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Open AccessJournal ArticleDOI

Junction Adhesion Molecule Is a Receptor for Reovirus

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TLDR
Reovirus interaction with cell-surface receptors is a critical determinant of both cell-type specific tropism and virus-induced intracellular signaling events that culminate in cell death.
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This article is published in Cell.The article was published on 2001-02-09 and is currently open access. It has received 627 citations till now. The article focuses on the topics: Tropism & Junctional Adhesion Molecule A.

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Microbial strategies to target, cross or disrupt epithelia.

TL;DR: Invasive bacteria or viruses may, by entering into cells, destabilize the junctions by targeting junction components directly or by inducing a series of events that lead to chemokine secretion, polymorphonuclear recruitment and inflammation.
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Tight junctions and tight junction proteins in mammalian epidermis

TL;DR: Tight junctions are barrier forming cell-cell junctions that are found in a variety of cell types and tissues but their existence in mammalian epidermis has been shown only in the last years.
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Hepatitis C virus entry

TL;DR: The mechanisms of HCV cell entry are described, beginning with the infectious virion in plasma and ending with fusion of the viral envelope and endosomal membrane.
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Expression of junctional adhesion molecule-A prevents spontaneous and random motility.

TL;DR: It is found that JAM-A absence increased the number of actin-containing protrusions, reduced the stability of microtubules and impaired the formation of focal adhesions, and was found to regulate effectors of motility that are also downstream of the PKCζ/GSK-3β axis.
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Type I interferons produced by hematopoietic cells protect mice against lethal infection by mammalian reovirus

TL;DR: Dendritic cells (DCs) were the major source of type I IFNs in PPs of reovirus-infected mice, whereas all cell types expressed the antiviral protein Mx-1, and indicates that cDCs are a significant source oftype I IFN production in vivo.
References
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Activators and target genes of Rel/NF-kappaB transcription factors.

TL;DR: It is argued that NF-κB functions more generally as a central regulator of stress responses and pairing stress responsiveness and anti-apoptotic pathways through the use of a common transcription factor may result in increased cell survival following stress insults.
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Isolation of a Common Receptor for Coxsackie B Viruses and Adenoviruses 2 and 5

TL;DR: Identification of CAR as a receptor for these two unrelated and structurally distinct viral pathogens is important for understanding viral pathogenesis and has implications for therapeutic gene delivery with adenovirus vectors.
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The Immunological Synapse: A Molecular Machine Controlling T Cell Activation

TL;DR: Immunological synapse formation is now shown to be an active and dynamic mechanism that allows T cells to distinguish potential antigenic ligands and was a determinative event for T cell proliferation.
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NF-κB is a target of AKT in anti-apoptotic PDGF signalling

TL;DR: A role for NF-κB in growth factor signalling is established and an anti-apoptotic Ras/PI(3)K/Akt/IKK/NF-κBs pathway is defined, thus linking anti-APoptotic signalling with transcription machinery.
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