Metalloprotease type III effectors that specifically cleave JNK and NF‐κB
Abstract Two major arms of the inflammatory response are the NF‐κB and c‐Jun N‐terminal kinase (JNK) pathways. Here, we show that enteropathogenic Escherichia coli (EPEC) employs the type III secretion system to target these two signalling arms by injecting host cells with two effector proteins, Nle...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Baruch, Kobi [verfasserIn] Gur‐Arie, Lihi [verfasserIn] Nadler, Chen [verfasserIn] Koby, Simi [verfasserIn] Yerushalmi, Gal [verfasserIn] Ben‐Neriah, Yinon [verfasserIn] Yogev, Orli [verfasserIn] Shaulian, Eitan [verfasserIn] Guttman, Chen [verfasserIn] Zarivach, Raz [verfasserIn] Rosenshine, Ilan [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2010 |
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| Schlagwörter: |
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| Anmerkung: |
© European Molecular Biology Organization 2011 |
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| Übergeordnetes Werk: |
Enthalten in: The EMBO Journal - Nature Publishing Group UK, 2023, 30(2010), 1 vom: 26. Nov., Seite 221-231 |
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| Übergeordnetes Werk: |
volume:30 ; year:2010 ; number:1 ; day:26 ; month:11 ; pages:221-231 |
| Links: |
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| DOI / URN: |
10.1038/emboj.2010.297 |
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| Katalog-ID: |
SPR057864934 |
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| 100 | 1 | |a Baruch, Kobi |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Metalloprotease type III effectors that specifically cleave JNK and NF‐κB |
| 264 | 1 | |c 2010 | |
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| 520 | |a Abstract Two major arms of the inflammatory response are the NF‐κB and c‐Jun N‐terminal kinase (JNK) pathways. Here, we show that enteropathogenic Escherichia coli (EPEC) employs the type III secretion system to target these two signalling arms by injecting host cells with two effector proteins, NleC and NleD. We provide evidence that NleC and NleD are Zn‐dependent endopeptidases that specifically clip and inactivate RelA (p65) and JNK, respectively, thus blocking NF‐κB and AP‐1 activation. We show that NleC and NleD co‐operate and complement other EPEC effectors in accomplishing maximal inhibition of IL‐8 secretion. This is a remarkable example of a pathogen using multiple effectors to manipulate systematically the host inflammatory response signalling network. | ||
| 520 | |a Abstract Enteropathogenic E. coli secretes multiple effector proteins that enable host‐cell colonization. Two effectors, NleC and NleD, are here shown to act as endopeptidases, cleaving p65 and JNK to inhibit the inflammatory response. | ||
| 650 | 4 | |a enteropathogenic |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a JNK |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a NF‐κB |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a NleC |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a NleD |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Gur‐Arie, Lihi |e verfasserin |4 aut | |
| 700 | 1 | |a Nadler, Chen |e verfasserin |4 aut | |
| 700 | 1 | |a Koby, Simi |e verfasserin |4 aut | |
| 700 | 1 | |a Yerushalmi, Gal |e verfasserin |4 aut | |
| 700 | 1 | |a Ben‐Neriah, Yinon |e verfasserin |4 aut | |
| 700 | 1 | |a Yogev, Orli |e verfasserin |4 aut | |
| 700 | 1 | |a Shaulian, Eitan |e verfasserin |4 aut | |
| 700 | 1 | |a Guttman, Chen |e verfasserin |4 aut | |
| 700 | 1 | |a Zarivach, Raz |e verfasserin |4 aut | |
| 700 | 1 | |a Rosenshine, Ilan |e verfasserin |4 aut | |
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| 912 | |a GBV_ILN_702 | ||
| 912 | |a GBV_ILN_2001 | ||
| 912 | |a GBV_ILN_2003 | ||
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| 912 | |a GBV_ILN_2005 | ||
| 912 | |a GBV_ILN_2006 | ||
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| 912 | |a GBV_ILN_2014 | ||
| 912 | |a GBV_ILN_2015 | ||
| 912 | |a GBV_ILN_2018 | ||
| 912 | |a GBV_ILN_2020 | ||
| 912 | |a GBV_ILN_2021 | ||
| 912 | |a GBV_ILN_2025 | ||
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| 912 | |a GBV_ILN_2038 | ||
| 912 | |a GBV_ILN_2044 | ||
| 912 | |a GBV_ILN_2048 | ||
| 912 | |a GBV_ILN_2049 | ||
| 912 | |a GBV_ILN_2050 | ||
| 912 | |a GBV_ILN_2055 | ||
| 912 | |a GBV_ILN_2056 | ||
| 912 | |a GBV_ILN_2057 | ||
| 912 | |a GBV_ILN_2059 | ||
| 912 | |a GBV_ILN_2061 | ||
| 912 | |a GBV_ILN_2064 | ||
| 912 | |a GBV_ILN_2068 | ||
| 912 | |a GBV_ILN_2088 | ||
| 912 | |a GBV_ILN_2093 | ||
| 912 | |a GBV_ILN_2106 | ||
| 912 | |a GBV_ILN_2108 | ||
| 912 | |a GBV_ILN_2110 | ||
| 912 | |a GBV_ILN_2111 | ||
| 912 | |a GBV_ILN_2113 | ||
| 912 | |a GBV_ILN_2118 | ||
| 912 | |a GBV_ILN_2119 | ||
| 912 | |a GBV_ILN_2122 | ||
| 912 | |a GBV_ILN_2129 | ||
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| 912 | |a GBV_ILN_4035 | ||
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| 912 | |a GBV_ILN_4046 | ||
| 912 | |a GBV_ILN_4112 | ||
| 912 | |a GBV_ILN_4125 | ||
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| 912 | |a GBV_ILN_4246 | ||
| 912 | |a GBV_ILN_4249 | ||
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| 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 | ||
| 912 | |a GBV_ILN_4324 | ||
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| 912 | |a GBV_ILN_4338 | ||
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10.1038/emboj.2010.297 doi (DE-627)SPR057864934 (SPR)emboj.2010.297-e DE-627 ger DE-627 rakwb eng Baruch, Kobi verfasserin aut Metalloprotease type III effectors that specifically cleave JNK and NF‐κB 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2011 Abstract Two major arms of the inflammatory response are the NF‐κB and c‐Jun N‐terminal kinase (JNK) pathways. Here, we show that enteropathogenic Escherichia coli (EPEC) employs the type III secretion system to target these two signalling arms by injecting host cells with two effector proteins, NleC and NleD. We provide evidence that NleC and NleD are Zn‐dependent endopeptidases that specifically clip and inactivate RelA (p65) and JNK, respectively, thus blocking NF‐κB and AP‐1 activation. We show that NleC and NleD co‐operate and complement other EPEC effectors in accomplishing maximal inhibition of IL‐8 secretion. This is a remarkable example of a pathogen using multiple effectors to manipulate systematically the host inflammatory response signalling network. Abstract Enteropathogenic E. coli secretes multiple effector proteins that enable host‐cell colonization. Two effectors, NleC and NleD, are here shown to act as endopeptidases, cleaving p65 and JNK to inhibit the inflammatory response. enteropathogenic (dpeaa)DE-He213 JNK (dpeaa)DE-He213 NF‐κB (dpeaa)DE-He213 NleC (dpeaa)DE-He213 NleD (dpeaa)DE-He213 Gur‐Arie, Lihi verfasserin aut Nadler, Chen verfasserin aut Koby, Simi verfasserin aut Yerushalmi, Gal verfasserin aut Ben‐Neriah, Yinon verfasserin aut Yogev, Orli verfasserin aut Shaulian, Eitan verfasserin aut Guttman, Chen verfasserin aut Zarivach, Raz verfasserin aut Rosenshine, Ilan verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 30(2010), 1 vom: 26. Nov., Seite 221-231 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:30 year:2010 number:1 day:26 month:11 pages:221-231 https://dx.doi.org/10.1038/emboj.2010.297 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 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_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 30 2010 1 26 11 221-231 |
| spelling |
10.1038/emboj.2010.297 doi (DE-627)SPR057864934 (SPR)emboj.2010.297-e DE-627 ger DE-627 rakwb eng Baruch, Kobi verfasserin aut Metalloprotease type III effectors that specifically cleave JNK and NF‐κB 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2011 Abstract Two major arms of the inflammatory response are the NF‐κB and c‐Jun N‐terminal kinase (JNK) pathways. Here, we show that enteropathogenic Escherichia coli (EPEC) employs the type III secretion system to target these two signalling arms by injecting host cells with two effector proteins, NleC and NleD. We provide evidence that NleC and NleD are Zn‐dependent endopeptidases that specifically clip and inactivate RelA (p65) and JNK, respectively, thus blocking NF‐κB and AP‐1 activation. We show that NleC and NleD co‐operate and complement other EPEC effectors in accomplishing maximal inhibition of IL‐8 secretion. This is a remarkable example of a pathogen using multiple effectors to manipulate systematically the host inflammatory response signalling network. Abstract Enteropathogenic E. coli secretes multiple effector proteins that enable host‐cell colonization. Two effectors, NleC and NleD, are here shown to act as endopeptidases, cleaving p65 and JNK to inhibit the inflammatory response. enteropathogenic (dpeaa)DE-He213 JNK (dpeaa)DE-He213 NF‐κB (dpeaa)DE-He213 NleC (dpeaa)DE-He213 NleD (dpeaa)DE-He213 Gur‐Arie, Lihi verfasserin aut Nadler, Chen verfasserin aut Koby, Simi verfasserin aut Yerushalmi, Gal verfasserin aut Ben‐Neriah, Yinon verfasserin aut Yogev, Orli verfasserin aut Shaulian, Eitan verfasserin aut Guttman, Chen verfasserin aut Zarivach, Raz verfasserin aut Rosenshine, Ilan verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 30(2010), 1 vom: 26. Nov., Seite 221-231 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:30 year:2010 number:1 day:26 month:11 pages:221-231 https://dx.doi.org/10.1038/emboj.2010.297 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 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_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 30 2010 1 26 11 221-231 |
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10.1038/emboj.2010.297 doi (DE-627)SPR057864934 (SPR)emboj.2010.297-e DE-627 ger DE-627 rakwb eng Baruch, Kobi verfasserin aut Metalloprotease type III effectors that specifically cleave JNK and NF‐κB 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2011 Abstract Two major arms of the inflammatory response are the NF‐κB and c‐Jun N‐terminal kinase (JNK) pathways. Here, we show that enteropathogenic Escherichia coli (EPEC) employs the type III secretion system to target these two signalling arms by injecting host cells with two effector proteins, NleC and NleD. We provide evidence that NleC and NleD are Zn‐dependent endopeptidases that specifically clip and inactivate RelA (p65) and JNK, respectively, thus blocking NF‐κB and AP‐1 activation. We show that NleC and NleD co‐operate and complement other EPEC effectors in accomplishing maximal inhibition of IL‐8 secretion. This is a remarkable example of a pathogen using multiple effectors to manipulate systematically the host inflammatory response signalling network. Abstract Enteropathogenic E. coli secretes multiple effector proteins that enable host‐cell colonization. Two effectors, NleC and NleD, are here shown to act as endopeptidases, cleaving p65 and JNK to inhibit the inflammatory response. enteropathogenic (dpeaa)DE-He213 JNK (dpeaa)DE-He213 NF‐κB (dpeaa)DE-He213 NleC (dpeaa)DE-He213 NleD (dpeaa)DE-He213 Gur‐Arie, Lihi verfasserin aut Nadler, Chen verfasserin aut Koby, Simi verfasserin aut Yerushalmi, Gal verfasserin aut Ben‐Neriah, Yinon verfasserin aut Yogev, Orli verfasserin aut Shaulian, Eitan verfasserin aut Guttman, Chen verfasserin aut Zarivach, Raz verfasserin aut Rosenshine, Ilan verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 30(2010), 1 vom: 26. Nov., Seite 221-231 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:30 year:2010 number:1 day:26 month:11 pages:221-231 https://dx.doi.org/10.1038/emboj.2010.297 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 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_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 30 2010 1 26 11 221-231 |
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10.1038/emboj.2010.297 doi (DE-627)SPR057864934 (SPR)emboj.2010.297-e DE-627 ger DE-627 rakwb eng Baruch, Kobi verfasserin aut Metalloprotease type III effectors that specifically cleave JNK and NF‐κB 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2011 Abstract Two major arms of the inflammatory response are the NF‐κB and c‐Jun N‐terminal kinase (JNK) pathways. Here, we show that enteropathogenic Escherichia coli (EPEC) employs the type III secretion system to target these two signalling arms by injecting host cells with two effector proteins, NleC and NleD. We provide evidence that NleC and NleD are Zn‐dependent endopeptidases that specifically clip and inactivate RelA (p65) and JNK, respectively, thus blocking NF‐κB and AP‐1 activation. We show that NleC and NleD co‐operate and complement other EPEC effectors in accomplishing maximal inhibition of IL‐8 secretion. This is a remarkable example of a pathogen using multiple effectors to manipulate systematically the host inflammatory response signalling network. Abstract Enteropathogenic E. coli secretes multiple effector proteins that enable host‐cell colonization. Two effectors, NleC and NleD, are here shown to act as endopeptidases, cleaving p65 and JNK to inhibit the inflammatory response. enteropathogenic (dpeaa)DE-He213 JNK (dpeaa)DE-He213 NF‐κB (dpeaa)DE-He213 NleC (dpeaa)DE-He213 NleD (dpeaa)DE-He213 Gur‐Arie, Lihi verfasserin aut Nadler, Chen verfasserin aut Koby, Simi verfasserin aut Yerushalmi, Gal verfasserin aut Ben‐Neriah, Yinon verfasserin aut Yogev, Orli verfasserin aut Shaulian, Eitan verfasserin aut Guttman, Chen verfasserin aut Zarivach, Raz verfasserin aut Rosenshine, Ilan verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 30(2010), 1 vom: 26. Nov., Seite 221-231 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:30 year:2010 number:1 day:26 month:11 pages:221-231 https://dx.doi.org/10.1038/emboj.2010.297 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 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_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 30 2010 1 26 11 221-231 |
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10.1038/emboj.2010.297 doi (DE-627)SPR057864934 (SPR)emboj.2010.297-e DE-627 ger DE-627 rakwb eng Baruch, Kobi verfasserin aut Metalloprotease type III effectors that specifically cleave JNK and NF‐κB 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2011 Abstract Two major arms of the inflammatory response are the NF‐κB and c‐Jun N‐terminal kinase (JNK) pathways. Here, we show that enteropathogenic Escherichia coli (EPEC) employs the type III secretion system to target these two signalling arms by injecting host cells with two effector proteins, NleC and NleD. We provide evidence that NleC and NleD are Zn‐dependent endopeptidases that specifically clip and inactivate RelA (p65) and JNK, respectively, thus blocking NF‐κB and AP‐1 activation. We show that NleC and NleD co‐operate and complement other EPEC effectors in accomplishing maximal inhibition of IL‐8 secretion. This is a remarkable example of a pathogen using multiple effectors to manipulate systematically the host inflammatory response signalling network. Abstract Enteropathogenic E. coli secretes multiple effector proteins that enable host‐cell colonization. Two effectors, NleC and NleD, are here shown to act as endopeptidases, cleaving p65 and JNK to inhibit the inflammatory response. enteropathogenic (dpeaa)DE-He213 JNK (dpeaa)DE-He213 NF‐κB (dpeaa)DE-He213 NleC (dpeaa)DE-He213 NleD (dpeaa)DE-He213 Gur‐Arie, Lihi verfasserin aut Nadler, Chen verfasserin aut Koby, Simi verfasserin aut Yerushalmi, Gal verfasserin aut Ben‐Neriah, Yinon verfasserin aut Yogev, Orli verfasserin aut Shaulian, Eitan verfasserin aut Guttman, Chen verfasserin aut Zarivach, Raz verfasserin aut Rosenshine, Ilan verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 30(2010), 1 vom: 26. Nov., Seite 221-231 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:30 year:2010 number:1 day:26 month:11 pages:221-231 https://dx.doi.org/10.1038/emboj.2010.297 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 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_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 30 2010 1 26 11 221-231 |
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Baruch, Kobi @@aut@@ Gur‐Arie, Lihi @@aut@@ Nadler, Chen @@aut@@ Koby, Simi @@aut@@ Yerushalmi, Gal @@aut@@ Ben‐Neriah, Yinon @@aut@@ Yogev, Orli @@aut@@ Shaulian, Eitan @@aut@@ Guttman, Chen @@aut@@ Zarivach, Raz @@aut@@ Rosenshine, Ilan @@aut@@ |
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Baruch, Kobi |
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Baruch, Kobi misc enteropathogenic misc JNK misc NF‐κB misc NleC misc NleD Metalloprotease type III effectors that specifically cleave JNK and NF‐κB |
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Metalloprotease type III effectors that specifically cleave JNK and NF‐κB enteropathogenic (dpeaa)DE-He213 JNK (dpeaa)DE-He213 NF‐κB (dpeaa)DE-He213 NleC (dpeaa)DE-He213 NleD (dpeaa)DE-He213 |
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Baruch, Kobi Gur‐Arie, Lihi Nadler, Chen Koby, Simi Yerushalmi, Gal Ben‐Neriah, Yinon Yogev, Orli Shaulian, Eitan Guttman, Chen Zarivach, Raz Rosenshine, Ilan |
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metalloprotease type iii effectors that specifically cleave jnk and nf‐κb |
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Metalloprotease type III effectors that specifically cleave JNK and NF‐κB |
| abstract |
Abstract Two major arms of the inflammatory response are the NF‐κB and c‐Jun N‐terminal kinase (JNK) pathways. Here, we show that enteropathogenic Escherichia coli (EPEC) employs the type III secretion system to target these two signalling arms by injecting host cells with two effector proteins, NleC and NleD. We provide evidence that NleC and NleD are Zn‐dependent endopeptidases that specifically clip and inactivate RelA (p65) and JNK, respectively, thus blocking NF‐κB and AP‐1 activation. We show that NleC and NleD co‐operate and complement other EPEC effectors in accomplishing maximal inhibition of IL‐8 secretion. This is a remarkable example of a pathogen using multiple effectors to manipulate systematically the host inflammatory response signalling network. Abstract Enteropathogenic E. coli secretes multiple effector proteins that enable host‐cell colonization. Two effectors, NleC and NleD, are here shown to act as endopeptidases, cleaving p65 and JNK to inhibit the inflammatory response. © European Molecular Biology Organization 2011 |
| abstractGer |
Abstract Two major arms of the inflammatory response are the NF‐κB and c‐Jun N‐terminal kinase (JNK) pathways. Here, we show that enteropathogenic Escherichia coli (EPEC) employs the type III secretion system to target these two signalling arms by injecting host cells with two effector proteins, NleC and NleD. We provide evidence that NleC and NleD are Zn‐dependent endopeptidases that specifically clip and inactivate RelA (p65) and JNK, respectively, thus blocking NF‐κB and AP‐1 activation. We show that NleC and NleD co‐operate and complement other EPEC effectors in accomplishing maximal inhibition of IL‐8 secretion. This is a remarkable example of a pathogen using multiple effectors to manipulate systematically the host inflammatory response signalling network. Abstract Enteropathogenic E. coli secretes multiple effector proteins that enable host‐cell colonization. Two effectors, NleC and NleD, are here shown to act as endopeptidases, cleaving p65 and JNK to inhibit the inflammatory response. © European Molecular Biology Organization 2011 |
| abstract_unstemmed |
Abstract Two major arms of the inflammatory response are the NF‐κB and c‐Jun N‐terminal kinase (JNK) pathways. Here, we show that enteropathogenic Escherichia coli (EPEC) employs the type III secretion system to target these two signalling arms by injecting host cells with two effector proteins, NleC and NleD. We provide evidence that NleC and NleD are Zn‐dependent endopeptidases that specifically clip and inactivate RelA (p65) and JNK, respectively, thus blocking NF‐κB and AP‐1 activation. We show that NleC and NleD co‐operate and complement other EPEC effectors in accomplishing maximal inhibition of IL‐8 secretion. This is a remarkable example of a pathogen using multiple effectors to manipulate systematically the host inflammatory response signalling network. Abstract Enteropathogenic E. coli secretes multiple effector proteins that enable host‐cell colonization. Two effectors, NleC and NleD, are here shown to act as endopeptidases, cleaving p65 and JNK to inhibit the inflammatory response. © European Molecular Biology Organization 2011 |
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1 |
| title_short |
Metalloprotease type III effectors that specifically cleave JNK and NF‐κB |
| url |
https://dx.doi.org/10.1038/emboj.2010.297 |
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| author2 |
Gur‐Arie, Lihi Nadler, Chen Koby, Simi Yerushalmi, Gal Ben‐Neriah, Yinon Yogev, Orli Shaulian, Eitan Guttman, Chen Zarivach, Raz Rosenshine, Ilan |
| author2Str |
Gur‐Arie, Lihi Nadler, Chen Koby, Simi Yerushalmi, Gal Ben‐Neriah, Yinon Yogev, Orli Shaulian, Eitan Guttman, Chen Zarivach, Raz Rosenshine, Ilan |
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10.1038/emboj.2010.297 |
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2024-10-18T04:52:43.927Z |
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| score |
7.402135 |