION' named entity 'DEPENDENT' named entity 'HELICASE' named entity 'CONTRAST' named entity 'RETENTION' named entity 'CIS' named entity 'INTERACTION' named entity 'DECREASED' named entity 'LINE' named entity 'ABILITY' named entity 'DEPLETION' named entity 'RESULTS' named entity 'COLOCALIZATION' named entity 'NOVEL' named entity 'INDUCTION' named entity 'IS A' named entity 'TUMOR NECROSIS FACTOR RECEPTOR' named entity 'NETWORK' named entity 'VIRAL INFECTION' named entity 'COMPARTMENTS' named entity 'RESPONSE' named entity 'IDENTIFICATION' named entity 'ITS' named entity 'ANTIVIRAL' named entity 'LEADING' named entity 'ER-' named entity 'TRANSPORT' named entity 'ROLE' named entity 'IMPORTANT' named entity 'COMPONENTS' named entity 'NF-KB' named entity 'TYPE I' named entity 'GOLGI APPARATUS' named entity 'IFN' named entity 'ENRICHED' named entity 'BOUND' named entity 'CONDITIONS' named entity 'INTRACELLULAR' named entity 'ALLOWING' named entity 'PROTEINS' named entity 'ASSOCIATION' named entity 'THESE' named entity 'FORMATION'

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