STING promotes NLRP3 localization in ER and facilitates NLRP3 deubiquitination to activate the inflammasome upon HSV-1 infection.

One of the fundamental reactions of the innate immune responses to pathogen infection is the release of pro-inflammatory cytokines, including IL-1β, processed by the NLRP3 inflammasome. The stimulator of interferon genes (STING) has the essential roles in innate immune response against pathogen infe...
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Autor*in:	Wenbiao Wang [verfasserIn] Dingwen Hu [verfasserIn] Caifeng Wu [verfasserIn] Yuqian Feng [verfasserIn] Aixin Li [verfasserIn] Weiyong Liu [verfasserIn] Yingchong Wang [verfasserIn] Keli Chen [verfasserIn] Mingfu Tian [verfasserIn] Feng Xiao [verfasserIn] Qi Zhang [verfasserIn] Muhammad Adnan Shereen [verfasserIn] Weijie Chen [verfasserIn] Pan Pan [verfasserIn] Pin Wan [verfasserIn] Kailang Wu [verfasserIn] Jianguo Wu [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2020

Übergeordnetes Werk:	In: PLoS Pathogens - Public Library of Science (PLoS), 2005, 16(2020), 3, p e1008335
Übergeordnetes Werk:	volume:16 ; year:2020 ; number:3, p e1008335

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.1371/journal.ppat.1008335

Katalog-ID:	DOAJ062568698

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520			\|a One of the fundamental reactions of the innate immune responses to pathogen infection is the release of pro-inflammatory cytokines, including IL-1β, processed by the NLRP3 inflammasome. The stimulator of interferon genes (STING) has the essential roles in innate immune response against pathogen infections. Here we reveal a distinct mechanism by which STING regulates the NLRP3 inflammasome activation, IL-1β secretion, and inflammatory responses in human cell lines, mice primary cells, and mice. Interestingly, upon HSV-1 infection and cytosolic DNA stimulation, STING binds to NLRP3 and promotes the inflammasome activation through two approaches. First, STING recruits NLRP3 and facilitates NLRP3 localization in the endoplasmic reticulum, thereby facilitating the inflammasome formation. Second, STING interacts with NLRP3 and attenuates K48- and K63-linked polyubiquitination of NLRP3, thereby promoting the inflammasome activation. Collectively, we demonstrate that the cGAS-STING-NLRP3 signaling is essential for host defense against HSV-1 infection.
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allfields	10.1371/journal.ppat.1008335 doi (DE-627)DOAJ062568698 (DE-599)DOAJ1f1ea353a43944d3ab8ede1e3144c959 DE-627 ger DE-627 rakwb eng RC581-607 QH301-705.5 Wenbiao Wang verfasserin aut STING promotes NLRP3 localization in ER and facilitates NLRP3 deubiquitination to activate the inflammasome upon HSV-1 infection. 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier One of the fundamental reactions of the innate immune responses to pathogen infection is the release of pro-inflammatory cytokines, including IL-1β, processed by the NLRP3 inflammasome. The stimulator of interferon genes (STING) has the essential roles in innate immune response against pathogen infections. Here we reveal a distinct mechanism by which STING regulates the NLRP3 inflammasome activation, IL-1β secretion, and inflammatory responses in human cell lines, mice primary cells, and mice. Interestingly, upon HSV-1 infection and cytosolic DNA stimulation, STING binds to NLRP3 and promotes the inflammasome activation through two approaches. First, STING recruits NLRP3 and facilitates NLRP3 localization in the endoplasmic reticulum, thereby facilitating the inflammasome formation. Second, STING interacts with NLRP3 and attenuates K48- and K63-linked polyubiquitination of NLRP3, thereby promoting the inflammasome activation. Collectively, we demonstrate that the cGAS-STING-NLRP3 signaling is essential for host defense against HSV-1 infection. Immunologic diseases. Allergy Biology (General) Dingwen Hu verfasserin aut Caifeng Wu verfasserin aut Yuqian Feng verfasserin aut Aixin Li verfasserin aut Weiyong Liu verfasserin aut Yingchong Wang verfasserin aut Keli Chen verfasserin aut Mingfu Tian verfasserin aut Feng Xiao verfasserin aut Qi Zhang verfasserin aut Muhammad Adnan Shereen verfasserin aut Weijie Chen verfasserin aut Pan Pan verfasserin aut Pin Wan verfasserin aut Kailang Wu verfasserin aut Jianguo Wu verfasserin aut In PLoS Pathogens Public Library of Science (PLoS), 2005 16(2020), 3, p e1008335 (DE-627)501074422 (DE-600)2205412-1 15537374 nnns volume:16 year:2020 number:3, p e1008335 https://doi.org/10.1371/journal.ppat.1008335 kostenfrei https://doaj.org/article/1f1ea353a43944d3ab8ede1e3144c959 kostenfrei https://doi.org/10.1371/journal.ppat.1008335 kostenfrei https://doaj.org/toc/1553-7366 Journal toc kostenfrei https://doaj.org/toc/1553-7374 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2020 3, p e1008335
spelling	10.1371/journal.ppat.1008335 doi (DE-627)DOAJ062568698 (DE-599)DOAJ1f1ea353a43944d3ab8ede1e3144c959 DE-627 ger DE-627 rakwb eng RC581-607 QH301-705.5 Wenbiao Wang verfasserin aut STING promotes NLRP3 localization in ER and facilitates NLRP3 deubiquitination to activate the inflammasome upon HSV-1 infection. 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier One of the fundamental reactions of the innate immune responses to pathogen infection is the release of pro-inflammatory cytokines, including IL-1β, processed by the NLRP3 inflammasome. The stimulator of interferon genes (STING) has the essential roles in innate immune response against pathogen infections. Here we reveal a distinct mechanism by which STING regulates the NLRP3 inflammasome activation, IL-1β secretion, and inflammatory responses in human cell lines, mice primary cells, and mice. Interestingly, upon HSV-1 infection and cytosolic DNA stimulation, STING binds to NLRP3 and promotes the inflammasome activation through two approaches. First, STING recruits NLRP3 and facilitates NLRP3 localization in the endoplasmic reticulum, thereby facilitating the inflammasome formation. Second, STING interacts with NLRP3 and attenuates K48- and K63-linked polyubiquitination of NLRP3, thereby promoting the inflammasome activation. Collectively, we demonstrate that the cGAS-STING-NLRP3 signaling is essential for host defense against HSV-1 infection. Immunologic diseases. Allergy Biology (General) Dingwen Hu verfasserin aut Caifeng Wu verfasserin aut Yuqian Feng verfasserin aut Aixin Li verfasserin aut Weiyong Liu verfasserin aut Yingchong Wang verfasserin aut Keli Chen verfasserin aut Mingfu Tian verfasserin aut Feng Xiao verfasserin aut Qi Zhang verfasserin aut Muhammad Adnan Shereen verfasserin aut Weijie Chen verfasserin aut Pan Pan verfasserin aut Pin Wan verfasserin aut Kailang Wu verfasserin aut Jianguo Wu verfasserin aut In PLoS Pathogens Public Library of Science (PLoS), 2005 16(2020), 3, p e1008335 (DE-627)501074422 (DE-600)2205412-1 15537374 nnns volume:16 year:2020 number:3, p e1008335 https://doi.org/10.1371/journal.ppat.1008335 kostenfrei https://doaj.org/article/1f1ea353a43944d3ab8ede1e3144c959 kostenfrei https://doi.org/10.1371/journal.ppat.1008335 kostenfrei https://doaj.org/toc/1553-7366 Journal toc kostenfrei https://doaj.org/toc/1553-7374 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2020 3, p e1008335
allfields_unstemmed	10.1371/journal.ppat.1008335 doi (DE-627)DOAJ062568698 (DE-599)DOAJ1f1ea353a43944d3ab8ede1e3144c959 DE-627 ger DE-627 rakwb eng RC581-607 QH301-705.5 Wenbiao Wang verfasserin aut STING promotes NLRP3 localization in ER and facilitates NLRP3 deubiquitination to activate the inflammasome upon HSV-1 infection. 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier One of the fundamental reactions of the innate immune responses to pathogen infection is the release of pro-inflammatory cytokines, including IL-1β, processed by the NLRP3 inflammasome. The stimulator of interferon genes (STING) has the essential roles in innate immune response against pathogen infections. Here we reveal a distinct mechanism by which STING regulates the NLRP3 inflammasome activation, IL-1β secretion, and inflammatory responses in human cell lines, mice primary cells, and mice. Interestingly, upon HSV-1 infection and cytosolic DNA stimulation, STING binds to NLRP3 and promotes the inflammasome activation through two approaches. First, STING recruits NLRP3 and facilitates NLRP3 localization in the endoplasmic reticulum, thereby facilitating the inflammasome formation. Second, STING interacts with NLRP3 and attenuates K48- and K63-linked polyubiquitination of NLRP3, thereby promoting the inflammasome activation. Collectively, we demonstrate that the cGAS-STING-NLRP3 signaling is essential for host defense against HSV-1 infection. Immunologic diseases. Allergy Biology (General) Dingwen Hu verfasserin aut Caifeng Wu verfasserin aut Yuqian Feng verfasserin aut Aixin Li verfasserin aut Weiyong Liu verfasserin aut Yingchong Wang verfasserin aut Keli Chen verfasserin aut Mingfu Tian verfasserin aut Feng Xiao verfasserin aut Qi Zhang verfasserin aut Muhammad Adnan Shereen verfasserin aut Weijie Chen verfasserin aut Pan Pan verfasserin aut Pin Wan verfasserin aut Kailang Wu verfasserin aut Jianguo Wu verfasserin aut In PLoS Pathogens Public Library of Science (PLoS), 2005 16(2020), 3, p e1008335 (DE-627)501074422 (DE-600)2205412-1 15537374 nnns volume:16 year:2020 number:3, p e1008335 https://doi.org/10.1371/journal.ppat.1008335 kostenfrei https://doaj.org/article/1f1ea353a43944d3ab8ede1e3144c959 kostenfrei https://doi.org/10.1371/journal.ppat.1008335 kostenfrei https://doaj.org/toc/1553-7366 Journal toc kostenfrei https://doaj.org/toc/1553-7374 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2020 3, p e1008335
allfieldsGer	10.1371/journal.ppat.1008335 doi (DE-627)DOAJ062568698 (DE-599)DOAJ1f1ea353a43944d3ab8ede1e3144c959 DE-627 ger DE-627 rakwb eng RC581-607 QH301-705.5 Wenbiao Wang verfasserin aut STING promotes NLRP3 localization in ER and facilitates NLRP3 deubiquitination to activate the inflammasome upon HSV-1 infection. 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier One of the fundamental reactions of the innate immune responses to pathogen infection is the release of pro-inflammatory cytokines, including IL-1β, processed by the NLRP3 inflammasome. The stimulator of interferon genes (STING) has the essential roles in innate immune response against pathogen infections. Here we reveal a distinct mechanism by which STING regulates the NLRP3 inflammasome activation, IL-1β secretion, and inflammatory responses in human cell lines, mice primary cells, and mice. Interestingly, upon HSV-1 infection and cytosolic DNA stimulation, STING binds to NLRP3 and promotes the inflammasome activation through two approaches. First, STING recruits NLRP3 and facilitates NLRP3 localization in the endoplasmic reticulum, thereby facilitating the inflammasome formation. Second, STING interacts with NLRP3 and attenuates K48- and K63-linked polyubiquitination of NLRP3, thereby promoting the inflammasome activation. Collectively, we demonstrate that the cGAS-STING-NLRP3 signaling is essential for host defense against HSV-1 infection. Immunologic diseases. Allergy Biology (General) Dingwen Hu verfasserin aut Caifeng Wu verfasserin aut Yuqian Feng verfasserin aut Aixin Li verfasserin aut Weiyong Liu verfasserin aut Yingchong Wang verfasserin aut Keli Chen verfasserin aut Mingfu Tian verfasserin aut Feng Xiao verfasserin aut Qi Zhang verfasserin aut Muhammad Adnan Shereen verfasserin aut Weijie Chen verfasserin aut Pan Pan verfasserin aut Pin Wan verfasserin aut Kailang Wu verfasserin aut Jianguo Wu verfasserin aut In PLoS Pathogens Public Library of Science (PLoS), 2005 16(2020), 3, p e1008335 (DE-627)501074422 (DE-600)2205412-1 15537374 nnns volume:16 year:2020 number:3, p e1008335 https://doi.org/10.1371/journal.ppat.1008335 kostenfrei https://doaj.org/article/1f1ea353a43944d3ab8ede1e3144c959 kostenfrei https://doi.org/10.1371/journal.ppat.1008335 kostenfrei https://doaj.org/toc/1553-7366 Journal toc kostenfrei https://doaj.org/toc/1553-7374 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2020 3, p e1008335
allfieldsSound	10.1371/journal.ppat.1008335 doi (DE-627)DOAJ062568698 (DE-599)DOAJ1f1ea353a43944d3ab8ede1e3144c959 DE-627 ger DE-627 rakwb eng RC581-607 QH301-705.5 Wenbiao Wang verfasserin aut STING promotes NLRP3 localization in ER and facilitates NLRP3 deubiquitination to activate the inflammasome upon HSV-1 infection. 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier One of the fundamental reactions of the innate immune responses to pathogen infection is the release of pro-inflammatory cytokines, including IL-1β, processed by the NLRP3 inflammasome. The stimulator of interferon genes (STING) has the essential roles in innate immune response against pathogen infections. Here we reveal a distinct mechanism by which STING regulates the NLRP3 inflammasome activation, IL-1β secretion, and inflammatory responses in human cell lines, mice primary cells, and mice. Interestingly, upon HSV-1 infection and cytosolic DNA stimulation, STING binds to NLRP3 and promotes the inflammasome activation through two approaches. First, STING recruits NLRP3 and facilitates NLRP3 localization in the endoplasmic reticulum, thereby facilitating the inflammasome formation. Second, STING interacts with NLRP3 and attenuates K48- and K63-linked polyubiquitination of NLRP3, thereby promoting the inflammasome activation. Collectively, we demonstrate that the cGAS-STING-NLRP3 signaling is essential for host defense against HSV-1 infection. Immunologic diseases. Allergy Biology (General) Dingwen Hu verfasserin aut Caifeng Wu verfasserin aut Yuqian Feng verfasserin aut Aixin Li verfasserin aut Weiyong Liu verfasserin aut Yingchong Wang verfasserin aut Keli Chen verfasserin aut Mingfu Tian verfasserin aut Feng Xiao verfasserin aut Qi Zhang verfasserin aut Muhammad Adnan Shereen verfasserin aut Weijie Chen verfasserin aut Pan Pan verfasserin aut Pin Wan verfasserin aut Kailang Wu verfasserin aut Jianguo Wu verfasserin aut In PLoS Pathogens Public Library of Science (PLoS), 2005 16(2020), 3, p e1008335 (DE-627)501074422 (DE-600)2205412-1 15537374 nnns volume:16 year:2020 number:3, p e1008335 https://doi.org/10.1371/journal.ppat.1008335 kostenfrei https://doaj.org/article/1f1ea353a43944d3ab8ede1e3144c959 kostenfrei https://doi.org/10.1371/journal.ppat.1008335 kostenfrei https://doaj.org/toc/1553-7366 Journal toc kostenfrei https://doaj.org/toc/1553-7374 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2020 3, p e1008335
language	English
source	In PLoS Pathogens 16(2020), 3, p e1008335 volume:16 year:2020 number:3, p e1008335
sourceStr	In PLoS Pathogens 16(2020), 3, p e1008335 volume:16 year:2020 number:3, p e1008335
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Immunologic diseases. Allergy Biology (General)
isfreeaccess_bool	true
container_title	PLoS Pathogens
authorswithroles_txt_mv	Wenbiao Wang @@aut@@ Dingwen Hu @@aut@@ Caifeng Wu @@aut@@ Yuqian Feng @@aut@@ Aixin Li @@aut@@ Weiyong Liu @@aut@@ Yingchong Wang @@aut@@ Keli Chen @@aut@@ Mingfu Tian @@aut@@ Feng Xiao @@aut@@ Qi Zhang @@aut@@ Muhammad Adnan Shereen @@aut@@ Weijie Chen @@aut@@ Pan Pan @@aut@@ Pin Wan @@aut@@ Kailang Wu @@aut@@ Jianguo Wu @@aut@@
publishDateDaySort_date	2020-01-01T00:00:00Z
hierarchy_top_id	501074422
id	DOAJ062568698
language_de	englisch
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callnumber-first	R - Medicine
author	Wenbiao Wang
spellingShingle	Wenbiao Wang misc RC581-607 misc QH301-705.5 misc Immunologic diseases. Allergy misc Biology (General) STING promotes NLRP3 localization in ER and facilitates NLRP3 deubiquitination to activate the inflammasome upon HSV-1 infection.
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topic_title	RC581-607 QH301-705.5 STING promotes NLRP3 localization in ER and facilitates NLRP3 deubiquitination to activate the inflammasome upon HSV-1 infection
topic	misc RC581-607 misc QH301-705.5 misc Immunologic diseases. Allergy misc Biology (General)
topic_unstemmed	misc RC581-607 misc QH301-705.5 misc Immunologic diseases. Allergy misc Biology (General)
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title	STING promotes NLRP3 localization in ER and facilitates NLRP3 deubiquitination to activate the inflammasome upon HSV-1 infection.
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title_full	STING promotes NLRP3 localization in ER and facilitates NLRP3 deubiquitination to activate the inflammasome upon HSV-1 infection
author_sort	Wenbiao Wang
journal	PLoS Pathogens
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author_browse	Wenbiao Wang Dingwen Hu Caifeng Wu Yuqian Feng Aixin Li Weiyong Liu Yingchong Wang Keli Chen Mingfu Tian Feng Xiao Qi Zhang Muhammad Adnan Shereen Weijie Chen Pan Pan Pin Wan Kailang Wu Jianguo Wu
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doi_str_mv	10.1371/journal.ppat.1008335
author2-role	verfasserin
title_sort	sting promotes nlrp3 localization in er and facilitates nlrp3 deubiquitination to activate the inflammasome upon hsv-1 infection
callnumber	RC581-607
title_auth	STING promotes NLRP3 localization in ER and facilitates NLRP3 deubiquitination to activate the inflammasome upon HSV-1 infection.
abstract	One of the fundamental reactions of the innate immune responses to pathogen infection is the release of pro-inflammatory cytokines, including IL-1β, processed by the NLRP3 inflammasome. The stimulator of interferon genes (STING) has the essential roles in innate immune response against pathogen infections. Here we reveal a distinct mechanism by which STING regulates the NLRP3 inflammasome activation, IL-1β secretion, and inflammatory responses in human cell lines, mice primary cells, and mice. Interestingly, upon HSV-1 infection and cytosolic DNA stimulation, STING binds to NLRP3 and promotes the inflammasome activation through two approaches. First, STING recruits NLRP3 and facilitates NLRP3 localization in the endoplasmic reticulum, thereby facilitating the inflammasome formation. Second, STING interacts with NLRP3 and attenuates K48- and K63-linked polyubiquitination of NLRP3, thereby promoting the inflammasome activation. Collectively, we demonstrate that the cGAS-STING-NLRP3 signaling is essential for host defense against HSV-1 infection.
abstractGer	One of the fundamental reactions of the innate immune responses to pathogen infection is the release of pro-inflammatory cytokines, including IL-1β, processed by the NLRP3 inflammasome. The stimulator of interferon genes (STING) has the essential roles in innate immune response against pathogen infections. Here we reveal a distinct mechanism by which STING regulates the NLRP3 inflammasome activation, IL-1β secretion, and inflammatory responses in human cell lines, mice primary cells, and mice. Interestingly, upon HSV-1 infection and cytosolic DNA stimulation, STING binds to NLRP3 and promotes the inflammasome activation through two approaches. First, STING recruits NLRP3 and facilitates NLRP3 localization in the endoplasmic reticulum, thereby facilitating the inflammasome formation. Second, STING interacts with NLRP3 and attenuates K48- and K63-linked polyubiquitination of NLRP3, thereby promoting the inflammasome activation. Collectively, we demonstrate that the cGAS-STING-NLRP3 signaling is essential for host defense against HSV-1 infection.
abstract_unstemmed	One of the fundamental reactions of the innate immune responses to pathogen infection is the release of pro-inflammatory cytokines, including IL-1β, processed by the NLRP3 inflammasome. The stimulator of interferon genes (STING) has the essential roles in innate immune response against pathogen infections. Here we reveal a distinct mechanism by which STING regulates the NLRP3 inflammasome activation, IL-1β secretion, and inflammatory responses in human cell lines, mice primary cells, and mice. Interestingly, upon HSV-1 infection and cytosolic DNA stimulation, STING binds to NLRP3 and promotes the inflammasome activation through two approaches. First, STING recruits NLRP3 and facilitates NLRP3 localization in the endoplasmic reticulum, thereby facilitating the inflammasome formation. Second, STING interacts with NLRP3 and attenuates K48- and K63-linked polyubiquitination of NLRP3, thereby promoting the inflammasome activation. Collectively, we demonstrate that the cGAS-STING-NLRP3 signaling is essential for host defense against HSV-1 infection.
collection_details	GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700
container_issue	3, p e1008335
title_short	STING promotes NLRP3 localization in ER and facilitates NLRP3 deubiquitination to activate the inflammasome upon HSV-1 infection.
url	https://doi.org/10.1371/journal.ppat.1008335 https://doaj.org/article/1f1ea353a43944d3ab8ede1e3144c959 https://doaj.org/toc/1553-7366 https://doaj.org/toc/1553-7374
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author2	Dingwen Hu Caifeng Wu Yuqian Feng Aixin Li Weiyong Liu Yingchong Wang Keli Chen Mingfu Tian Feng Xiao Qi Zhang Muhammad Adnan Shereen Weijie Chen Pan Pan Pin Wan Kailang Wu Jianguo Wu
author2Str	Dingwen Hu Caifeng Wu Yuqian Feng Aixin Li Weiyong Liu Yingchong Wang Keli Chen Mingfu Tian Feng Xiao Qi Zhang Muhammad Adnan Shereen Weijie Chen Pan Pan Pin Wan Kailang Wu Jianguo Wu
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doi_str	10.1371/journal.ppat.1008335
callnumber-a	RC581-607
up_date	2024-07-04T02:08:29.361Z
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STING promotes NLRP3 localization in ER and facilitates NLRP3 deubiquitination to activate the inflammasome upon HSV-1 infection.

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