SrasV1, PubMed, Checkpoint, bibRecord, 000970

SARS-Coronavirus Open Reading Frame-3a drives multimodal necrotic cell death.

Identifieur interne : 000970 ( PubMed/Checkpoint ); précédent : 000969; suivant : 000971

SARS-Coronavirus Open Reading Frame-3a drives multimodal necrotic cell death.

Auteurs : Yuan Yue [République populaire de Chine] ; Neel R. Nabar [États-Unis] ; Chong-Shan Shi [États-Unis] ; Olena Kamenyeva [États-Unis] ; Xun Xiao [République populaire de Chine] ; Il-Young Hwang [États-Unis] ; Min Wang [République populaire de Chine] ; John H. Kehrl [États-Unis]

Source :

Cell death & disease [ 2041-4889 ] ; 2018.

RBID : pubmed:30185776

Descripteurs français

KwdFr :
- Apoptose (physiologie), Autophagie (physiologie), Cadres ouverts de lecture (génétique), Cellules A549, Cellules HEK293, Cellules HeLa, Humains, Inflammasomes (métabolisme), Lignée cellulaire, Lignée cellulaire tumorale, Lysosomes (anatomopathologie), Lysosomes (métabolisme), Lysosomes (virologie), Membranes intracellulaires (anatomopathologie), Membranes intracellulaires (virologie), Nécrose (anatomopathologie), Nécrose (métabolisme), Nécrose (virologie), Receptor-Interacting Protein Serine-Threonine Kinases (métabolisme), Syndrome respiratoire aigu sévère (anatomopathologie), Syndrome respiratoire aigu sévère (virologie), Virus du SRAS (génétique), Virus du SRAS (pathogénicité).
MESH :
- anatomopathologie : Lysosomes, Membranes intracellulaires, Nécrose, Syndrome respiratoire aigu sévère.
- génétique : Cadres ouverts de lecture, Virus du SRAS.
- métabolisme : Inflammasomes, Lysosomes, Nécrose, Receptor-Interacting Protein Serine-Threonine Kinases.
- pathogénicité : Virus du SRAS.
- physiologie : Apoptose, Autophagie.
- virologie : Lysosomes, Membranes intracellulaires, Nécrose, Syndrome respiratoire aigu sévère.
- Cellules A549, Cellules HEK293, Cellules HeLa, Humains, Lignée cellulaire, Lignée cellulaire tumorale.

English descriptors

KwdEn :
- A549 Cells, Apoptosis (physiology), Autophagy (physiology), Cell Line, Cell Line, Tumor, HEK293 Cells, HeLa Cells, Humans, Inflammasomes (metabolism), Intracellular Membranes (pathology), Intracellular Membranes (virology), Lysosomes (metabolism), Lysosomes (pathology), Lysosomes (virology), Necrosis (metabolism), Necrosis (pathology), Necrosis (virology), Open Reading Frames (genetics), Receptor-Interacting Protein Serine-Threonine Kinases (metabolism), SARS Virus (genetics), SARS Virus (pathogenicity), Severe Acute Respiratory Syndrome (pathology), Severe Acute Respiratory Syndrome (virology).
MESH :
- chemical , metabolism : Inflammasomes, Receptor-Interacting Protein Serine-Threonine Kinases.
- genetics : Open Reading Frames, SARS Virus.
- metabolism : Lysosomes, Necrosis.
- pathogenicity : SARS Virus.
- pathology : Intracellular Membranes, Lysosomes, Necrosis, Severe Acute Respiratory Syndrome.
- physiology : Apoptosis, Autophagy.
- virology : Intracellular Membranes, Lysosomes, Necrosis, Severe Acute Respiratory Syndrome.
- A549 Cells, Cell Line, Cell Line, Tumor, HEK293 Cells, HeLa Cells, Humans.

Abstract

The molecular mechanisms underlying the severe lung pathology that occurs during SARS-CoV infections remain incompletely understood. The largest of the SARS-CoV accessory protein open reading frames (SARS 3a) oligomerizes, dynamically inserting into late endosomal, lysosomal, and trans-Golgi-network membranes. While previously implicated in a non-inflammatory apoptotic cell death pathway, here we extend the range of SARS 3a pathophysiologic targets by examining its effects on necrotic cell death pathways. We show that SARS 3a interacts with Receptor Interacting Protein 3 (Rip3), which augments the oligomerization of SARS 3a helping drive necrotic cell death. In addition, by inserting into lysosomal membranes SARS 3a triggers lysosomal damage and dysfunction. Consequently, Transcription Factor EB (TFEB) translocates to the nucleus increasing the transcription of autophagy- and lysosome-related genes. Finally, SARS 3a activates caspase-1 either directly or via an enhanced potassium efflux, which triggers NLRP3 inflammasome assembly. In summary, Rip3-mediated oligomerization of SARS 3a causes necrotic cell death, lysosomal damage, and caspase-1 activation-all likely contributing to the clinical manifestations of SARS-CoV infection.

DOI: 10.1038/s41419-018-0917-y
PubMed: 30185776

Affiliations:

République populaire de Chine, États-Unis

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Le document en format XML

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<term>Cellules HEK293</term>
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<front><div type="abstract" xml:lang="en">The molecular mechanisms underlying the severe lung pathology that occurs during SARS-CoV infections remain incompletely understood. The largest of the SARS-CoV accessory protein open reading frames (SARS 3a) oligomerizes, dynamically inserting into late endosomal, lysosomal, and trans-Golgi-network membranes. While previously implicated in a non-inflammatory apoptotic cell death pathway, here we extend the range of SARS 3a pathophysiologic targets by examining its effects on necrotic cell death pathways. We show that SARS 3a interacts with Receptor Interacting Protein 3 (Rip3), which augments the oligomerization of SARS 3a helping drive necrotic cell death. In addition, by inserting into lysosomal membranes SARS 3a triggers lysosomal damage and dysfunction. Consequently, Transcription Factor EB (TFEB) translocates to the nucleus increasing the transcription of autophagy- and lysosome-related genes. Finally, SARS 3a activates caspase-1 either directly or via an enhanced potassium efflux, which triggers NLRP3 inflammasome assembly. In summary, Rip3-mediated oligomerization of SARS 3a causes necrotic cell death, lysosomal damage, and caspase-1 activation-all likely contributing to the clinical manifestations of SARS-CoV infection.</div>
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<Month>09</Month>
<Day>05</Day>
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<Title>Cell death & disease</Title>
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<Abstract><AbstractText>The molecular mechanisms underlying the severe lung pathology that occurs during SARS-CoV infections remain incompletely understood. The largest of the SARS-CoV accessory protein open reading frames (SARS 3a) oligomerizes, dynamically inserting into late endosomal, lysosomal, and trans-Golgi-network membranes. While previously implicated in a non-inflammatory apoptotic cell death pathway, here we extend the range of SARS 3a pathophysiologic targets by examining its effects on necrotic cell death pathways. We show that SARS 3a interacts with Receptor Interacting Protein 3 (Rip3), which augments the oligomerization of SARS 3a helping drive necrotic cell death. In addition, by inserting into lysosomal membranes SARS 3a triggers lysosomal damage and dysfunction. Consequently, Transcription Factor EB (TFEB) translocates to the nucleus increasing the transcription of autophagy- and lysosome-related genes. Finally, SARS 3a activates caspase-1 either directly or via an enhanced potassium efflux, which triggers NLRP3 inflammasome assembly. In summary, Rip3-mediated oligomerization of SARS 3a causes necrotic cell death, lysosomal damage, and caspase-1 activation-all likely contributing to the clinical manifestations of SARS-CoV infection.</AbstractText>
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<Initials>Y</Initials>
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<AffiliationInfo><Affiliation>B Cell Molecular Immunology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, 20892, USA.</Affiliation>
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<ArticleIdList><ArticleId IdType="pubmed">30185776</ArticleId>
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</ArticleIdList>
<ReferenceList><Reference><Citation>Lancet. 2003 May 24;361(9371):1761-6</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12781533</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Blood. 2005 Oct 1;106(7):2366-74</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15860669</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2006 Aug 15;103(33):12540-5</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16894145</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>MBio. 2018 May 22;9(3):null</Citation>
<ArticleIdList><ArticleId IdType="pubmed">29789363</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>FEBS Lett. 2006 Dec 22;580(30):6807-12</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17141229</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Emerg Microbes Infect. 2017 Jun 7;6(6):e51</Citation>
<ArticleIdList><ArticleId IdType="pubmed">28588290</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Rev Microbiol. 2016 Aug;14(8):523-34</Citation>
<ArticleIdList><ArticleId IdType="pubmed">27344959</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>PLoS One. 2012;7(1):e29542</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22253733</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell. 2012 Jan 20;148(1-2):213-27</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22265413</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Med. 2014 Feb;20(2):204-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">24441827</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>PLoS Genet. 2017 Mar 29;13(3):e1006695</Citation>
<ArticleIdList><ArticleId IdType="pubmed">28355222</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Autophagy. 2016 Aug 2;12(8):1240-58</Citation>
<ArticleIdList><ArticleId IdType="pubmed">27171064</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2015 Apr 21;112(16):5017-22</Citation>
<ArticleIdList><ArticleId IdType="pubmed">25852146</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Biomark Res. 2014 Jan 07;2(1):1</Citation>
<ArticleIdList><ArticleId IdType="pubmed">24398220</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Autophagy. 2016 Aug 2;12(8):1372-89</Citation>
<ArticleIdList><ArticleId IdType="pubmed">27172265</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>PLoS Pathog. 2017 Apr 14;13(4):e1006326</Citation>
<ArticleIdList><ArticleId IdType="pubmed">28410401</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Microbiol Immunol Infect. 2017 Jun;50(3):277-285</Citation>
<ArticleIdList><ArticleId IdType="pubmed">26320399</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Cell Biol. 2015 Mar;17(3):288-99</Citation>
<ArticleIdList><ArticleId IdType="pubmed">25720963</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>EMBO J. 2016 Mar 1;35(5):479-95</Citation>
<ArticleIdList><ArticleId IdType="pubmed">26813791</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Hum Pathol. 2003 Aug;34(8):743-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">14506633</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Microbes Infect. 2011 Feb;13(2):179-88</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21035562</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Infect Dis. 2007 Aug 1;196(3):405-15</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17597455</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Immunol. 2014 Sep 15;193(6):3080-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">25135833</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Respirology. 2003 Nov;8 Suppl:S6-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15018126</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell Microbiol. 2017 Aug;19(8):</Citation>
<ArticleIdList><ArticleId IdType="pubmed">28476074</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Virol. 2010 Jan;84(2):1097-109</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19889773</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Genes Dev. 2013 Aug 1;27(15):1640-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23913919</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell Res. 2015 Jun;25(6):707-25</Citation>
<ArticleIdList><ArticleId IdType="pubmed">25952668</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Yale J Biol Med. 2017 Jun 23;90(2):301-315</Citation>
<ArticleIdList><ArticleId IdType="pubmed">28656016</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell. 2016 Dec 15;167(7):1693-1704</Citation>
<ArticleIdList><ArticleId IdType="pubmed">27984721</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell Host Microbe. 2016 Feb 10;19(2):181-93</Citation>
<ArticleIdList><ArticleId IdType="pubmed">26867177</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell. 2009 Jun 12;137(6):1100-11</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19524512</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Virol. 2007 Jan;81(2):548-57</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17108024</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Immunity. 2011 Dec 23;35(6):908-18</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22195746</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nature. 2016 Feb 18;530(7590):354-7</Citation>
<ArticleIdList><ArticleId IdType="pubmed">26814970</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Science. 2009 Jul 17;325(5938):332-6</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19498109</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Clin Invest. 2013 Jul;123(7):2773-4</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23863635</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Trends Microbiol. 2015 Jan;23(1):55-63</Citation>
<ArticleIdList><ArticleId IdType="pubmed">25456015</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell Rep. 2013 Jan 31;3(1):200-10</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23333278</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Annu Rev Immunol. 2008;26:421-52</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18303997</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Science. 2014 Mar 21;343(6177):1357-60</Citation>
<ArticleIdList><ArticleId IdType="pubmed">24557836</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Autophagy. 2015;11(8):1408-24</Citation>
<ArticleIdList><ArticleId IdType="pubmed">26114578</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Toxicol Pathol. 2007 Jun;35(4):495-516</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17562483</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Allergy Clin Immunol. 2012 Apr;129(4):1116-25.e6</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22227418</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Cell. 2014 Nov 20;56(4):481-95</Citation>
<ArticleIdList><ArticleId IdType="pubmed">25459880</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Virol. 2005 Jun;79(12):7819-26</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15919935</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Virus Res. 2008 Apr;133(1):113-21</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18045721</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell Death Differ. 2009 Jan;16(1):3-11</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18846107</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Trends Cell Biol. 2017 Nov;27(11):800-809</Citation>
<ArticleIdList><ArticleId IdType="pubmed">28642032</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Am J Pathol. 2007 Apr;170(4):1136-47</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17392154</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Biochim Biophys Acta. 2016 Apr;1865(2):228-36</Citation>
<ArticleIdList><ArticleId IdType="pubmed">26968619</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Annu Rev Pathol. 2008;3:99-126</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18039143</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Cell. 2014 Apr 10;54(1):133-146</Citation>
<ArticleIdList><ArticleId IdType="pubmed">24703947</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Immunol. 2017 Jun;86:10-15</Citation>
<ArticleIdList><ArticleId IdType="pubmed">28249679</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
</PubmedData>
</pubmed>
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SARS-Coronavirus Open Reading Frame-3a drives multimodal necrotic cell death.

SARS-Coronavirus Open Reading Frame-3a drives multimodal necrotic cell death.

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