PXD022271

PXD022271 is an original dataset announced via ProteomeXchange.

Title	Ubiquitin Ligase Enzyme FANCL Inhibits Peste des petits ruminants Virus Replication by Inducing Type I Interferon Production through Promoting Phosphorylation of TBK1
Description	Peste des petits ruminants virus (PPRV) infection causes highly contagious and severe disease in domestic and wild ruminants. It is widely reported that PRRV infection causes considerable innate immunosuppression in its host and promotes viral replication. However, how does the host rescue the innate immune response to counteract this immunosuppression during viral replication is poorly understood. The goat fetal fibroblasts (GFFs) have been commonly used as host-original cells to investigate the pathogenesis of PPRV. To explore the mechanisms of how host counteracts PPRV-mediated innate immunosuppression, a high-throughput quantitation proteomic approach (iTRAQ in conjunction with LC-MS/MS) was used to investigate the proteome landscape of GFFs in response to PPRV infection. Eventually, the proteomic analysis gained 497 up-regulated proteins and 358 down-regulated proteins (PPRV-infected cells versus mock-infected cells). The complement and coagulation cascades, protein digestion and absorption, and cytokine-cytokine receptor interaction pathways were significantly regulated in response to PPRV infection. ErmineJ analysis of the differentially expressed proteins (DEPs) identified the significantly enriched GO categories for response to interferon-gamma and positive regulation of ERK1 and ERK2 cascade. In addition, many immune related proteins, such as interferon gamma, 2'-5'-oligoadenylate synthase-like protein, toll-like receptor 9, toll-like receptor 6, NOD1, plasminogen activator inhibitor 1, and Wnt-5a were significantly upregulated. This suggested that the innate immune response was triggered during PPRV infection in GFFs. We subsequently identified that the E3 ubiquitin ligase FANCL was critically involved in regulation of the innate immune response during PPRV infection. FANCL inhibited PPRV infection by enhancing type I interferon (IFN) and interferon-stimulated genes (ISGs) expression. Further study indicated that FANCL induced type I IFN production by promoting TBK1 phosphorylation, and therefore impairing PPRV-mediated immunosuppression and revealing an antiviral function against PPRV.
HostingRepository	PRIDE
AnnounceDate	2021-07-26
AnnouncementXML	Submission_2021-07-26_10:03:34.492.xml
DigitalObjectIdentifier
ReviewLevel	Peer-reviewed dataset
DatasetOrigin	Original dataset
RepositorySupport	Unsupported dataset by repository
PrimarySubmitter	Shuying Chen
SpeciesList	scientific name: Ovis aries; NCBI TaxID: 9940;
ModificationList	No PTMs are included in the dataset
Instrument	Q Exactive HF

Revision	Datetime	Status	ChangeLog Entry
0	2020-10-30 07:49:08	ID requested
⏵ 1	2021-07-26 10:03:35	announced

Chen S, Yang F, Cao W, Liu H, Wen B, Sun Y, Zheng H, Wang J, Zhu Z, Quantitative Proteomics Reveals a Novel Role of the E3 Ubiquitin-Protein Ligase FANCL in the Activation of the Innate Immune Response through Regulation of TBK1 Phosphorylation during Peste des Petits Ruminants Virus Infection. J Proteome Res, 20(8):4113-4130(2021) [pubmed]

submitter keyword: Peste des petits ruminants virus

quantitative proteomics

FANCL

innate immune response

TBK1

Haixue Zheng
contact affiliation	State Key Laboratory of Veterinary Etiological Biology, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, Gansu, PR China
contact email	zhenghaixue@caas.cn
lab head
Shuying Chen
contact affiliation	College of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi
contact email	chenshuying0709@qq.com
dataset submitter

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PRIDE project URI

• PRIDE
  1. PXD022271
     1. Label: PRIDE project
     2. Name: Ubiquitin Ligase Enzyme FANCL Inhibits Peste des petits ruminants Virus Replication by Inducing Type I Interferon Production through Promoting Phosphorylation of TBK1