Alterations in the iron homeostasis network: A driving force for macrophage-mediated hepatitis C virus persistency. - Wikidata - awgldk - TriplyDB

Alterations in the iron homeostasis network: A driving force for macrophage-mediated hepatitis C virus persistency.

Alterations in the iron homeostasis network: A driving force for macrophage-mediated hepatitis C virus persistency.

http://www.wikidata.org/entity/Q37189857

about

The iron homeostasis network and hepatitis C virus - a new challenge in the era of directly acting antivirals Relationship between Hepatitis C Virus Infection and Iron Overload.Low hepcidin in liver fibrosis and cirrhosis; a tale of progressive disorder and a case for a new biochemical marker.

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Alterations in the iron homeostasis network: A driving force for macrophage-mediated hepatitis C virus persistency.

http://www.wikidata.org/entity/Q37189857

description

article científic

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article scientifique

@fr

articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 08 April 2016

@en

vedecký článok

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vetenskaplig artikel

@sv

videnskabelig artikel

@da

vědecký článek

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name

Alterations in the iron homeos ...... hepatitis C virus persistency.

@en

Alterations in the iron homeos ...... hepatitis C virus persistency.

@nl

type

label

Alterations in the iron homeos ...... hepatitis C virus persistency.

@en

Alterations in the iron homeos ...... hepatitis C virus persistency.

@nl

prefLabel

Alterations in the iron homeos ...... hepatitis C virus persistency.

@en

Alterations in the iron homeos ...... hepatitis C virus persistency.

@nl

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21505594.2016.1175700

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Alterations in the iron homeos ...... hepatitis C virus persistency.

@en

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Agoritsa Varaklioti

http://www.w3.org/2001/XMLSchema#string

Alexios Dimitriadis

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Avgi Mamalaki

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Dionyssios Giannimaras

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Eirini Karamichali

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Eleni Kyratzopoulou

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John Koskinas

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Pelagia Foka

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Urania Georgopoulou

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P2860

A novel mammalian iron-regulated protein involved in intracellular iron metabolism

Hepcidin regulates cellular iron efflux by binding to ferroportin and inducing its internalization

Efficient trans-Encapsidation of Hepatitis C Virus RNAs into Infectious Virus-Like Particles

Induction of a Striking Systemic Cytokine Cascade prior to Peak Viremia in Acute Human Immunodeficiency Virus Type 1 Infection, in Contrast to More Modest and Delayed Responses in Acute Hepatitis B and C Virus Infections

A Functional Genomic Screen Identifies Cellular Cofactors of Hepatitis C Virus Replication

Ironing out Ferroportin

The role of the iron responsive element in the control of ferroportin1/IREG1/MTP1 gene expression

Hepcidin, a putative mediator of anemia of inflammation, is a type II acute-phase protein

Evidence for a lack of a direct transcriptional suppression of the iron regulatory peptide hepcidin by hypoxia-inducible factors

Cell-cell contact-mediated hepatitis C virus (HCV) transfer, productive infection, and replication and their requirement for HCV receptors.

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