Residues in a Highly Conserved Claudin-1 Motif Are Required for Hepatitis C Virus Entry and Mediate the Formation of Cell-Cell Contacts (Q27488396)

1

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Claire Bertaux

3

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Francis Kajumo

4

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Tatjana Dragic

CD81 and Claudin 1 Coreceptor Association: Role in Hepatitis C Virus Entry

5

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publication date

June 2009

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published in

Journal of Virology

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volume

83

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issue

11

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page(s)

5477-84

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cites work

1 reference

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The tight junction proteins claudin-1, -6, and -9 are entry cofactors for hepatitis C virus

20 March 2017

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Correlation of the Tight Junction-like Distribution of Claudin-1 to the Cellular Tropism of Hepatitis C Virus

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Claudin-6 and claudin-9 function as additional coreceptors for hepatitis C virus

20 March 2017

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Scavenger receptor BI and BII expression levels modulate hepatitis C virus infectivity

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Hepatitis C Virus Entry Requires a Critical Postinternalization Step and Delivery to Early Endosomes via Clathrin-Coated Vesicles

20 March 2017

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Different Domains of CD81 Mediate Distinct Stages of Hepatitis C Virus Pseudoparticle Entry

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Phosphorylation of claudin-3 at threonine 192 by cAMP-dependent protein kinase regulates tight junction barrier function in ovarian cancer cells

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Human serum facilitates hepatitis C virus infection, and neutralizing responses inversely correlate with viral replication kinetics at the acute phase of hepatitis C virus infection

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Claudin-1 and -2: novel integral membrane proteins localizing at tight junctions with no sequence similarity to occludin

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Claudin-1 is a hepatitis C virus co-receptor required for a late step in entry

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Claudin extracellular domains determine paracellular charge selectivity and resistance but not tight junction fibril architecture

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CD81 is an entry coreceptor for hepatitis C virus

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Familial hypomagnesemia with hypercalciuria and nephrocalcinosis: blocking endocytosis restores surface expression of a novel Claudin-16 mutant that lacks the entire C-terminal cytosolic tail.

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27 November 2018

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27 November 2018

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27 November 2018

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