Cell fate in antiviral response arises in the crosstalk of IRF, NF-κB and JAK/STAT pathways

Innate immunity combines intra- and intercellular signalling to develop responses that limit pathogen spread. Here the authors analyse feedback and feedforward loops connecting IRF3, NF-κB and STAT pathways, and suggest they allow coordinating cell fate decisions in cellular populations in response...

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Autores principales:	Maciej Czerkies, Zbigniew Korwek, Wiktor Prus, Marek Kochańczyk, Joanna Jaruszewicz-Błońska, Karolina Tudelska, Sławomir Błoński, Marek Kimmel, Allan R. Brasier, Tomasz Lipniacki
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2018
Materias:	Science Q
Acceso en línea:	https://doaj.org/article/2cd07c1b1ec6412cbcb7351e15f8b2da
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spelling	oai:doaj.org-article:2cd07c1b1ec6412cbcb7351e15f8b2da2021-12-02T13:27:23ZCell fate in antiviral response arises in the crosstalk of IRF, NF-κB and JAK/STAT pathways10.1038/s41467-017-02640-82041-1723https://doaj.org/article/2cd07c1b1ec6412cbcb7351e15f8b2da2018-02-01T00:00:00Zhttps://doi.org/10.1038/s41467-017-02640-8https://doaj.org/toc/2041-1723Innate immunity combines intra- and intercellular signalling to develop responses that limit pathogen spread. Here the authors analyse feedback and feedforward loops connecting IRF3, NF-κB and STAT pathways, and suggest they allow coordinating cell fate decisions in cellular populations in response to the virus-mimicking agent poly(I:C).Maciej CzerkiesZbigniew KorwekWiktor PrusMarek KochańczykJoanna Jaruszewicz-BłońskaKarolina TudelskaSławomir BłońskiMarek KimmelAllan R. BrasierTomasz LipniackiNature PortfolioarticleScienceQENNature Communications, Vol 9, Iss 1, Pp 1-14 (2018)
institution	DOAJ
collection	DOAJ
language	EN
topic	Science Q
spellingShingle	Science Q Maciej Czerkies Zbigniew Korwek Wiktor Prus Marek Kochańczyk Joanna Jaruszewicz-Błońska Karolina Tudelska Sławomir Błoński Marek Kimmel Allan R. Brasier Tomasz Lipniacki Cell fate in antiviral response arises in the crosstalk of IRF, NF-κB and JAK/STAT pathways
description	Innate immunity combines intra- and intercellular signalling to develop responses that limit pathogen spread. Here the authors analyse feedback and feedforward loops connecting IRF3, NF-κB and STAT pathways, and suggest they allow coordinating cell fate decisions in cellular populations in response to the virus-mimicking agent poly(I:C).
format	article
author	Maciej Czerkies Zbigniew Korwek Wiktor Prus Marek Kochańczyk Joanna Jaruszewicz-Błońska Karolina Tudelska Sławomir Błoński Marek Kimmel Allan R. Brasier Tomasz Lipniacki
author_facet	Maciej Czerkies Zbigniew Korwek Wiktor Prus Marek Kochańczyk Joanna Jaruszewicz-Błońska Karolina Tudelska Sławomir Błoński Marek Kimmel Allan R. Brasier Tomasz Lipniacki
author_sort	Maciej Czerkies
title	Cell fate in antiviral response arises in the crosstalk of IRF, NF-κB and JAK/STAT pathways
title_short	Cell fate in antiviral response arises in the crosstalk of IRF, NF-κB and JAK/STAT pathways
title_full	Cell fate in antiviral response arises in the crosstalk of IRF, NF-κB and JAK/STAT pathways
title_fullStr	Cell fate in antiviral response arises in the crosstalk of IRF, NF-κB and JAK/STAT pathways
title_full_unstemmed	Cell fate in antiviral response arises in the crosstalk of IRF, NF-κB and JAK/STAT pathways
title_sort	cell fate in antiviral response arises in the crosstalk of irf, nf-κb and jak/stat pathways
publisher	Nature Portfolio
publishDate	2018
url	https://doaj.org/article/2cd07c1b1ec6412cbcb7351e15f8b2da
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Cell fate in antiviral response arises in the crosstalk of IRF, NF-κB and JAK/STAT pathways

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