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  An orthogonal proteomic survey uncovers novel Zika virus host factors

Scaturro, P., Stukalov, A., Haas, D. A., Cortese, M., Draganova, K., Plaszczyca, A., et al. (2018). An orthogonal proteomic survey uncovers novel Zika virus host factors. Nature, 561(7722), 253-257. doi:10.1038/s41586-018-0484-5.

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Item Permalink: http://hdl.handle.net/21.11116/0000-0002-F3F5-7 Version Permalink: http://hdl.handle.net/21.11116/0000-0002-F3F6-6
Genre: Journal Article

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 Creators:
Scaturro, Pietro1, Author              
Stukalov, Alexey1, Author              
Haas, Darya A.1, Author              
Cortese, Mirko2, Author
Draganova, Kalina2, Author
Plaszczyca, Anna2, Author
Bartenschlager, Ralf2, Author
Goetz, Magdalena2, Author
Pichlmair, Andreas1, Author              
Affiliations:
1Pichlmair, Andreas / Innate Immunity, Max Planck Institute of Biochemistry, Max Planck Society, ou_1565166              
2external, ou_persistent22              

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Free keywords: EMBRYONIC STEM-CELLS; DENGUE VIRUS; PROTEIN; PHOSPHOPROTEOMICS; DIFFERENTIATION; ENRICHMENT; INFECTION; PLATFORM; GENOME; KINASEScience & Technology - Other Topics;
 Abstract: Zika virus (ZIKV) has recently emerged as a global health concern owing to its widespread diffusion and its association with severe neurological symptoms and microcephaly in newborns(1). However, the molecular mechanisms that are responsible for the pathogenicity of ZIKV remain largely unknown. Here we use human neural progenitor cells and the neuronal cell line SK-N-BE2 in an integrated proteomics approach to characterize the cellular responses to viral infection at the proteome and phosphoproteome level, and use affinity proteomics to identify cellular targets of ZIKV proteins. Using this approach, we identify 386 ZIKV-interacting proteins, ZIKV-specific and pan-flaviviral activities as well as host factors with known functions in neuronal development, retinal defects and infertility. Moreover, our analysis identified 1,216 phosphorylation sites that are specifically up-or downregulated after ZIKV infection, indicating profound modulation of fundamental signalling pathways such as AKT, MAPK-ERK and ATM-ATR and thereby providing mechanistic insights into the proliferation arrest elicited by ZIKV infection. Functionally, our integrative study identifies ZIKV host-dependency factors and provides a comprehensive framework for a system-level understanding of ZIKV-induced perturbations at the levels of proteins and cellular pathways.

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Language(s): eng - English
 Dates: 2018
 Publication Status: Published in print
 Pages: 23
 Publishing info: -
 Table of Contents: -
 Rev. Method: -
 Identifiers: ISI: 000444437900046
DOI: 10.1038/s41586-018-0484-5
 Degree: -

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Title: Nature
  Abbreviation : Nature
Source Genre: Journal
 Creator(s):
Affiliations:
Publ. Info: London : Nature Publishing Group
Pages: - Volume / Issue: 561 (7722) Sequence Number: - Start / End Page: 253 - 257 Identifier: ISSN: 0028-0836
CoNE: https://pure.mpg.de/cone/journals/resource/954925427238