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Ahmet Civas

Researcher at University of Paris

Publications -  15
Citations -  2360

Ahmet Civas is an academic researcher from University of Paris. The author has contributed to research in topics: Promoter & Gene. The author has an hindex of 12, co-authored 14 publications receiving 2077 citations. Previous affiliations of Ahmet Civas include Paris Descartes University.

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Activation of the NLRP3 inflammasome in dendritic cells induces IL-1β–dependent adaptive immunity against tumors

TL;DR: It is shown that dying tumor cells release ATP, which then acts on P2X7 purinergic receptors from DCs and triggers the NOD-like receptor family, pyrin domain containing-3 protein (NLRP3)-dependent caspase-1 activation complex ('inflammasome'), allowing for the secretion of interleukin-1 β (IL-1β).
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RIG-I-like receptors: sensing and responding to RNA virus infection.

TL;DR: This review will focus on RIG-I-like receptor (RLR) signal transduction and the regulatory mechanisms - ubiquitination, deubiquitinations, ISGylation - underlying this important host response to virus infection.
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The role of differential expression of human interferon--a genes in antiviral immunity.

TL;DR: New data describing how IRF3 and IRF7 regulate the temporal and quantitative differences in the expression of the multigenic IFN-A family enhances the understanding of the selective advantage of the multiplicity ofIFN-alpha subtypes in the regulation of innate and adaptive immunity.
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Differential regulation of human interferon A gene expression by interferon regulatory factors 3 and 7.

TL;DR: This regulatory mechanism contributes to differential expression of IFN-A genes and may be critical for alpha interferon production in different cell types by RIG-I-dependent signals, leading to innate antiviral immune responses.
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Impairment of Interferon-Induced IRF-7 Gene Expression due to Inhibition of ISGF3 Formation by Trichostatin A

TL;DR: Treatment of cells with trichostatin A (TSA), a deacetylase inhibitor, inhibits the virus-induced activation of IFN-α/β promoters and dramatically reduces the ability of different ISG promoters to respond to IFN stimulation, suggesting that an acetylation/deacetylation mechanism participates in the regulation of cellular distribution and function of STAT2 in IFn- α/β signaling.