About: Exchange Protein Directly Activated by cAMP Modulates Ebola Virus Uptake into Vascular Endothelial Cells

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About: Exchange Protein Directly Activated by cAMP Modulates Ebola Virus Uptake into Vascular Endothelial Cells 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
has title	Exchange Protein Directly Activated by cAMP Modulates Ebola Virus Uptake into Vascular Endothelial Cells
Creator	Zhou, Jia Li, Xiang Chang, Qing Wakamiya, Maki Popov, Vsevolod Ksiazek, Thomas Drelich, Aleksandra Gong, Bin He, Xi Judy, Barbara Lu, Fanglin Yu, Shangyi
Source	Medline; PMC
abstract	Members of the family Filoviridae, including Ebola virus (EBOV) and Marburg virus (MARV), cause severe hemorrhagic fever in humans and nonhuman primates. Given their high lethality, a comprehensive understanding of filoviral pathogenesis is urgently needed. In the present studies, we revealed that the exchange protein directly activated by cAMP 1 (EPAC1) gene deletion protects vasculature in ex vivo explants from EBOV infection. Importantly, pharmacological inhibition of EPAC1 using EPAC-specific inhibitors (ESIs) mimicked the EPAC1 knockout phenotype in the ex vivo model. ESI treatment dramatically decreased EBOV infectivity in both ex vivo vasculature and in vitro vascular endothelial cells (ECs). Furthermore, postexposure protection of ECs against EBOV infection was conferred using ESIs. Protective efficacy of ESIs in ECs was observed also in MARV infection. Additional studies using a vesicular stomatitis virus pseudotype that expresses EBOV glycoprotein (EGP-VSV) confirmed that ESIs reduced infection in ECs. Ultrastructural studies suggested that ESIs blocked EGP-VSV internalization via inhibition of macropinocytosis. The inactivation of EPAC1 affects the early stage of viral entry after viral binding to the cell surface, but before early endosome formation, in a phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)-dependent manner. Our study delineated a new critical role of EPAC1 during EBOV uptake into ECs.
has issue date	2018-10-16(xsd:dateTime)
bibo:doi	10.3390/v10100563
bibo:pmid	30332733
has license	cc-by
sha1sum (hex)	0396bc111213d601eeb67ae191530309bdbb6220
schema:url	https://doi.org/10.3390/v10100563
resource representing a document's title	Exchange Protein Directly Activated by cAMP Modulates Ebola Virus Uptake into Vascular Endothelial Cells
has PubMed Central identifier	PMC6213290
has PubMed identifier	30332733
schema:publication	Viruses
resource representing a document's body	covid:0396bc111213d601eeb67ae191530309bdbb6220#body_text
is schema:about of	named entity 'VASCULAR' named entity 'comprehensive' named entity 'Our' named entity 'vascular' named entity 'protein' named entity 'infection' named entity 'vasculature' named entity 'Endothelial' named entity 'ECS' named entity 'MEMBERS' named entity 'EBOLA VIRUS' named entity 'THEIR' named entity 'INHIBITION' named entity 'UNDERSTANDING' named entity 'STUDIES' named entity 'SEVERE' named entity 'INFECTION' named entity 'VIRAL ENTRY' named entity '2C5' named entity 'PHOSPHATIDYLINOSITOL' named entity 'OUR' named entity 'ENDOTHELIAL CELLS' named entity 'LETHALITY' named entity 'KINASE' named entity 'KNOCKOUT' covid:arg/0396bc111213d601eeb67ae191530309bdbb6220 named entity 'CRITICAL' named entity 'USING' named entity 'MODEL' named entity 'OBSERVED' named entity 'UPTAKE' named entity 'VESICULAR STOMATITIS VIRUS' named entity 'COMPREHENSIVE' named entity 'BINDING' named entity 'NONHUMAN PRIMATES' named entity 'EARLY STAGE' named entity 'ENDOTHELIAL CELLS' named entity 'EXCHANGE PROTEIN DIRECTLY ACTIVATED BY CAMP' named entity 'EXCHANGE PROTEIN DIRECTLY ACTIVATED BY CAMP 1' named entity 'PATHOGENESIS' named entity 'TREATMENT' named entity 'CONFIRMED' named entity 'EGP' named entity 'STUDY' named entity 'EPAC' named entity 'HEMORRHAGIC FEVER' named entity 'PROTECTION' named entity 'IN VITRO' named entity 'GENE DELETION' named entity 'NEEDED' named entity 'EPAC1' named entity 'VASCULATURE' named entity 'PHENOTYPE' named entity 'CELL SURFACE' named entity 'INACTIVATION' named entity 'ROLE' named entity 'HIGH' named entity 'INHIBITION OF MACROPINOCYTOSIS' named entity 'EARLY ENDOSOME' named entity 'DECREASED' named entity 'EFFICACY' named entity 'VIRAL' named entity 'INFECTIVITY' named entity 'PRESENT' named entity 'EBOLA VIRUS' named entity 'VASCULAR' named entity 'HUMANS' named entity 'BLOCKED' named entity 'PHARMACOLOGICAL' named entity 'INTERNALIZATION'

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