Factor inhibiting HIF negatively regulates antiviral innate immunity via hydroxylation of IKKϵ

Summary: Activation of type I interferon (IFN-1) signaling is essential to protect host cells from viral infection. The full spectrum of IFN-I induction requires the activation of a number of cellular factors, including IκB kinase epsilon (IKKϵ). However, the regulation of IKKϵ activation in respons...
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Autor*in:	Xiaolian Cai [verfasserIn] Rui Wang [verfasserIn] Junji Zhu [verfasserIn] Xiong Li [verfasserIn] Xing Liu [verfasserIn] Gang Ouyang [verfasserIn] Jing Wang [verfasserIn] Zhi Li [verfasserIn] Chunchun Zhu [verfasserIn] Hongyan Deng [verfasserIn] Wuhan Xiao [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2024

Schlagwörter:	CP: Immunology

Übergeordnetes Werk:	In: Cell Reports - Elsevier, 2015, 43(2024), 1, Seite 113606-
Übergeordnetes Werk:	volume:43 ; year:2024 ; number:1 ; pages:113606-

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1016/j.celrep.2023.113606

Katalog-ID:	DOAJ098988735

Internformat


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245	1	0	\|a Factor inhibiting HIF negatively regulates antiviral innate immunity via hydroxylation of IKKϵ
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520			\|a Summary: Activation of type I interferon (IFN-1) signaling is essential to protect host cells from viral infection. The full spectrum of IFN-I induction requires the activation of a number of cellular factors, including IκB kinase epsilon (IKKϵ). However, the regulation of IKKϵ activation in response to viral infection remains largely unknown. Here, we show that factor inhibiting hypoxia-inducible factor (HIF) (FIH), an asparaginyl hydroxylase, interacts with IKKϵ and catalyzes asparagine hydroxylation of IKKϵ at Asn-254, Asn-700, and Asn-701, resulting in the suppression of IKKϵ activation. FIH-mediated hydroxylation of IKKϵ prevents IKKϵ binding to TBK1 and TRAF3 and attenuates the cIAP1/cIAP2/TRAF2 E3 ubiquitin ligase complex-catalyzed K63-linked polyubiquitination of IKKϵ at Lys-416. In addition, Fih-deficient mice and zebrafish are more resistant to viral infection. This work uncovers a previously unrecognized role of FIH in suppressing IKKϵ activation for IFN signaling and antiviral immune responses.
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700	0		\|a Zhi Li \|e verfasserin \|4 aut
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700	0		\|a Hongyan Deng \|e verfasserin \|4 aut
700	0		\|a Wuhan Xiao \|e verfasserin \|4 aut
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912			\|a GBV_ILN_4393
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allfields	10.1016/j.celrep.2023.113606 doi (DE-627)DOAJ098988735 (DE-599)DOAJe55c7040396c450483076f98c4f42e87 DE-627 ger DE-627 rakwb eng QH301-705.5 Xiaolian Cai verfasserin aut Factor inhibiting HIF negatively regulates antiviral innate immunity via hydroxylation of IKKϵ 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: Activation of type I interferon (IFN-1) signaling is essential to protect host cells from viral infection. The full spectrum of IFN-I induction requires the activation of a number of cellular factors, including IκB kinase epsilon (IKKϵ). However, the regulation of IKKϵ activation in response to viral infection remains largely unknown. Here, we show that factor inhibiting hypoxia-inducible factor (HIF) (FIH), an asparaginyl hydroxylase, interacts with IKKϵ and catalyzes asparagine hydroxylation of IKKϵ at Asn-254, Asn-700, and Asn-701, resulting in the suppression of IKKϵ activation. FIH-mediated hydroxylation of IKKϵ prevents IKKϵ binding to TBK1 and TRAF3 and attenuates the cIAP1/cIAP2/TRAF2 E3 ubiquitin ligase complex-catalyzed K63-linked polyubiquitination of IKKϵ at Lys-416. In addition, Fih-deficient mice and zebrafish are more resistant to viral infection. This work uncovers a previously unrecognized role of FIH in suppressing IKKϵ activation for IFN signaling and antiviral immune responses. CP: Immunology Biology (General) Rui Wang verfasserin aut Junji Zhu verfasserin aut Xiong Li verfasserin aut Xing Liu verfasserin aut Gang Ouyang verfasserin aut Jing Wang verfasserin aut Zhi Li verfasserin aut Chunchun Zhu verfasserin aut Hongyan Deng verfasserin aut Wuhan Xiao verfasserin aut In Cell Reports Elsevier, 2015 43(2024), 1, Seite 113606- (DE-627)684964562 (DE-600)2649101-1 22111247 nnns volume:43 year:2024 number:1 pages:113606- https://doi.org/10.1016/j.celrep.2023.113606 kostenfrei https://doaj.org/article/e55c7040396c450483076f98c4f42e87 kostenfrei http://www.sciencedirect.com/science/article/pii/S2211124723016182 kostenfrei https://doaj.org/toc/2211-1247 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 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_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 43 2024 1 113606-
spelling	10.1016/j.celrep.2023.113606 doi (DE-627)DOAJ098988735 (DE-599)DOAJe55c7040396c450483076f98c4f42e87 DE-627 ger DE-627 rakwb eng QH301-705.5 Xiaolian Cai verfasserin aut Factor inhibiting HIF negatively regulates antiviral innate immunity via hydroxylation of IKKϵ 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: Activation of type I interferon (IFN-1) signaling is essential to protect host cells from viral infection. The full spectrum of IFN-I induction requires the activation of a number of cellular factors, including IκB kinase epsilon (IKKϵ). However, the regulation of IKKϵ activation in response to viral infection remains largely unknown. Here, we show that factor inhibiting hypoxia-inducible factor (HIF) (FIH), an asparaginyl hydroxylase, interacts with IKKϵ and catalyzes asparagine hydroxylation of IKKϵ at Asn-254, Asn-700, and Asn-701, resulting in the suppression of IKKϵ activation. FIH-mediated hydroxylation of IKKϵ prevents IKKϵ binding to TBK1 and TRAF3 and attenuates the cIAP1/cIAP2/TRAF2 E3 ubiquitin ligase complex-catalyzed K63-linked polyubiquitination of IKKϵ at Lys-416. In addition, Fih-deficient mice and zebrafish are more resistant to viral infection. This work uncovers a previously unrecognized role of FIH in suppressing IKKϵ activation for IFN signaling and antiviral immune responses. CP: Immunology Biology (General) Rui Wang verfasserin aut Junji Zhu verfasserin aut Xiong Li verfasserin aut Xing Liu verfasserin aut Gang Ouyang verfasserin aut Jing Wang verfasserin aut Zhi Li verfasserin aut Chunchun Zhu verfasserin aut Hongyan Deng verfasserin aut Wuhan Xiao verfasserin aut In Cell Reports Elsevier, 2015 43(2024), 1, Seite 113606- (DE-627)684964562 (DE-600)2649101-1 22111247 nnns volume:43 year:2024 number:1 pages:113606- https://doi.org/10.1016/j.celrep.2023.113606 kostenfrei https://doaj.org/article/e55c7040396c450483076f98c4f42e87 kostenfrei http://www.sciencedirect.com/science/article/pii/S2211124723016182 kostenfrei https://doaj.org/toc/2211-1247 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 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_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 43 2024 1 113606-
allfields_unstemmed	10.1016/j.celrep.2023.113606 doi (DE-627)DOAJ098988735 (DE-599)DOAJe55c7040396c450483076f98c4f42e87 DE-627 ger DE-627 rakwb eng QH301-705.5 Xiaolian Cai verfasserin aut Factor inhibiting HIF negatively regulates antiviral innate immunity via hydroxylation of IKKϵ 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: Activation of type I interferon (IFN-1) signaling is essential to protect host cells from viral infection. The full spectrum of IFN-I induction requires the activation of a number of cellular factors, including IκB kinase epsilon (IKKϵ). However, the regulation of IKKϵ activation in response to viral infection remains largely unknown. Here, we show that factor inhibiting hypoxia-inducible factor (HIF) (FIH), an asparaginyl hydroxylase, interacts with IKKϵ and catalyzes asparagine hydroxylation of IKKϵ at Asn-254, Asn-700, and Asn-701, resulting in the suppression of IKKϵ activation. FIH-mediated hydroxylation of IKKϵ prevents IKKϵ binding to TBK1 and TRAF3 and attenuates the cIAP1/cIAP2/TRAF2 E3 ubiquitin ligase complex-catalyzed K63-linked polyubiquitination of IKKϵ at Lys-416. In addition, Fih-deficient mice and zebrafish are more resistant to viral infection. This work uncovers a previously unrecognized role of FIH in suppressing IKKϵ activation for IFN signaling and antiviral immune responses. CP: Immunology Biology (General) Rui Wang verfasserin aut Junji Zhu verfasserin aut Xiong Li verfasserin aut Xing Liu verfasserin aut Gang Ouyang verfasserin aut Jing Wang verfasserin aut Zhi Li verfasserin aut Chunchun Zhu verfasserin aut Hongyan Deng verfasserin aut Wuhan Xiao verfasserin aut In Cell Reports Elsevier, 2015 43(2024), 1, Seite 113606- (DE-627)684964562 (DE-600)2649101-1 22111247 nnns volume:43 year:2024 number:1 pages:113606- https://doi.org/10.1016/j.celrep.2023.113606 kostenfrei https://doaj.org/article/e55c7040396c450483076f98c4f42e87 kostenfrei http://www.sciencedirect.com/science/article/pii/S2211124723016182 kostenfrei https://doaj.org/toc/2211-1247 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 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_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 43 2024 1 113606-
allfieldsGer	10.1016/j.celrep.2023.113606 doi (DE-627)DOAJ098988735 (DE-599)DOAJe55c7040396c450483076f98c4f42e87 DE-627 ger DE-627 rakwb eng QH301-705.5 Xiaolian Cai verfasserin aut Factor inhibiting HIF negatively regulates antiviral innate immunity via hydroxylation of IKKϵ 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: Activation of type I interferon (IFN-1) signaling is essential to protect host cells from viral infection. The full spectrum of IFN-I induction requires the activation of a number of cellular factors, including IκB kinase epsilon (IKKϵ). However, the regulation of IKKϵ activation in response to viral infection remains largely unknown. Here, we show that factor inhibiting hypoxia-inducible factor (HIF) (FIH), an asparaginyl hydroxylase, interacts with IKKϵ and catalyzes asparagine hydroxylation of IKKϵ at Asn-254, Asn-700, and Asn-701, resulting in the suppression of IKKϵ activation. FIH-mediated hydroxylation of IKKϵ prevents IKKϵ binding to TBK1 and TRAF3 and attenuates the cIAP1/cIAP2/TRAF2 E3 ubiquitin ligase complex-catalyzed K63-linked polyubiquitination of IKKϵ at Lys-416. In addition, Fih-deficient mice and zebrafish are more resistant to viral infection. This work uncovers a previously unrecognized role of FIH in suppressing IKKϵ activation for IFN signaling and antiviral immune responses. CP: Immunology Biology (General) Rui Wang verfasserin aut Junji Zhu verfasserin aut Xiong Li verfasserin aut Xing Liu verfasserin aut Gang Ouyang verfasserin aut Jing Wang verfasserin aut Zhi Li verfasserin aut Chunchun Zhu verfasserin aut Hongyan Deng verfasserin aut Wuhan Xiao verfasserin aut In Cell Reports Elsevier, 2015 43(2024), 1, Seite 113606- (DE-627)684964562 (DE-600)2649101-1 22111247 nnns volume:43 year:2024 number:1 pages:113606- https://doi.org/10.1016/j.celrep.2023.113606 kostenfrei https://doaj.org/article/e55c7040396c450483076f98c4f42e87 kostenfrei http://www.sciencedirect.com/science/article/pii/S2211124723016182 kostenfrei https://doaj.org/toc/2211-1247 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 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_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 43 2024 1 113606-
allfieldsSound	10.1016/j.celrep.2023.113606 doi (DE-627)DOAJ098988735 (DE-599)DOAJe55c7040396c450483076f98c4f42e87 DE-627 ger DE-627 rakwb eng QH301-705.5 Xiaolian Cai verfasserin aut Factor inhibiting HIF negatively regulates antiviral innate immunity via hydroxylation of IKKϵ 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: Activation of type I interferon (IFN-1) signaling is essential to protect host cells from viral infection. The full spectrum of IFN-I induction requires the activation of a number of cellular factors, including IκB kinase epsilon (IKKϵ). However, the regulation of IKKϵ activation in response to viral infection remains largely unknown. Here, we show that factor inhibiting hypoxia-inducible factor (HIF) (FIH), an asparaginyl hydroxylase, interacts with IKKϵ and catalyzes asparagine hydroxylation of IKKϵ at Asn-254, Asn-700, and Asn-701, resulting in the suppression of IKKϵ activation. FIH-mediated hydroxylation of IKKϵ prevents IKKϵ binding to TBK1 and TRAF3 and attenuates the cIAP1/cIAP2/TRAF2 E3 ubiquitin ligase complex-catalyzed K63-linked polyubiquitination of IKKϵ at Lys-416. In addition, Fih-deficient mice and zebrafish are more resistant to viral infection. This work uncovers a previously unrecognized role of FIH in suppressing IKKϵ activation for IFN signaling and antiviral immune responses. CP: Immunology Biology (General) Rui Wang verfasserin aut Junji Zhu verfasserin aut Xiong Li verfasserin aut Xing Liu verfasserin aut Gang Ouyang verfasserin aut Jing Wang verfasserin aut Zhi Li verfasserin aut Chunchun Zhu verfasserin aut Hongyan Deng verfasserin aut Wuhan Xiao verfasserin aut In Cell Reports Elsevier, 2015 43(2024), 1, Seite 113606- (DE-627)684964562 (DE-600)2649101-1 22111247 nnns volume:43 year:2024 number:1 pages:113606- https://doi.org/10.1016/j.celrep.2023.113606 kostenfrei https://doaj.org/article/e55c7040396c450483076f98c4f42e87 kostenfrei http://www.sciencedirect.com/science/article/pii/S2211124723016182 kostenfrei https://doaj.org/toc/2211-1247 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 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_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 43 2024 1 113606-
language	English
source	In Cell Reports 43(2024), 1, Seite 113606- volume:43 year:2024 number:1 pages:113606-
sourceStr	In Cell Reports 43(2024), 1, Seite 113606- volume:43 year:2024 number:1 pages:113606-
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	CP: Immunology Biology (General)
isfreeaccess_bool	true
container_title	Cell Reports
authorswithroles_txt_mv	Xiaolian Cai @@aut@@ Rui Wang @@aut@@ Junji Zhu @@aut@@ Xiong Li @@aut@@ Xing Liu @@aut@@ Gang Ouyang @@aut@@ Jing Wang @@aut@@ Zhi Li @@aut@@ Chunchun Zhu @@aut@@ Hongyan Deng @@aut@@ Wuhan Xiao @@aut@@
publishDateDaySort_date	2024-01-01T00:00:00Z
hierarchy_top_id	684964562
id	DOAJ098988735
language_de	englisch
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callnumber-first	Q - Science
author	Xiaolian Cai
spellingShingle	Xiaolian Cai misc QH301-705.5 misc CP: Immunology misc Biology (General) Factor inhibiting HIF negatively regulates antiviral innate immunity via hydroxylation of IKKϵ
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topic_title	QH301-705.5 Factor inhibiting HIF negatively regulates antiviral innate immunity via hydroxylation of IKKϵ CP: Immunology
topic	misc QH301-705.5 misc CP: Immunology misc Biology (General)
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title	Factor inhibiting HIF negatively regulates antiviral innate immunity via hydroxylation of IKKϵ
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title_full	Factor inhibiting HIF negatively regulates antiviral innate immunity via hydroxylation of IKKϵ
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author_browse	Xiaolian Cai Rui Wang Junji Zhu Xiong Li Xing Liu Gang Ouyang Jing Wang Zhi Li Chunchun Zhu Hongyan Deng Wuhan Xiao
container_volume	43
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author-letter	Xiaolian Cai
doi_str_mv	10.1016/j.celrep.2023.113606
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title_sort	factor inhibiting hif negatively regulates antiviral innate immunity via hydroxylation of ikkϵ
callnumber	QH301-705.5
title_auth	Factor inhibiting HIF negatively regulates antiviral innate immunity via hydroxylation of IKKϵ
abstract	Summary: Activation of type I interferon (IFN-1) signaling is essential to protect host cells from viral infection. The full spectrum of IFN-I induction requires the activation of a number of cellular factors, including IκB kinase epsilon (IKKϵ). However, the regulation of IKKϵ activation in response to viral infection remains largely unknown. Here, we show that factor inhibiting hypoxia-inducible factor (HIF) (FIH), an asparaginyl hydroxylase, interacts with IKKϵ and catalyzes asparagine hydroxylation of IKKϵ at Asn-254, Asn-700, and Asn-701, resulting in the suppression of IKKϵ activation. FIH-mediated hydroxylation of IKKϵ prevents IKKϵ binding to TBK1 and TRAF3 and attenuates the cIAP1/cIAP2/TRAF2 E3 ubiquitin ligase complex-catalyzed K63-linked polyubiquitination of IKKϵ at Lys-416. In addition, Fih-deficient mice and zebrafish are more resistant to viral infection. This work uncovers a previously unrecognized role of FIH in suppressing IKKϵ activation for IFN signaling and antiviral immune responses.
abstractGer	Summary: Activation of type I interferon (IFN-1) signaling is essential to protect host cells from viral infection. The full spectrum of IFN-I induction requires the activation of a number of cellular factors, including IκB kinase epsilon (IKKϵ). However, the regulation of IKKϵ activation in response to viral infection remains largely unknown. Here, we show that factor inhibiting hypoxia-inducible factor (HIF) (FIH), an asparaginyl hydroxylase, interacts with IKKϵ and catalyzes asparagine hydroxylation of IKKϵ at Asn-254, Asn-700, and Asn-701, resulting in the suppression of IKKϵ activation. FIH-mediated hydroxylation of IKKϵ prevents IKKϵ binding to TBK1 and TRAF3 and attenuates the cIAP1/cIAP2/TRAF2 E3 ubiquitin ligase complex-catalyzed K63-linked polyubiquitination of IKKϵ at Lys-416. In addition, Fih-deficient mice and zebrafish are more resistant to viral infection. This work uncovers a previously unrecognized role of FIH in suppressing IKKϵ activation for IFN signaling and antiviral immune responses.
abstract_unstemmed	Summary: Activation of type I interferon (IFN-1) signaling is essential to protect host cells from viral infection. The full spectrum of IFN-I induction requires the activation of a number of cellular factors, including IκB kinase epsilon (IKKϵ). However, the regulation of IKKϵ activation in response to viral infection remains largely unknown. Here, we show that factor inhibiting hypoxia-inducible factor (HIF) (FIH), an asparaginyl hydroxylase, interacts with IKKϵ and catalyzes asparagine hydroxylation of IKKϵ at Asn-254, Asn-700, and Asn-701, resulting in the suppression of IKKϵ activation. FIH-mediated hydroxylation of IKKϵ prevents IKKϵ binding to TBK1 and TRAF3 and attenuates the cIAP1/cIAP2/TRAF2 E3 ubiquitin ligase complex-catalyzed K63-linked polyubiquitination of IKKϵ at Lys-416. In addition, Fih-deficient mice and zebrafish are more resistant to viral infection. This work uncovers a previously unrecognized role of FIH in suppressing IKKϵ activation for IFN signaling and antiviral immune responses.
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container_issue	1
title_short	Factor inhibiting HIF negatively regulates antiviral innate immunity via hydroxylation of IKKϵ
url	https://doi.org/10.1016/j.celrep.2023.113606 https://doaj.org/article/e55c7040396c450483076f98c4f42e87 http://www.sciencedirect.com/science/article/pii/S2211124723016182 https://doaj.org/toc/2211-1247
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author2	Rui Wang Junji Zhu Xiong Li Xing Liu Gang Ouyang Jing Wang Zhi Li Chunchun Zhu Hongyan Deng Wuhan Xiao
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up_date	2024-07-03T20:23:43.250Z
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Factor inhibiting HIF negatively regulates antiviral innate immunity via hydroxylation of IKKϵ

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