Targeting Viral Proteostasis Limits Influenza Virus, HIV, and Dengue Virus Infection
- Autores
- Heaton, Nicholas S.; Moshkina, Natasha; Fenouil, Romain; Gardner, Thomas J.; Aguirre, Sebastian; Shah, Priya S.; Zhao, Nan; Manganaro, Lara; Hultquist, Judd F.; Noel, Justine; Sachs, David H.; Hamilton, Jennifer; Leon, Paul E.; Chawdury, Amit; Tripathi, Shashank; Melegari, Camilla; Campisi, Laura; Hai, Rong; Metreveli, Giorgi; Gamarnik, Andrea Vanesa; García Sastre, Adolfo; Greenbaum, Benjamin; Simon, Viviana; Fernandez Sesma, Ana; Krogan, Nevan J.; Mulder, Lubbertus C.F.; van Bakel, Harm; Tortorella, Domenico; Taunton, Jack; Palese, Peter; Marazzi, Ivan
- Año de publicación
- 2016
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- Viruses are obligate parasites and thus require the machinery of the host cell to replicate. Inhibition of host factors co-opted during active infection is a strategy hosts use to suppress viral replication and a potential pan-antiviral therapy. To define the cellular proteins and processes required for a virus during infection is thus crucial to understanding the mechanisms of virally induced disease. In this report, we generated fully infectious tagged influenza viruses and used infection-based proteomics to identify pivotal arms of cellular signaling required for influenza virus growth and infectivity. Using mathematical modeling and genetic and pharmacologic approaches, we revealed that modulation of Sec61-mediated cotranslational translocation selectively impaired glycoprotein proteostasis of influenza as well as HIV and dengue viruses and led to inhibition of viral growth and infectivity. Thus, by studying virus-human protein-protein interactions in the context of active replication, we have identified targetable host factors for broad-spectrum antiviral therapies. Viruses are obligate parasites dependent on the host cell machinery. Using infection-based proteomics, biochemistry, and mathematical modeling, Marazzi and colleagues reveal that targeting host factors controlling essential cellular functions can provide broad-spectrum antiviral effects. Loss-of-function and chemical inhibition of one such factor, Sec61, inhibited influenza, HIV, and dengue virus replication.
Fil: Heaton, Nicholas S.. Icahn School Of Medicine At Mount Sinai; Estados Unidos
Fil: Moshkina, Natasha. Icahn School Of Medicine At Mount Sinai; Estados Unidos
Fil: Fenouil, Romain. Icahn School Of Medicine At Mount Sinai; Estados Unidos
Fil: Gardner, Thomas J.. Icahn School Of Medicine At Mount Sinai; Estados Unidos
Fil: Aguirre, Sebastian. Icahn School Of Medicine At Mount Sinai; Estados Unidos
Fil: Shah, Priya S.. University of California; Estados Unidos
Fil: Zhao, Nan. Icahn School Of Medicine At Mount Sinai; Estados Unidos
Fil: Manganaro, Lara. Icahn School Of Medicine At Mount Sinai; Estados Unidos
Fil: Hultquist, Judd F.. University of California; Estados Unidos
Fil: Noel, Justine. Icahn School Of Medicine At Mount Sinai; Estados Unidos
Fil: Sachs, David H.. Icahn School Of Medicine At Mount Sinai; Estados Unidos
Fil: Hamilton, Jennifer. Icahn School Of Medicine At Mount Sinai; Estados Unidos
Fil: Leon, Paul E.. Icahn School Of Medicine At Mount Sinai; Estados Unidos
Fil: Chawdury, Amit. Icahn School Of Medicine At Mount Sinai; Estados Unidos
Fil: Tripathi, Shashank. Icahn School Of Medicine At Mount Sinai; Estados Unidos
Fil: Melegari, Camilla. Icahn School Of Medicine At Mount Sinai; Estados Unidos
Fil: Campisi, Laura. Icahn School Of Medicine At Mount Sinai; Estados Unidos
Fil: Hai, Rong. Icahn School Of Medicine At Mount Sinai; Estados Unidos
Fil: Metreveli, Giorgi. Icahn School Of Medicine At Mount Sinai; Estados Unidos
Fil: Gamarnik, Andrea Vanesa. Fundación Instituto Leloir; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina
Fil: García Sastre, Adolfo. Icahn School Of Medicine At Mount Sinai; Estados Unidos
Fil: Greenbaum, Benjamin. Icahn School Of Medicine At Mount Sinai; Estados Unidos
Fil: Simon, Viviana. Icahn School Of Medicine At Mount Sinai; Estados Unidos
Fil: Fernandez Sesma, Ana. Icahn School Of Medicine At Mount Sinai; Estados Unidos
Fil: Krogan, Nevan J.. University of California; Estados Unidos
Fil: Mulder, Lubbertus C.F.. Icahn School Of Medicine At Mount Sinai; Estados Unidos
Fil: van Bakel, Harm. Icahn School Of Medicine At Mount Sinai; Estados Unidos
Fil: Tortorella, Domenico. Icahn School Of Medicine At Mount Sinai; Estados Unidos
Fil: Taunton, Jack. University of California; Estados Unidos
Fil: Palese, Peter. Icahn School Of Medicine At Mount Sinai; Estados Unidos
Fil: Marazzi, Ivan. Icahn School Of Medicine At Mount Sinai; Estados Unidos - Materia
-
Viral Proteastasis
Dengue Virus
Host-Virus Interactions
Antivirals - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
- Repositorio
.jpg)
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/54245
Ver los metadatos del registro completo
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Targeting Viral Proteostasis Limits Influenza Virus, HIV, and Dengue Virus InfectionHeaton, Nicholas S.Moshkina, NatashaFenouil, RomainGardner, Thomas J.Aguirre, SebastianShah, Priya S.Zhao, NanManganaro, LaraHultquist, Judd F.Noel, JustineSachs, David H.Hamilton, JenniferLeon, Paul E.Chawdury, AmitTripathi, ShashankMelegari, CamillaCampisi, LauraHai, RongMetreveli, GiorgiGamarnik, Andrea VanesaGarcía Sastre, AdolfoGreenbaum, BenjaminSimon, VivianaFernandez Sesma, AnaKrogan, Nevan J.Mulder, Lubbertus C.F.van Bakel, HarmTortorella, DomenicoTaunton, JackPalese, PeterMarazzi, IvanViral ProteastasisDengue VirusHost-Virus InteractionsAntiviralshttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Viruses are obligate parasites and thus require the machinery of the host cell to replicate. Inhibition of host factors co-opted during active infection is a strategy hosts use to suppress viral replication and a potential pan-antiviral therapy. To define the cellular proteins and processes required for a virus during infection is thus crucial to understanding the mechanisms of virally induced disease. In this report, we generated fully infectious tagged influenza viruses and used infection-based proteomics to identify pivotal arms of cellular signaling required for influenza virus growth and infectivity. Using mathematical modeling and genetic and pharmacologic approaches, we revealed that modulation of Sec61-mediated cotranslational translocation selectively impaired glycoprotein proteostasis of influenza as well as HIV and dengue viruses and led to inhibition of viral growth and infectivity. Thus, by studying virus-human protein-protein interactions in the context of active replication, we have identified targetable host factors for broad-spectrum antiviral therapies. Viruses are obligate parasites dependent on the host cell machinery. Using infection-based proteomics, biochemistry, and mathematical modeling, Marazzi and colleagues reveal that targeting host factors controlling essential cellular functions can provide broad-spectrum antiviral effects. Loss-of-function and chemical inhibition of one such factor, Sec61, inhibited influenza, HIV, and dengue virus replication.Fil: Heaton, Nicholas S.. Icahn School Of Medicine At Mount Sinai; Estados UnidosFil: Moshkina, Natasha. Icahn School Of Medicine At Mount Sinai; Estados UnidosFil: Fenouil, Romain. Icahn School Of Medicine At Mount Sinai; Estados UnidosFil: Gardner, Thomas J.. Icahn School Of Medicine At Mount Sinai; Estados UnidosFil: Aguirre, Sebastian. Icahn School Of Medicine At Mount Sinai; Estados UnidosFil: Shah, Priya S.. University of California; Estados UnidosFil: Zhao, Nan. Icahn School Of Medicine At Mount Sinai; Estados UnidosFil: Manganaro, Lara. Icahn School Of Medicine At Mount Sinai; Estados UnidosFil: Hultquist, Judd F.. University of California; Estados UnidosFil: Noel, Justine. Icahn School Of Medicine At Mount Sinai; Estados UnidosFil: Sachs, David H.. Icahn School Of Medicine At Mount Sinai; Estados UnidosFil: Hamilton, Jennifer. Icahn School Of Medicine At Mount Sinai; Estados UnidosFil: Leon, Paul E.. Icahn School Of Medicine At Mount Sinai; Estados UnidosFil: Chawdury, Amit. Icahn School Of Medicine At Mount Sinai; Estados UnidosFil: Tripathi, Shashank. Icahn School Of Medicine At Mount Sinai; Estados UnidosFil: Melegari, Camilla. Icahn School Of Medicine At Mount Sinai; Estados UnidosFil: Campisi, Laura. Icahn School Of Medicine At Mount Sinai; Estados UnidosFil: Hai, Rong. Icahn School Of Medicine At Mount Sinai; Estados UnidosFil: Metreveli, Giorgi. Icahn School Of Medicine At Mount Sinai; Estados UnidosFil: Gamarnik, Andrea Vanesa. Fundación Instituto Leloir; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; ArgentinaFil: García Sastre, Adolfo. Icahn School Of Medicine At Mount Sinai; Estados UnidosFil: Greenbaum, Benjamin. Icahn School Of Medicine At Mount Sinai; Estados UnidosFil: Simon, Viviana. Icahn School Of Medicine At Mount Sinai; Estados UnidosFil: Fernandez Sesma, Ana. Icahn School Of Medicine At Mount Sinai; Estados UnidosFil: Krogan, Nevan J.. University of California; Estados UnidosFil: Mulder, Lubbertus C.F.. Icahn School Of Medicine At Mount Sinai; Estados UnidosFil: van Bakel, Harm. Icahn School Of Medicine At Mount Sinai; Estados UnidosFil: Tortorella, Domenico. Icahn School Of Medicine At Mount Sinai; Estados UnidosFil: Taunton, Jack. University of California; Estados UnidosFil: Palese, Peter. Icahn School Of Medicine At Mount Sinai; Estados UnidosFil: Marazzi, Ivan. Icahn School Of Medicine At Mount Sinai; Estados UnidosCell Press2016-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/54245Heaton, Nicholas S.; Moshkina, Natasha; Fenouil, Romain; Gardner, Thomas J.; Aguirre, Sebastian; et al.; Targeting Viral Proteostasis Limits Influenza Virus, HIV, and Dengue Virus Infection; Cell Press; Immunity; 44; 1; 1-2016; 46-581074-76131097-4180CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1016/j.immuni.2015.12.017info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S1074761315005439info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T09:44:09Zoai:ri.conicet.gov.ar:11336/54245instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 09:44:09.805CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
| dc.title.none.fl_str_mv |
Targeting Viral Proteostasis Limits Influenza Virus, HIV, and Dengue Virus Infection |
| title |
Targeting Viral Proteostasis Limits Influenza Virus, HIV, and Dengue Virus Infection |
| spellingShingle |
Targeting Viral Proteostasis Limits Influenza Virus, HIV, and Dengue Virus Infection Heaton, Nicholas S. Viral Proteastasis Dengue Virus Host-Virus Interactions Antivirals |
| title_short |
Targeting Viral Proteostasis Limits Influenza Virus, HIV, and Dengue Virus Infection |
| title_full |
Targeting Viral Proteostasis Limits Influenza Virus, HIV, and Dengue Virus Infection |
| title_fullStr |
Targeting Viral Proteostasis Limits Influenza Virus, HIV, and Dengue Virus Infection |
| title_full_unstemmed |
Targeting Viral Proteostasis Limits Influenza Virus, HIV, and Dengue Virus Infection |
| title_sort |
Targeting Viral Proteostasis Limits Influenza Virus, HIV, and Dengue Virus Infection |
| dc.creator.none.fl_str_mv |
Heaton, Nicholas S. Moshkina, Natasha Fenouil, Romain Gardner, Thomas J. Aguirre, Sebastian Shah, Priya S. Zhao, Nan Manganaro, Lara Hultquist, Judd F. Noel, Justine Sachs, David H. Hamilton, Jennifer Leon, Paul E. Chawdury, Amit Tripathi, Shashank Melegari, Camilla Campisi, Laura Hai, Rong Metreveli, Giorgi Gamarnik, Andrea Vanesa García Sastre, Adolfo Greenbaum, Benjamin Simon, Viviana Fernandez Sesma, Ana Krogan, Nevan J. Mulder, Lubbertus C.F. van Bakel, Harm Tortorella, Domenico Taunton, Jack Palese, Peter Marazzi, Ivan |
| author |
Heaton, Nicholas S. |
| author_facet |
Heaton, Nicholas S. Moshkina, Natasha Fenouil, Romain Gardner, Thomas J. Aguirre, Sebastian Shah, Priya S. Zhao, Nan Manganaro, Lara Hultquist, Judd F. Noel, Justine Sachs, David H. Hamilton, Jennifer Leon, Paul E. Chawdury, Amit Tripathi, Shashank Melegari, Camilla Campisi, Laura Hai, Rong Metreveli, Giorgi Gamarnik, Andrea Vanesa García Sastre, Adolfo Greenbaum, Benjamin Simon, Viviana Fernandez Sesma, Ana Krogan, Nevan J. Mulder, Lubbertus C.F. van Bakel, Harm Tortorella, Domenico Taunton, Jack Palese, Peter Marazzi, Ivan |
| author_role |
author |
| author2 |
Moshkina, Natasha Fenouil, Romain Gardner, Thomas J. Aguirre, Sebastian Shah, Priya S. Zhao, Nan Manganaro, Lara Hultquist, Judd F. Noel, Justine Sachs, David H. Hamilton, Jennifer Leon, Paul E. Chawdury, Amit Tripathi, Shashank Melegari, Camilla Campisi, Laura Hai, Rong Metreveli, Giorgi Gamarnik, Andrea Vanesa García Sastre, Adolfo Greenbaum, Benjamin Simon, Viviana Fernandez Sesma, Ana Krogan, Nevan J. Mulder, Lubbertus C.F. van Bakel, Harm Tortorella, Domenico Taunton, Jack Palese, Peter Marazzi, Ivan |
| author2_role |
author author author author author author author author author author author author author author author author author author author author author author author author author author author author author author |
| dc.subject.none.fl_str_mv |
Viral Proteastasis Dengue Virus Host-Virus Interactions Antivirals |
| topic |
Viral Proteastasis Dengue Virus Host-Virus Interactions Antivirals |
| purl_subject.fl_str_mv |
https://purl.org/becyt/ford/1.6 https://purl.org/becyt/ford/1 |
| dc.description.none.fl_txt_mv |
Viruses are obligate parasites and thus require the machinery of the host cell to replicate. Inhibition of host factors co-opted during active infection is a strategy hosts use to suppress viral replication and a potential pan-antiviral therapy. To define the cellular proteins and processes required for a virus during infection is thus crucial to understanding the mechanisms of virally induced disease. In this report, we generated fully infectious tagged influenza viruses and used infection-based proteomics to identify pivotal arms of cellular signaling required for influenza virus growth and infectivity. Using mathematical modeling and genetic and pharmacologic approaches, we revealed that modulation of Sec61-mediated cotranslational translocation selectively impaired glycoprotein proteostasis of influenza as well as HIV and dengue viruses and led to inhibition of viral growth and infectivity. Thus, by studying virus-human protein-protein interactions in the context of active replication, we have identified targetable host factors for broad-spectrum antiviral therapies. Viruses are obligate parasites dependent on the host cell machinery. Using infection-based proteomics, biochemistry, and mathematical modeling, Marazzi and colleagues reveal that targeting host factors controlling essential cellular functions can provide broad-spectrum antiviral effects. Loss-of-function and chemical inhibition of one such factor, Sec61, inhibited influenza, HIV, and dengue virus replication. Fil: Heaton, Nicholas S.. Icahn School Of Medicine At Mount Sinai; Estados Unidos Fil: Moshkina, Natasha. Icahn School Of Medicine At Mount Sinai; Estados Unidos Fil: Fenouil, Romain. Icahn School Of Medicine At Mount Sinai; Estados Unidos Fil: Gardner, Thomas J.. Icahn School Of Medicine At Mount Sinai; Estados Unidos Fil: Aguirre, Sebastian. Icahn School Of Medicine At Mount Sinai; Estados Unidos Fil: Shah, Priya S.. University of California; Estados Unidos Fil: Zhao, Nan. Icahn School Of Medicine At Mount Sinai; Estados Unidos Fil: Manganaro, Lara. Icahn School Of Medicine At Mount Sinai; Estados Unidos Fil: Hultquist, Judd F.. University of California; Estados Unidos Fil: Noel, Justine. Icahn School Of Medicine At Mount Sinai; Estados Unidos Fil: Sachs, David H.. Icahn School Of Medicine At Mount Sinai; Estados Unidos Fil: Hamilton, Jennifer. Icahn School Of Medicine At Mount Sinai; Estados Unidos Fil: Leon, Paul E.. Icahn School Of Medicine At Mount Sinai; Estados Unidos Fil: Chawdury, Amit. Icahn School Of Medicine At Mount Sinai; Estados Unidos Fil: Tripathi, Shashank. Icahn School Of Medicine At Mount Sinai; Estados Unidos Fil: Melegari, Camilla. Icahn School Of Medicine At Mount Sinai; Estados Unidos Fil: Campisi, Laura. Icahn School Of Medicine At Mount Sinai; Estados Unidos Fil: Hai, Rong. Icahn School Of Medicine At Mount Sinai; Estados Unidos Fil: Metreveli, Giorgi. Icahn School Of Medicine At Mount Sinai; Estados Unidos Fil: Gamarnik, Andrea Vanesa. Fundación Instituto Leloir; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina Fil: García Sastre, Adolfo. Icahn School Of Medicine At Mount Sinai; Estados Unidos Fil: Greenbaum, Benjamin. Icahn School Of Medicine At Mount Sinai; Estados Unidos Fil: Simon, Viviana. Icahn School Of Medicine At Mount Sinai; Estados Unidos Fil: Fernandez Sesma, Ana. Icahn School Of Medicine At Mount Sinai; Estados Unidos Fil: Krogan, Nevan J.. University of California; Estados Unidos Fil: Mulder, Lubbertus C.F.. Icahn School Of Medicine At Mount Sinai; Estados Unidos Fil: van Bakel, Harm. Icahn School Of Medicine At Mount Sinai; Estados Unidos Fil: Tortorella, Domenico. Icahn School Of Medicine At Mount Sinai; Estados Unidos Fil: Taunton, Jack. University of California; Estados Unidos Fil: Palese, Peter. Icahn School Of Medicine At Mount Sinai; Estados Unidos Fil: Marazzi, Ivan. Icahn School Of Medicine At Mount Sinai; Estados Unidos |
| description |
Viruses are obligate parasites and thus require the machinery of the host cell to replicate. Inhibition of host factors co-opted during active infection is a strategy hosts use to suppress viral replication and a potential pan-antiviral therapy. To define the cellular proteins and processes required for a virus during infection is thus crucial to understanding the mechanisms of virally induced disease. In this report, we generated fully infectious tagged influenza viruses and used infection-based proteomics to identify pivotal arms of cellular signaling required for influenza virus growth and infectivity. Using mathematical modeling and genetic and pharmacologic approaches, we revealed that modulation of Sec61-mediated cotranslational translocation selectively impaired glycoprotein proteostasis of influenza as well as HIV and dengue viruses and led to inhibition of viral growth and infectivity. Thus, by studying virus-human protein-protein interactions in the context of active replication, we have identified targetable host factors for broad-spectrum antiviral therapies. Viruses are obligate parasites dependent on the host cell machinery. Using infection-based proteomics, biochemistry, and mathematical modeling, Marazzi and colleagues reveal that targeting host factors controlling essential cellular functions can provide broad-spectrum antiviral effects. Loss-of-function and chemical inhibition of one such factor, Sec61, inhibited influenza, HIV, and dengue virus replication. |
| publishDate |
2016 |
| dc.date.none.fl_str_mv |
2016-01 |
| dc.type.none.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo |
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article |
| status_str |
publishedVersion |
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http://hdl.handle.net/11336/54245 Heaton, Nicholas S.; Moshkina, Natasha; Fenouil, Romain; Gardner, Thomas J.; Aguirre, Sebastian; et al.; Targeting Viral Proteostasis Limits Influenza Virus, HIV, and Dengue Virus Infection; Cell Press; Immunity; 44; 1; 1-2016; 46-58 1074-7613 1097-4180 CONICET Digital CONICET |
| url |
http://hdl.handle.net/11336/54245 |
| identifier_str_mv |
Heaton, Nicholas S.; Moshkina, Natasha; Fenouil, Romain; Gardner, Thomas J.; Aguirre, Sebastian; et al.; Targeting Viral Proteostasis Limits Influenza Virus, HIV, and Dengue Virus Infection; Cell Press; Immunity; 44; 1; 1-2016; 46-58 1074-7613 1097-4180 CONICET Digital CONICET |
| dc.language.none.fl_str_mv |
eng |
| language |
eng |
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info:eu-repo/semantics/altIdentifier/doi/10.1016/j.immuni.2015.12.017 info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S1074761315005439 |
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info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
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openAccess |
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https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
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application/pdf application/pdf |
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Cell Press |
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Cell Press |
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CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas |
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dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar |
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