Proteasome dysfunction triggers activation of SKN-1A/Nrf1 by the aspartic protease DDI-1

Proteasomes are essential for protein homeostasis in eukaryotes. To preserve cellular function, transcription of proteasome subunit genes is induced in response to proteasome dysfunction caused by pathogen attacks or proteasome inhibitor drugs. In Caenorhabditis elegans, this response requires SKN-1...
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Gespeichert in:

Autor*in:	Nicolas J Lehrbach [verfasserIn] Gary Ruvkun [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2016

Schlagwörter:	proteasome aspartic protease peptide N-glycanase SKN-1A/Nrf1 ER traffic

Übergeordnetes Werk:	In: eLife - eLife Sciences Publications Ltd, 2013, 5(2016)
Übergeordnetes Werk:	volume:5 ; year:2016

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.7554/eLife.17721

Katalog-ID:	DOAJ005645778

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allfields	10.7554/eLife.17721 doi (DE-627)DOAJ005645778 (DE-599)DOAJe966d8b746c7454c85b4fd3fe4aa8c88 DE-627 ger DE-627 rakwb eng QH301-705.5 Nicolas J Lehrbach verfasserin aut Proteasome dysfunction triggers activation of SKN-1A/Nrf1 by the aspartic protease DDI-1 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Proteasomes are essential for protein homeostasis in eukaryotes. To preserve cellular function, transcription of proteasome subunit genes is induced in response to proteasome dysfunction caused by pathogen attacks or proteasome inhibitor drugs. In Caenorhabditis elegans, this response requires SKN-1, a transcription factor related to mammalian Nrf1/2. Here, we use comprehensive genetic analyses to identify the pathway required for C. elegans to detect proteasome dysfunction and activate SKN-1. Genes required for SKN-1 activation encode regulators of ER traffic, a peptide N-glycanase, and DDI-1, a conserved aspartic protease. DDI-1 expression is induced by proteasome dysfunction, and we show that DDI-1 is required to cleave and activate an ER-associated isoform of SKN-1. Mammalian Nrf1 is also ER-associated and subject to proteolytic cleavage, suggesting a conserved mechanism of proteasome surveillance. Targeting mammalian DDI1 protease could mitigate effects of proteasome dysfunction in aging and protein aggregation disorders, or increase effectiveness of proteasome inhibitor cancer chemotherapies. proteasome aspartic protease peptide N-glycanase SKN-1A/Nrf1 ER traffic Medicine R Science Q Biology (General) Gary Ruvkun verfasserin aut In eLife eLife Sciences Publications Ltd, 2013 5(2016) (DE-627)728518384 (DE-600)2687154-3 2050084X nnns volume:5 year:2016 https://doi.org/10.7554/eLife.17721 kostenfrei https://doaj.org/article/e966d8b746c7454c85b4fd3fe4aa8c88 kostenfrei https://elifesciences.org/articles/17721 kostenfrei https://doaj.org/toc/2050-084X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 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_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2016
spelling	10.7554/eLife.17721 doi (DE-627)DOAJ005645778 (DE-599)DOAJe966d8b746c7454c85b4fd3fe4aa8c88 DE-627 ger DE-627 rakwb eng QH301-705.5 Nicolas J Lehrbach verfasserin aut Proteasome dysfunction triggers activation of SKN-1A/Nrf1 by the aspartic protease DDI-1 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Proteasomes are essential for protein homeostasis in eukaryotes. To preserve cellular function, transcription of proteasome subunit genes is induced in response to proteasome dysfunction caused by pathogen attacks or proteasome inhibitor drugs. In Caenorhabditis elegans, this response requires SKN-1, a transcription factor related to mammalian Nrf1/2. Here, we use comprehensive genetic analyses to identify the pathway required for C. elegans to detect proteasome dysfunction and activate SKN-1. Genes required for SKN-1 activation encode regulators of ER traffic, a peptide N-glycanase, and DDI-1, a conserved aspartic protease. DDI-1 expression is induced by proteasome dysfunction, and we show that DDI-1 is required to cleave and activate an ER-associated isoform of SKN-1. Mammalian Nrf1 is also ER-associated and subject to proteolytic cleavage, suggesting a conserved mechanism of proteasome surveillance. Targeting mammalian DDI1 protease could mitigate effects of proteasome dysfunction in aging and protein aggregation disorders, or increase effectiveness of proteasome inhibitor cancer chemotherapies. proteasome aspartic protease peptide N-glycanase SKN-1A/Nrf1 ER traffic Medicine R Science Q Biology (General) Gary Ruvkun verfasserin aut In eLife eLife Sciences Publications Ltd, 2013 5(2016) (DE-627)728518384 (DE-600)2687154-3 2050084X nnns volume:5 year:2016 https://doi.org/10.7554/eLife.17721 kostenfrei https://doaj.org/article/e966d8b746c7454c85b4fd3fe4aa8c88 kostenfrei https://elifesciences.org/articles/17721 kostenfrei https://doaj.org/toc/2050-084X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 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_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2016
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allfieldsSound	10.7554/eLife.17721 doi (DE-627)DOAJ005645778 (DE-599)DOAJe966d8b746c7454c85b4fd3fe4aa8c88 DE-627 ger DE-627 rakwb eng QH301-705.5 Nicolas J Lehrbach verfasserin aut Proteasome dysfunction triggers activation of SKN-1A/Nrf1 by the aspartic protease DDI-1 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Proteasomes are essential for protein homeostasis in eukaryotes. To preserve cellular function, transcription of proteasome subunit genes is induced in response to proteasome dysfunction caused by pathogen attacks or proteasome inhibitor drugs. In Caenorhabditis elegans, this response requires SKN-1, a transcription factor related to mammalian Nrf1/2. Here, we use comprehensive genetic analyses to identify the pathway required for C. elegans to detect proteasome dysfunction and activate SKN-1. Genes required for SKN-1 activation encode regulators of ER traffic, a peptide N-glycanase, and DDI-1, a conserved aspartic protease. DDI-1 expression is induced by proteasome dysfunction, and we show that DDI-1 is required to cleave and activate an ER-associated isoform of SKN-1. Mammalian Nrf1 is also ER-associated and subject to proteolytic cleavage, suggesting a conserved mechanism of proteasome surveillance. Targeting mammalian DDI1 protease could mitigate effects of proteasome dysfunction in aging and protein aggregation disorders, or increase effectiveness of proteasome inhibitor cancer chemotherapies. proteasome aspartic protease peptide N-glycanase SKN-1A/Nrf1 ER traffic Medicine R Science Q Biology (General) Gary Ruvkun verfasserin aut In eLife eLife Sciences Publications Ltd, 2013 5(2016) (DE-627)728518384 (DE-600)2687154-3 2050084X nnns volume:5 year:2016 https://doi.org/10.7554/eLife.17721 kostenfrei https://doaj.org/article/e966d8b746c7454c85b4fd3fe4aa8c88 kostenfrei https://elifesciences.org/articles/17721 kostenfrei https://doaj.org/toc/2050-084X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 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_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2016
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author	Nicolas J Lehrbach
spellingShingle	Nicolas J Lehrbach misc QH301-705.5 misc proteasome misc aspartic protease misc peptide N-glycanase misc SKN-1A/Nrf1 misc ER traffic misc Medicine misc R misc Science misc Q misc Biology (General) Proteasome dysfunction triggers activation of SKN-1A/Nrf1 by the aspartic protease DDI-1
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topic_title	QH301-705.5 Proteasome dysfunction triggers activation of SKN-1A/Nrf1 by the aspartic protease DDI-1 proteasome aspartic protease peptide N-glycanase SKN-1A/Nrf1 ER traffic
topic	misc QH301-705.5 misc proteasome misc aspartic protease misc peptide N-glycanase misc SKN-1A/Nrf1 misc ER traffic misc Medicine misc R misc Science misc Q misc Biology (General)
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title	Proteasome dysfunction triggers activation of SKN-1A/Nrf1 by the aspartic protease DDI-1
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title_full	Proteasome dysfunction triggers activation of SKN-1A/Nrf1 by the aspartic protease DDI-1
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title_sort	proteasome dysfunction triggers activation of skn-1a/nrf1 by the aspartic protease ddi-1
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title_auth	Proteasome dysfunction triggers activation of SKN-1A/Nrf1 by the aspartic protease DDI-1
abstract	Proteasomes are essential for protein homeostasis in eukaryotes. To preserve cellular function, transcription of proteasome subunit genes is induced in response to proteasome dysfunction caused by pathogen attacks or proteasome inhibitor drugs. In Caenorhabditis elegans, this response requires SKN-1, a transcription factor related to mammalian Nrf1/2. Here, we use comprehensive genetic analyses to identify the pathway required for C. elegans to detect proteasome dysfunction and activate SKN-1. Genes required for SKN-1 activation encode regulators of ER traffic, a peptide N-glycanase, and DDI-1, a conserved aspartic protease. DDI-1 expression is induced by proteasome dysfunction, and we show that DDI-1 is required to cleave and activate an ER-associated isoform of SKN-1. Mammalian Nrf1 is also ER-associated and subject to proteolytic cleavage, suggesting a conserved mechanism of proteasome surveillance. Targeting mammalian DDI1 protease could mitigate effects of proteasome dysfunction in aging and protein aggregation disorders, or increase effectiveness of proteasome inhibitor cancer chemotherapies.
abstractGer	Proteasomes are essential for protein homeostasis in eukaryotes. To preserve cellular function, transcription of proteasome subunit genes is induced in response to proteasome dysfunction caused by pathogen attacks or proteasome inhibitor drugs. In Caenorhabditis elegans, this response requires SKN-1, a transcription factor related to mammalian Nrf1/2. Here, we use comprehensive genetic analyses to identify the pathway required for C. elegans to detect proteasome dysfunction and activate SKN-1. Genes required for SKN-1 activation encode regulators of ER traffic, a peptide N-glycanase, and DDI-1, a conserved aspartic protease. DDI-1 expression is induced by proteasome dysfunction, and we show that DDI-1 is required to cleave and activate an ER-associated isoform of SKN-1. Mammalian Nrf1 is also ER-associated and subject to proteolytic cleavage, suggesting a conserved mechanism of proteasome surveillance. Targeting mammalian DDI1 protease could mitigate effects of proteasome dysfunction in aging and protein aggregation disorders, or increase effectiveness of proteasome inhibitor cancer chemotherapies.
abstract_unstemmed	Proteasomes are essential for protein homeostasis in eukaryotes. To preserve cellular function, transcription of proteasome subunit genes is induced in response to proteasome dysfunction caused by pathogen attacks or proteasome inhibitor drugs. In Caenorhabditis elegans, this response requires SKN-1, a transcription factor related to mammalian Nrf1/2. Here, we use comprehensive genetic analyses to identify the pathway required for C. elegans to detect proteasome dysfunction and activate SKN-1. Genes required for SKN-1 activation encode regulators of ER traffic, a peptide N-glycanase, and DDI-1, a conserved aspartic protease. DDI-1 expression is induced by proteasome dysfunction, and we show that DDI-1 is required to cleave and activate an ER-associated isoform of SKN-1. Mammalian Nrf1 is also ER-associated and subject to proteolytic cleavage, suggesting a conserved mechanism of proteasome surveillance. Targeting mammalian DDI1 protease could mitigate effects of proteasome dysfunction in aging and protein aggregation disorders, or increase effectiveness of proteasome inhibitor cancer chemotherapies.
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title_short	Proteasome dysfunction triggers activation of SKN-1A/Nrf1 by the aspartic protease DDI-1
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