Paxillin mediates ATP-induced activation of P2X7 receptor and NLRP3 inflammasome

Abstract Background Extracellular adenosine triphosphate (ATP), a key danger-associated molecular pattern (DAMP) molecule, is released to the extracellular medium during inflammation by injured parenchymal cells, dying leukocytes, and activated platelets. ATP directly activates the plasma membrane c...
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Autor*in:	Wenbiao Wang [verfasserIn] Dingwen Hu [verfasserIn] Yuqian Feng [verfasserIn] Caifeng Wu [verfasserIn] Yunting Song [verfasserIn] Weiyong Liu [verfasserIn] Aixin Li [verfasserIn] Yingchong Wang [verfasserIn] Keli Chen [verfasserIn] Mingfu Tian [verfasserIn] Feng Xiao [verfasserIn] Qi Zhang [verfasserIn] Weijie Chen [verfasserIn] Pan Pan [verfasserIn] Pin Wan [verfasserIn] Yingle Liu [verfasserIn] Huiyao Lan [verfasserIn] Kailang Wu [verfasserIn] Jianguo Wu [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2020

Schlagwörter:	Adenosine triphosphate, ATP P2X7 receptor Paxillin The NACHT, LRR, and PYD domain-containing protein 3, NLRP3 Ubiquitin-specific peptidase 13, USP13

Übergeordnetes Werk:	In: BMC Biology - BMC, 2003, 18(2020), 1, Seite 22
Übergeordnetes Werk:	volume:18 ; year:2020 ; number:1 ; pages:22

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1186/s12915-020-00918-w

Katalog-ID:	DOAJ017032571

Internformat


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245	1	0	\|a Paxillin mediates ATP-induced activation of P2X7 receptor and NLRP3 inflammasome
264		1	\|c 2020
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520			\|a Abstract Background Extracellular adenosine triphosphate (ATP), a key danger-associated molecular pattern (DAMP) molecule, is released to the extracellular medium during inflammation by injured parenchymal cells, dying leukocytes, and activated platelets. ATP directly activates the plasma membrane channel P2X7 receptor (P2X7R), leading to an intracellular influx of K+, a key trigger inducing NLRP3 inflammasome activation. However, the mechanism underlying P2X7R-mediated activation of NLRP3 inflammasome is poorly understood, and additional molecular mediators have not been identified. Here, we demonstrate that Paxillin is the molecule connecting the P2X7 receptor and NLRP3 inflammasome through protein interactions. Results We show a distinct mechanism by which Paxillin promotes ATP-induced activation of the P2X7 receptor and NLRP3 inflammasome. Extracellular ATP induces Paxillin phosphorylation and then facilitates Paxillin-NLRP3 interaction. Interestingly, Paxillin enhances NLRP3 deubiquitination and activates NLRP3 inflammasome upon ATP treatment and K+ efflux. Moreover, we demonstrated that USP13 is a key enzyme for Paxillin-mediated NLRP3 deubiquitination upon ATP treatment. Notably, extracellular ATP promotes Paxillin and NLRP3 migration from the cytosol to the plasma membrane and facilitates P2X7R-Paxillin interaction and PaxillinNLRP3 association, resulting in the formation of the P2X7R-Paxillin-NLRP3 complex. Functionally, Paxillin is essential for ATP-induced NLRP3 inflammasome activation in mouse BMDMs and BMDCs as well as in human PBMCs and THP-1-differentiated macrophages. Conclusions We have identified paxillin as a mediator of NLRP3 inflammasome activation. Paxillin plays key roles in ATP-induced activation of the P2X7 receptor and NLRP3 inflammasome by facilitating the formation of the P2X7R-Paxillin-NLRP3 complex.
650		4	\|a Adenosine triphosphate, ATP
650		4	\|a P2X7 receptor
650		4	\|a Paxillin
650		4	\|a The NACHT, LRR, and PYD domain-containing protein 3, NLRP3
650		4	\|a Ubiquitin-specific peptidase 13, USP13
653		0	\|a Biology (General)
700	0		\|a Dingwen Hu \|e verfasserin \|4 aut
700	0		\|a Yuqian Feng \|e verfasserin \|4 aut
700	0		\|a Caifeng Wu \|e verfasserin \|4 aut
700	0		\|a Yunting Song \|e verfasserin \|4 aut
700	0		\|a Weiyong Liu \|e verfasserin \|4 aut
700	0		\|a Aixin Li \|e verfasserin \|4 aut
700	0		\|a Yingchong Wang \|e verfasserin \|4 aut
700	0		\|a Keli Chen \|e verfasserin \|4 aut
700	0		\|a Mingfu Tian \|e verfasserin \|4 aut
700	0		\|a Feng Xiao \|e verfasserin \|4 aut
700	0		\|a Qi Zhang \|e verfasserin \|4 aut
700	0		\|a Weijie Chen \|e verfasserin \|4 aut
700	0		\|a Pan Pan \|e verfasserin \|4 aut
700	0		\|a Pin Wan \|e verfasserin \|4 aut
700	0		\|a Yingle Liu \|e verfasserin \|4 aut
700	0		\|a Huiyao Lan \|e verfasserin \|4 aut
700	0		\|a Kailang Wu \|e verfasserin \|4 aut
700	0		\|a Jianguo Wu \|e verfasserin \|4 aut
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912			\|a GBV_ILN_23
912			\|a GBV_ILN_24
912			\|a GBV_ILN_31
912			\|a GBV_ILN_39
912			\|a GBV_ILN_40
912			\|a GBV_ILN_60
912			\|a GBV_ILN_62
912			\|a GBV_ILN_63
912			\|a GBV_ILN_65
912			\|a GBV_ILN_69
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912			\|a GBV_ILN_151
912			\|a GBV_ILN_161
912			\|a GBV_ILN_170
912			\|a GBV_ILN_206
912			\|a GBV_ILN_213
912			\|a GBV_ILN_230
912			\|a GBV_ILN_285
912			\|a GBV_ILN_293
912			\|a GBV_ILN_602
912			\|a GBV_ILN_702
912			\|a GBV_ILN_2001
912			\|a GBV_ILN_2003
912			\|a GBV_ILN_2005
912			\|a GBV_ILN_2006
912			\|a GBV_ILN_2008
912			\|a GBV_ILN_2009
912			\|a GBV_ILN_2010
912			\|a GBV_ILN_2011
912			\|a GBV_ILN_2014
912			\|a GBV_ILN_2015
912			\|a GBV_ILN_2020
912			\|a GBV_ILN_2021
912			\|a GBV_ILN_2025
912			\|a GBV_ILN_2031
912			\|a GBV_ILN_2038
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912			\|a GBV_ILN_2048
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912			\|a GBV_ILN_2056
912			\|a GBV_ILN_2057
912			\|a GBV_ILN_2061
912			\|a GBV_ILN_2111
912			\|a GBV_ILN_2113
912			\|a GBV_ILN_2190
912			\|a GBV_ILN_4012
912			\|a GBV_ILN_4037
912			\|a GBV_ILN_4112
912			\|a GBV_ILN_4125
912			\|a GBV_ILN_4126
912			\|a GBV_ILN_4249
912			\|a GBV_ILN_4305
912			\|a GBV_ILN_4306
912			\|a GBV_ILN_4307
912			\|a GBV_ILN_4313
912			\|a GBV_ILN_4322
912			\|a GBV_ILN_4323
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author_variant	w w ww d h dh y f yf c w cw y s ys w l wl a l al y w yw k c kc m t mt f x fx q z qz w c wc p p pp p w pw y l yl h l hl k w kw j w jw
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hierarchy_sort_str	2020
callnumber-subject-code	QH
publishDate	2020
allfields	10.1186/s12915-020-00918-w doi (DE-627)DOAJ017032571 (DE-599)DOAJ6501c92b4b5045cb996039eebe55494a DE-627 ger DE-627 rakwb eng QH301-705.5 Wenbiao Wang verfasserin aut Paxillin mediates ATP-induced activation of P2X7 receptor and NLRP3 inflammasome 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Extracellular adenosine triphosphate (ATP), a key danger-associated molecular pattern (DAMP) molecule, is released to the extracellular medium during inflammation by injured parenchymal cells, dying leukocytes, and activated platelets. ATP directly activates the plasma membrane channel P2X7 receptor (P2X7R), leading to an intracellular influx of K+, a key trigger inducing NLRP3 inflammasome activation. However, the mechanism underlying P2X7R-mediated activation of NLRP3 inflammasome is poorly understood, and additional molecular mediators have not been identified. Here, we demonstrate that Paxillin is the molecule connecting the P2X7 receptor and NLRP3 inflammasome through protein interactions. Results We show a distinct mechanism by which Paxillin promotes ATP-induced activation of the P2X7 receptor and NLRP3 inflammasome. Extracellular ATP induces Paxillin phosphorylation and then facilitates Paxillin-NLRP3 interaction. Interestingly, Paxillin enhances NLRP3 deubiquitination and activates NLRP3 inflammasome upon ATP treatment and K+ efflux. Moreover, we demonstrated that USP13 is a key enzyme for Paxillin-mediated NLRP3 deubiquitination upon ATP treatment. Notably, extracellular ATP promotes Paxillin and NLRP3 migration from the cytosol to the plasma membrane and facilitates P2X7R-Paxillin interaction and PaxillinNLRP3 association, resulting in the formation of the P2X7R-Paxillin-NLRP3 complex. Functionally, Paxillin is essential for ATP-induced NLRP3 inflammasome activation in mouse BMDMs and BMDCs as well as in human PBMCs and THP-1-differentiated macrophages. Conclusions We have identified paxillin as a mediator of NLRP3 inflammasome activation. Paxillin plays key roles in ATP-induced activation of the P2X7 receptor and NLRP3 inflammasome by facilitating the formation of the P2X7R-Paxillin-NLRP3 complex. Adenosine triphosphate, ATP P2X7 receptor Paxillin The NACHT, LRR, and PYD domain-containing protein 3, NLRP3 Ubiquitin-specific peptidase 13, USP13 Biology (General) Dingwen Hu verfasserin aut Yuqian Feng verfasserin aut Caifeng Wu verfasserin aut Yunting Song verfasserin aut Weiyong Liu verfasserin aut Aixin Li verfasserin aut Yingchong Wang verfasserin aut Keli Chen verfasserin aut Mingfu Tian verfasserin aut Feng Xiao verfasserin aut Qi Zhang verfasserin aut Weijie Chen verfasserin aut Pan Pan verfasserin aut Pin Wan verfasserin aut Yingle Liu verfasserin aut Huiyao Lan verfasserin aut Kailang Wu verfasserin aut Jianguo Wu verfasserin aut In BMC Biology BMC, 2003 18(2020), 1, Seite 22 (DE-627)377757241 (DE-600)2133020-7 17417007 nnns volume:18 year:2020 number:1 pages:22 https://doi.org/10.1186/s12915-020-00918-w kostenfrei https://doaj.org/article/6501c92b4b5045cb996039eebe55494a kostenfrei https://doi.org/10.1186/s12915-020-00918-w kostenfrei https://doaj.org/toc/1741-7007 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_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_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_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 18 2020 1 22
spelling	10.1186/s12915-020-00918-w doi (DE-627)DOAJ017032571 (DE-599)DOAJ6501c92b4b5045cb996039eebe55494a DE-627 ger DE-627 rakwb eng QH301-705.5 Wenbiao Wang verfasserin aut Paxillin mediates ATP-induced activation of P2X7 receptor and NLRP3 inflammasome 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Extracellular adenosine triphosphate (ATP), a key danger-associated molecular pattern (DAMP) molecule, is released to the extracellular medium during inflammation by injured parenchymal cells, dying leukocytes, and activated platelets. ATP directly activates the plasma membrane channel P2X7 receptor (P2X7R), leading to an intracellular influx of K+, a key trigger inducing NLRP3 inflammasome activation. However, the mechanism underlying P2X7R-mediated activation of NLRP3 inflammasome is poorly understood, and additional molecular mediators have not been identified. Here, we demonstrate that Paxillin is the molecule connecting the P2X7 receptor and NLRP3 inflammasome through protein interactions. Results We show a distinct mechanism by which Paxillin promotes ATP-induced activation of the P2X7 receptor and NLRP3 inflammasome. Extracellular ATP induces Paxillin phosphorylation and then facilitates Paxillin-NLRP3 interaction. Interestingly, Paxillin enhances NLRP3 deubiquitination and activates NLRP3 inflammasome upon ATP treatment and K+ efflux. Moreover, we demonstrated that USP13 is a key enzyme for Paxillin-mediated NLRP3 deubiquitination upon ATP treatment. Notably, extracellular ATP promotes Paxillin and NLRP3 migration from the cytosol to the plasma membrane and facilitates P2X7R-Paxillin interaction and PaxillinNLRP3 association, resulting in the formation of the P2X7R-Paxillin-NLRP3 complex. Functionally, Paxillin is essential for ATP-induced NLRP3 inflammasome activation in mouse BMDMs and BMDCs as well as in human PBMCs and THP-1-differentiated macrophages. Conclusions We have identified paxillin as a mediator of NLRP3 inflammasome activation. Paxillin plays key roles in ATP-induced activation of the P2X7 receptor and NLRP3 inflammasome by facilitating the formation of the P2X7R-Paxillin-NLRP3 complex. Adenosine triphosphate, ATP P2X7 receptor Paxillin The NACHT, LRR, and PYD domain-containing protein 3, NLRP3 Ubiquitin-specific peptidase 13, USP13 Biology (General) Dingwen Hu verfasserin aut Yuqian Feng verfasserin aut Caifeng Wu verfasserin aut Yunting Song verfasserin aut Weiyong Liu verfasserin aut Aixin Li verfasserin aut Yingchong Wang verfasserin aut Keli Chen verfasserin aut Mingfu Tian verfasserin aut Feng Xiao verfasserin aut Qi Zhang verfasserin aut Weijie Chen verfasserin aut Pan Pan verfasserin aut Pin Wan verfasserin aut Yingle Liu verfasserin aut Huiyao Lan verfasserin aut Kailang Wu verfasserin aut Jianguo Wu verfasserin aut In BMC Biology BMC, 2003 18(2020), 1, Seite 22 (DE-627)377757241 (DE-600)2133020-7 17417007 nnns volume:18 year:2020 number:1 pages:22 https://doi.org/10.1186/s12915-020-00918-w kostenfrei https://doaj.org/article/6501c92b4b5045cb996039eebe55494a kostenfrei https://doi.org/10.1186/s12915-020-00918-w kostenfrei https://doaj.org/toc/1741-7007 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_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_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_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 18 2020 1 22
allfields_unstemmed	10.1186/s12915-020-00918-w doi (DE-627)DOAJ017032571 (DE-599)DOAJ6501c92b4b5045cb996039eebe55494a DE-627 ger DE-627 rakwb eng QH301-705.5 Wenbiao Wang verfasserin aut Paxillin mediates ATP-induced activation of P2X7 receptor and NLRP3 inflammasome 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Extracellular adenosine triphosphate (ATP), a key danger-associated molecular pattern (DAMP) molecule, is released to the extracellular medium during inflammation by injured parenchymal cells, dying leukocytes, and activated platelets. ATP directly activates the plasma membrane channel P2X7 receptor (P2X7R), leading to an intracellular influx of K+, a key trigger inducing NLRP3 inflammasome activation. However, the mechanism underlying P2X7R-mediated activation of NLRP3 inflammasome is poorly understood, and additional molecular mediators have not been identified. Here, we demonstrate that Paxillin is the molecule connecting the P2X7 receptor and NLRP3 inflammasome through protein interactions. Results We show a distinct mechanism by which Paxillin promotes ATP-induced activation of the P2X7 receptor and NLRP3 inflammasome. Extracellular ATP induces Paxillin phosphorylation and then facilitates Paxillin-NLRP3 interaction. Interestingly, Paxillin enhances NLRP3 deubiquitination and activates NLRP3 inflammasome upon ATP treatment and K+ efflux. Moreover, we demonstrated that USP13 is a key enzyme for Paxillin-mediated NLRP3 deubiquitination upon ATP treatment. Notably, extracellular ATP promotes Paxillin and NLRP3 migration from the cytosol to the plasma membrane and facilitates P2X7R-Paxillin interaction and PaxillinNLRP3 association, resulting in the formation of the P2X7R-Paxillin-NLRP3 complex. Functionally, Paxillin is essential for ATP-induced NLRP3 inflammasome activation in mouse BMDMs and BMDCs as well as in human PBMCs and THP-1-differentiated macrophages. Conclusions We have identified paxillin as a mediator of NLRP3 inflammasome activation. Paxillin plays key roles in ATP-induced activation of the P2X7 receptor and NLRP3 inflammasome by facilitating the formation of the P2X7R-Paxillin-NLRP3 complex. Adenosine triphosphate, ATP P2X7 receptor Paxillin The NACHT, LRR, and PYD domain-containing protein 3, NLRP3 Ubiquitin-specific peptidase 13, USP13 Biology (General) Dingwen Hu verfasserin aut Yuqian Feng verfasserin aut Caifeng Wu verfasserin aut Yunting Song verfasserin aut Weiyong Liu verfasserin aut Aixin Li verfasserin aut Yingchong Wang verfasserin aut Keli Chen verfasserin aut Mingfu Tian verfasserin aut Feng Xiao verfasserin aut Qi Zhang verfasserin aut Weijie Chen verfasserin aut Pan Pan verfasserin aut Pin Wan verfasserin aut Yingle Liu verfasserin aut Huiyao Lan verfasserin aut Kailang Wu verfasserin aut Jianguo Wu verfasserin aut In BMC Biology BMC, 2003 18(2020), 1, Seite 22 (DE-627)377757241 (DE-600)2133020-7 17417007 nnns volume:18 year:2020 number:1 pages:22 https://doi.org/10.1186/s12915-020-00918-w kostenfrei https://doaj.org/article/6501c92b4b5045cb996039eebe55494a kostenfrei https://doi.org/10.1186/s12915-020-00918-w kostenfrei https://doaj.org/toc/1741-7007 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_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_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_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 18 2020 1 22
allfieldsGer	10.1186/s12915-020-00918-w doi (DE-627)DOAJ017032571 (DE-599)DOAJ6501c92b4b5045cb996039eebe55494a DE-627 ger DE-627 rakwb eng QH301-705.5 Wenbiao Wang verfasserin aut Paxillin mediates ATP-induced activation of P2X7 receptor and NLRP3 inflammasome 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Extracellular adenosine triphosphate (ATP), a key danger-associated molecular pattern (DAMP) molecule, is released to the extracellular medium during inflammation by injured parenchymal cells, dying leukocytes, and activated platelets. ATP directly activates the plasma membrane channel P2X7 receptor (P2X7R), leading to an intracellular influx of K+, a key trigger inducing NLRP3 inflammasome activation. However, the mechanism underlying P2X7R-mediated activation of NLRP3 inflammasome is poorly understood, and additional molecular mediators have not been identified. Here, we demonstrate that Paxillin is the molecule connecting the P2X7 receptor and NLRP3 inflammasome through protein interactions. Results We show a distinct mechanism by which Paxillin promotes ATP-induced activation of the P2X7 receptor and NLRP3 inflammasome. Extracellular ATP induces Paxillin phosphorylation and then facilitates Paxillin-NLRP3 interaction. Interestingly, Paxillin enhances NLRP3 deubiquitination and activates NLRP3 inflammasome upon ATP treatment and K+ efflux. Moreover, we demonstrated that USP13 is a key enzyme for Paxillin-mediated NLRP3 deubiquitination upon ATP treatment. Notably, extracellular ATP promotes Paxillin and NLRP3 migration from the cytosol to the plasma membrane and facilitates P2X7R-Paxillin interaction and PaxillinNLRP3 association, resulting in the formation of the P2X7R-Paxillin-NLRP3 complex. Functionally, Paxillin is essential for ATP-induced NLRP3 inflammasome activation in mouse BMDMs and BMDCs as well as in human PBMCs and THP-1-differentiated macrophages. Conclusions We have identified paxillin as a mediator of NLRP3 inflammasome activation. Paxillin plays key roles in ATP-induced activation of the P2X7 receptor and NLRP3 inflammasome by facilitating the formation of the P2X7R-Paxillin-NLRP3 complex. Adenosine triphosphate, ATP P2X7 receptor Paxillin The NACHT, LRR, and PYD domain-containing protein 3, NLRP3 Ubiquitin-specific peptidase 13, USP13 Biology (General) Dingwen Hu verfasserin aut Yuqian Feng verfasserin aut Caifeng Wu verfasserin aut Yunting Song verfasserin aut Weiyong Liu verfasserin aut Aixin Li verfasserin aut Yingchong Wang verfasserin aut Keli Chen verfasserin aut Mingfu Tian verfasserin aut Feng Xiao verfasserin aut Qi Zhang verfasserin aut Weijie Chen verfasserin aut Pan Pan verfasserin aut Pin Wan verfasserin aut Yingle Liu verfasserin aut Huiyao Lan verfasserin aut Kailang Wu verfasserin aut Jianguo Wu verfasserin aut In BMC Biology BMC, 2003 18(2020), 1, Seite 22 (DE-627)377757241 (DE-600)2133020-7 17417007 nnns volume:18 year:2020 number:1 pages:22 https://doi.org/10.1186/s12915-020-00918-w kostenfrei https://doaj.org/article/6501c92b4b5045cb996039eebe55494a kostenfrei https://doi.org/10.1186/s12915-020-00918-w kostenfrei https://doaj.org/toc/1741-7007 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_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_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_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 18 2020 1 22
allfieldsSound	10.1186/s12915-020-00918-w doi (DE-627)DOAJ017032571 (DE-599)DOAJ6501c92b4b5045cb996039eebe55494a DE-627 ger DE-627 rakwb eng QH301-705.5 Wenbiao Wang verfasserin aut Paxillin mediates ATP-induced activation of P2X7 receptor and NLRP3 inflammasome 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Extracellular adenosine triphosphate (ATP), a key danger-associated molecular pattern (DAMP) molecule, is released to the extracellular medium during inflammation by injured parenchymal cells, dying leukocytes, and activated platelets. ATP directly activates the plasma membrane channel P2X7 receptor (P2X7R), leading to an intracellular influx of K+, a key trigger inducing NLRP3 inflammasome activation. However, the mechanism underlying P2X7R-mediated activation of NLRP3 inflammasome is poorly understood, and additional molecular mediators have not been identified. Here, we demonstrate that Paxillin is the molecule connecting the P2X7 receptor and NLRP3 inflammasome through protein interactions. Results We show a distinct mechanism by which Paxillin promotes ATP-induced activation of the P2X7 receptor and NLRP3 inflammasome. Extracellular ATP induces Paxillin phosphorylation and then facilitates Paxillin-NLRP3 interaction. Interestingly, Paxillin enhances NLRP3 deubiquitination and activates NLRP3 inflammasome upon ATP treatment and K+ efflux. Moreover, we demonstrated that USP13 is a key enzyme for Paxillin-mediated NLRP3 deubiquitination upon ATP treatment. Notably, extracellular ATP promotes Paxillin and NLRP3 migration from the cytosol to the plasma membrane and facilitates P2X7R-Paxillin interaction and PaxillinNLRP3 association, resulting in the formation of the P2X7R-Paxillin-NLRP3 complex. Functionally, Paxillin is essential for ATP-induced NLRP3 inflammasome activation in mouse BMDMs and BMDCs as well as in human PBMCs and THP-1-differentiated macrophages. Conclusions We have identified paxillin as a mediator of NLRP3 inflammasome activation. Paxillin plays key roles in ATP-induced activation of the P2X7 receptor and NLRP3 inflammasome by facilitating the formation of the P2X7R-Paxillin-NLRP3 complex. Adenosine triphosphate, ATP P2X7 receptor Paxillin The NACHT, LRR, and PYD domain-containing protein 3, NLRP3 Ubiquitin-specific peptidase 13, USP13 Biology (General) Dingwen Hu verfasserin aut Yuqian Feng verfasserin aut Caifeng Wu verfasserin aut Yunting Song verfasserin aut Weiyong Liu verfasserin aut Aixin Li verfasserin aut Yingchong Wang verfasserin aut Keli Chen verfasserin aut Mingfu Tian verfasserin aut Feng Xiao verfasserin aut Qi Zhang verfasserin aut Weijie Chen verfasserin aut Pan Pan verfasserin aut Pin Wan verfasserin aut Yingle Liu verfasserin aut Huiyao Lan verfasserin aut Kailang Wu verfasserin aut Jianguo Wu verfasserin aut In BMC Biology BMC, 2003 18(2020), 1, Seite 22 (DE-627)377757241 (DE-600)2133020-7 17417007 nnns volume:18 year:2020 number:1 pages:22 https://doi.org/10.1186/s12915-020-00918-w kostenfrei https://doaj.org/article/6501c92b4b5045cb996039eebe55494a kostenfrei https://doi.org/10.1186/s12915-020-00918-w kostenfrei https://doaj.org/toc/1741-7007 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_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_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_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 18 2020 1 22
language	English
source	In BMC Biology 18(2020), 1, Seite 22 volume:18 year:2020 number:1 pages:22
sourceStr	In BMC Biology 18(2020), 1, Seite 22 volume:18 year:2020 number:1 pages:22
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Adenosine triphosphate, ATP P2X7 receptor Paxillin The NACHT, LRR, and PYD domain-containing protein 3, NLRP3 Ubiquitin-specific peptidase 13, USP13 Biology (General)
isfreeaccess_bool	true
container_title	BMC Biology
authorswithroles_txt_mv	Wenbiao Wang @@aut@@ Dingwen Hu @@aut@@ Yuqian Feng @@aut@@ Caifeng Wu @@aut@@ Yunting Song @@aut@@ Weiyong Liu @@aut@@ Aixin Li @@aut@@ Yingchong Wang @@aut@@ Keli Chen @@aut@@ Mingfu Tian @@aut@@ Feng Xiao @@aut@@ Qi Zhang @@aut@@ Weijie Chen @@aut@@ Pan Pan @@aut@@ Pin Wan @@aut@@ Yingle Liu @@aut@@ Huiyao Lan @@aut@@ Kailang Wu @@aut@@ Jianguo Wu @@aut@@
publishDateDaySort_date	2020-01-01T00:00:00Z
hierarchy_top_id	377757241
id	DOAJ017032571
language_de	englisch
fullrecord	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ017032571</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230310085135.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230226s2020 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1186/s12915-020-00918-w</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ017032571</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ6501c92b4b5045cb996039eebe55494a</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">QH301-705.5</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Wenbiao Wang</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Paxillin mediates ATP-induced activation of P2X7 receptor and NLRP3 inflammasome</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2020</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract Background Extracellular adenosine triphosphate (ATP), a key danger-associated molecular pattern (DAMP) molecule, is released to the extracellular medium during inflammation by injured parenchymal cells, dying leukocytes, and activated platelets. ATP directly activates the plasma membrane channel P2X7 receptor (P2X7R), leading to an intracellular influx of K+, a key trigger inducing NLRP3 inflammasome activation. However, the mechanism underlying P2X7R-mediated activation of NLRP3 inflammasome is poorly understood, and additional molecular mediators have not been identified. Here, we demonstrate that Paxillin is the molecule connecting the P2X7 receptor and NLRP3 inflammasome through protein interactions. Results We show a distinct mechanism by which Paxillin promotes ATP-induced activation of the P2X7 receptor and NLRP3 inflammasome. Extracellular ATP induces Paxillin phosphorylation and then facilitates Paxillin-NLRP3 interaction. Interestingly, Paxillin enhances NLRP3 deubiquitination and activates NLRP3 inflammasome upon ATP treatment and K+ efflux. Moreover, we demonstrated that USP13 is a key enzyme for Paxillin-mediated NLRP3 deubiquitination upon ATP treatment. Notably, extracellular ATP promotes Paxillin and NLRP3 migration from the cytosol to the plasma membrane and facilitates P2X7R-Paxillin interaction and PaxillinNLRP3 association, resulting in the formation of the P2X7R-Paxillin-NLRP3 complex. Functionally, Paxillin is essential for ATP-induced NLRP3 inflammasome activation in mouse BMDMs and BMDCs as well as in human PBMCs and THP-1-differentiated macrophages. Conclusions We have identified paxillin as a mediator of NLRP3 inflammasome activation. 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callnumber-first	Q - Science
author	Wenbiao Wang
spellingShingle	Wenbiao Wang misc QH301-705.5 misc Adenosine triphosphate, ATP misc P2X7 receptor misc Paxillin misc The NACHT, LRR, and PYD domain-containing protein 3, NLRP3 misc Ubiquitin-specific peptidase 13, USP13 misc Biology (General) Paxillin mediates ATP-induced activation of P2X7 receptor and NLRP3 inflammasome
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topic_title	QH301-705.5 Paxillin mediates ATP-induced activation of P2X7 receptor and NLRP3 inflammasome Adenosine triphosphate, ATP P2X7 receptor Paxillin The NACHT, LRR, and PYD domain-containing protein 3, NLRP3 Ubiquitin-specific peptidase 13, USP13
topic	misc QH301-705.5 misc Adenosine triphosphate, ATP misc P2X7 receptor misc Paxillin misc The NACHT, LRR, and PYD domain-containing protein 3, NLRP3 misc Ubiquitin-specific peptidase 13, USP13 misc Biology (General)
topic_unstemmed	misc QH301-705.5 misc Adenosine triphosphate, ATP misc P2X7 receptor misc Paxillin misc The NACHT, LRR, and PYD domain-containing protein 3, NLRP3 misc Ubiquitin-specific peptidase 13, USP13 misc Biology (General)
topic_browse	misc QH301-705.5 misc Adenosine triphosphate, ATP misc P2X7 receptor misc Paxillin misc The NACHT, LRR, and PYD domain-containing protein 3, NLRP3 misc Ubiquitin-specific peptidase 13, USP13 misc Biology (General)
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title	Paxillin mediates ATP-induced activation of P2X7 receptor and NLRP3 inflammasome
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title_full	Paxillin mediates ATP-induced activation of P2X7 receptor and NLRP3 inflammasome
author_sort	Wenbiao Wang
journal	BMC Biology
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author_browse	Wenbiao Wang Dingwen Hu Yuqian Feng Caifeng Wu Yunting Song Weiyong Liu Aixin Li Yingchong Wang Keli Chen Mingfu Tian Feng Xiao Qi Zhang Weijie Chen Pan Pan Pin Wan Yingle Liu Huiyao Lan Kailang Wu Jianguo Wu
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doi_str_mv	10.1186/s12915-020-00918-w
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title_sort	paxillin mediates atp-induced activation of p2x7 receptor and nlrp3 inflammasome
callnumber	QH301-705.5
title_auth	Paxillin mediates ATP-induced activation of P2X7 receptor and NLRP3 inflammasome
abstract	Abstract Background Extracellular adenosine triphosphate (ATP), a key danger-associated molecular pattern (DAMP) molecule, is released to the extracellular medium during inflammation by injured parenchymal cells, dying leukocytes, and activated platelets. ATP directly activates the plasma membrane channel P2X7 receptor (P2X7R), leading to an intracellular influx of K+, a key trigger inducing NLRP3 inflammasome activation. However, the mechanism underlying P2X7R-mediated activation of NLRP3 inflammasome is poorly understood, and additional molecular mediators have not been identified. Here, we demonstrate that Paxillin is the molecule connecting the P2X7 receptor and NLRP3 inflammasome through protein interactions. Results We show a distinct mechanism by which Paxillin promotes ATP-induced activation of the P2X7 receptor and NLRP3 inflammasome. Extracellular ATP induces Paxillin phosphorylation and then facilitates Paxillin-NLRP3 interaction. Interestingly, Paxillin enhances NLRP3 deubiquitination and activates NLRP3 inflammasome upon ATP treatment and K+ efflux. Moreover, we demonstrated that USP13 is a key enzyme for Paxillin-mediated NLRP3 deubiquitination upon ATP treatment. Notably, extracellular ATP promotes Paxillin and NLRP3 migration from the cytosol to the plasma membrane and facilitates P2X7R-Paxillin interaction and PaxillinNLRP3 association, resulting in the formation of the P2X7R-Paxillin-NLRP3 complex. Functionally, Paxillin is essential for ATP-induced NLRP3 inflammasome activation in mouse BMDMs and BMDCs as well as in human PBMCs and THP-1-differentiated macrophages. Conclusions We have identified paxillin as a mediator of NLRP3 inflammasome activation. Paxillin plays key roles in ATP-induced activation of the P2X7 receptor and NLRP3 inflammasome by facilitating the formation of the P2X7R-Paxillin-NLRP3 complex.
abstractGer	Abstract Background Extracellular adenosine triphosphate (ATP), a key danger-associated molecular pattern (DAMP) molecule, is released to the extracellular medium during inflammation by injured parenchymal cells, dying leukocytes, and activated platelets. ATP directly activates the plasma membrane channel P2X7 receptor (P2X7R), leading to an intracellular influx of K+, a key trigger inducing NLRP3 inflammasome activation. However, the mechanism underlying P2X7R-mediated activation of NLRP3 inflammasome is poorly understood, and additional molecular mediators have not been identified. Here, we demonstrate that Paxillin is the molecule connecting the P2X7 receptor and NLRP3 inflammasome through protein interactions. Results We show a distinct mechanism by which Paxillin promotes ATP-induced activation of the P2X7 receptor and NLRP3 inflammasome. Extracellular ATP induces Paxillin phosphorylation and then facilitates Paxillin-NLRP3 interaction. Interestingly, Paxillin enhances NLRP3 deubiquitination and activates NLRP3 inflammasome upon ATP treatment and K+ efflux. Moreover, we demonstrated that USP13 is a key enzyme for Paxillin-mediated NLRP3 deubiquitination upon ATP treatment. Notably, extracellular ATP promotes Paxillin and NLRP3 migration from the cytosol to the plasma membrane and facilitates P2X7R-Paxillin interaction and PaxillinNLRP3 association, resulting in the formation of the P2X7R-Paxillin-NLRP3 complex. Functionally, Paxillin is essential for ATP-induced NLRP3 inflammasome activation in mouse BMDMs and BMDCs as well as in human PBMCs and THP-1-differentiated macrophages. Conclusions We have identified paxillin as a mediator of NLRP3 inflammasome activation. Paxillin plays key roles in ATP-induced activation of the P2X7 receptor and NLRP3 inflammasome by facilitating the formation of the P2X7R-Paxillin-NLRP3 complex.
abstract_unstemmed	Abstract Background Extracellular adenosine triphosphate (ATP), a key danger-associated molecular pattern (DAMP) molecule, is released to the extracellular medium during inflammation by injured parenchymal cells, dying leukocytes, and activated platelets. ATP directly activates the plasma membrane channel P2X7 receptor (P2X7R), leading to an intracellular influx of K+, a key trigger inducing NLRP3 inflammasome activation. However, the mechanism underlying P2X7R-mediated activation of NLRP3 inflammasome is poorly understood, and additional molecular mediators have not been identified. Here, we demonstrate that Paxillin is the molecule connecting the P2X7 receptor and NLRP3 inflammasome through protein interactions. Results We show a distinct mechanism by which Paxillin promotes ATP-induced activation of the P2X7 receptor and NLRP3 inflammasome. Extracellular ATP induces Paxillin phosphorylation and then facilitates Paxillin-NLRP3 interaction. Interestingly, Paxillin enhances NLRP3 deubiquitination and activates NLRP3 inflammasome upon ATP treatment and K+ efflux. Moreover, we demonstrated that USP13 is a key enzyme for Paxillin-mediated NLRP3 deubiquitination upon ATP treatment. Notably, extracellular ATP promotes Paxillin and NLRP3 migration from the cytosol to the plasma membrane and facilitates P2X7R-Paxillin interaction and PaxillinNLRP3 association, resulting in the formation of the P2X7R-Paxillin-NLRP3 complex. Functionally, Paxillin is essential for ATP-induced NLRP3 inflammasome activation in mouse BMDMs and BMDCs as well as in human PBMCs and THP-1-differentiated macrophages. Conclusions We have identified paxillin as a mediator of NLRP3 inflammasome activation. Paxillin plays key roles in ATP-induced activation of the P2X7 receptor and NLRP3 inflammasome by facilitating the formation of the P2X7R-Paxillin-NLRP3 complex.
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title_short	Paxillin mediates ATP-induced activation of P2X7 receptor and NLRP3 inflammasome
url	https://doi.org/10.1186/s12915-020-00918-w https://doaj.org/article/6501c92b4b5045cb996039eebe55494a https://doaj.org/toc/1741-7007
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author2Str	Dingwen Hu Yuqian Feng Caifeng Wu Yunting Song Weiyong Liu Aixin Li Yingchong Wang Keli Chen Mingfu Tian Feng Xiao Qi Zhang Weijie Chen Pan Pan Pin Wan Yingle Liu Huiyao Lan Kailang Wu Jianguo Wu
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up_date	2024-07-04T00:02:55.834Z
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fullrecord_marcxml	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ017032571</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230310085135.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230226s2020 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1186/s12915-020-00918-w</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ017032571</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ6501c92b4b5045cb996039eebe55494a</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">QH301-705.5</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Wenbiao Wang</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Paxillin mediates ATP-induced activation of P2X7 receptor and NLRP3 inflammasome</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2020</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract Background Extracellular adenosine triphosphate (ATP), a key danger-associated molecular pattern (DAMP) molecule, is released to the extracellular medium during inflammation by injured parenchymal cells, dying leukocytes, and activated platelets. ATP directly activates the plasma membrane channel P2X7 receptor (P2X7R), leading to an intracellular influx of K+, a key trigger inducing NLRP3 inflammasome activation. However, the mechanism underlying P2X7R-mediated activation of NLRP3 inflammasome is poorly understood, and additional molecular mediators have not been identified. Here, we demonstrate that Paxillin is the molecule connecting the P2X7 receptor and NLRP3 inflammasome through protein interactions. Results We show a distinct mechanism by which Paxillin promotes ATP-induced activation of the P2X7 receptor and NLRP3 inflammasome. Extracellular ATP induces Paxillin phosphorylation and then facilitates Paxillin-NLRP3 interaction. Interestingly, Paxillin enhances NLRP3 deubiquitination and activates NLRP3 inflammasome upon ATP treatment and K+ efflux. Moreover, we demonstrated that USP13 is a key enzyme for Paxillin-mediated NLRP3 deubiquitination upon ATP treatment. Notably, extracellular ATP promotes Paxillin and NLRP3 migration from the cytosol to the plasma membrane and facilitates P2X7R-Paxillin interaction and PaxillinNLRP3 association, resulting in the formation of the P2X7R-Paxillin-NLRP3 complex. Functionally, Paxillin is essential for ATP-induced NLRP3 inflammasome activation in mouse BMDMs and BMDCs as well as in human PBMCs and THP-1-differentiated macrophages. Conclusions We have identified paxillin as a mediator of NLRP3 inflammasome activation. Paxillin plays key roles in ATP-induced activation of the P2X7 receptor and NLRP3 inflammasome by facilitating the formation of the P2X7R-Paxillin-NLRP3 complex.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Adenosine triphosphate, ATP</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">P2X7 receptor</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Paxillin</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">The NACHT, LRR, and PYD domain-containing protein 3, NLRP3</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Ubiquitin-specific peptidase 13, USP13</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Biology (General)</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Dingwen Hu</subfield><subfield code="e">verfasserin</subfield><subfield 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Paxillin mediates ATP-induced activation of P2X7 receptor and NLRP3 inflammasome

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