Subcellular hot spots of GPCR signaling promote vascular inflammation

G-coupled protein receptors (GPCRs) comprise the largest class of druggable targets. Signaling by GPCRs is initiated from subcellular hot spots including the plasma membrane, signalosomes and endosomes to contribute to vascular inflammation. GPCR-G protein signaling at the plasma membrane causes end...

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Autores:
Tipo de recurso:
Article of investigation
Fecha de publicación:
2020
Institución:
Universidad de Bogotá Jorge Tadeo Lozano
Repositorio:
Expeditio: repositorio UTadeo
Idioma:
eng
OAI Identifier:
oai:expeditiorepositorio.utadeo.edu.co:20.500.12010/12479
Acceso en línea:
https://doi.org/10.1016/j.coemr.2020.07.011
http://hdl.handle.net/20.500.12010/12479
Palabra clave:
Arrestins
COVID-19
Endosomes
Endothelial
MALT1
JAK-STAT
NFκB
p38 MAPK
Síndrome respiratorio agudo grave
COVID-19
SARS-CoV-2
Coronavirus
Rights
License
Acceso restringido
id UTADEO2_ba2247e84351c1f4bab0068bce37bd04
oai_identifier_str oai:expeditiorepositorio.utadeo.edu.co:20.500.12010/12479
network_acronym_str UTADEO2
network_name_str Expeditio: repositorio UTadeo
repository_id_str
dc.title.spa.fl_str_mv Subcellular hot spots of GPCR signaling promote vascular inflammation
title Subcellular hot spots of GPCR signaling promote vascular inflammation
spellingShingle Subcellular hot spots of GPCR signaling promote vascular inflammation
Arrestins
COVID-19
Endosomes
Endothelial
MALT1
JAK-STAT
NFκB
p38 MAPK
Síndrome respiratorio agudo grave
COVID-19
SARS-CoV-2
Coronavirus
title_short Subcellular hot spots of GPCR signaling promote vascular inflammation
title_full Subcellular hot spots of GPCR signaling promote vascular inflammation
title_fullStr Subcellular hot spots of GPCR signaling promote vascular inflammation
title_full_unstemmed Subcellular hot spots of GPCR signaling promote vascular inflammation
title_sort Subcellular hot spots of GPCR signaling promote vascular inflammation
dc.subject.spa.fl_str_mv Arrestins
COVID-19
Endosomes
Endothelial
MALT1
JAK-STAT
NFκB
p38 MAPK
topic Arrestins
COVID-19
Endosomes
Endothelial
MALT1
JAK-STAT
NFκB
p38 MAPK
Síndrome respiratorio agudo grave
COVID-19
SARS-CoV-2
Coronavirus
dc.subject.lemb.spa.fl_str_mv Síndrome respiratorio agudo grave
COVID-19
SARS-CoV-2
Coronavirus
description G-coupled protein receptors (GPCRs) comprise the largest class of druggable targets. Signaling by GPCRs is initiated from subcellular hot spots including the plasma membrane, signalosomes and endosomes to contribute to vascular inflammation. GPCR-G protein signaling at the plasma membrane causes endothelial barrier disruption and also cross-talks with growth factor receptors to promote proinflammatory signaling. A second surge of GPCR signaling is initiated by cytoplasmic NFκB activation mediated by β-arrestins and CARMA-Bcl10-MALT1 signalosomes. Once internalized, ubiquitinated GPCRs initiate signaling from endosomes via assembly of the transforming growth factor-β-activated kinase binding protein-1 (TAB1)-TAB2-p38 MAPK complex to promote vascular inflammation. Understanding the complexities of GPCR signaling is critical for development of new strategies to treat vascular inflammation such as that associated with COVID-19.
publishDate 2020
dc.date.accessioned.none.fl_str_mv 2020-08-31T17:51:19Z
dc.date.available.none.fl_str_mv 2020-08-31T17:51:19Z
dc.date.created.none.fl_str_mv 2020
dc.type.local.spa.fl_str_mv Artículo
dc.type.coar.spa.fl_str_mv http://purl.org/coar/resource_type/c_2df8fbb1
format http://purl.org/coar/resource_type/c_2df8fbb1
dc.identifier.issn.spa.fl_str_mv 2451-9650
dc.identifier.other.spa.fl_str_mv https://doi.org/10.1016/j.coemr.2020.07.011
dc.identifier.uri.none.fl_str_mv http://hdl.handle.net/20.500.12010/12479
dc.identifier.doi.spa.fl_str_mv https://doi.org/10.1016/j.coemr.2020.07.011
identifier_str_mv 2451-9650
url https://doi.org/10.1016/j.coemr.2020.07.011
http://hdl.handle.net/20.500.12010/12479
dc.language.iso.spa.fl_str_mv eng
language eng
dc.rights.coar.fl_str_mv http://purl.org/coar/access_right/c_f1cf
dc.rights.local.spa.fl_str_mv Acceso restringido
rights_invalid_str_mv Acceso restringido
http://purl.org/coar/access_right/c_f1cf
dc.format.extent.spa.fl_str_mv 19 páginas
dc.format.mimetype.spa.fl_str_mv image/jepg
dc.publisher.spa.fl_str_mv Current Opinion in Endocrine and Metabolic Research
dc.source.spa.fl_str_mv reponame:Expeditio Repositorio Institucional UJTL
instname:Universidad de Bogotá Jorge Tadeo Lozano
instname_str Universidad de Bogotá Jorge Tadeo Lozano
institution Universidad de Bogotá Jorge Tadeo Lozano
reponame_str Expeditio Repositorio Institucional UJTL
collection Expeditio Repositorio Institucional UJTL
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spelling 2020-08-31T17:51:19Z2020-08-31T17:51:19Z20202451-9650https://doi.org/10.1016/j.coemr.2020.07.011http://hdl.handle.net/20.500.12010/12479https://doi.org/10.1016/j.coemr.2020.07.011G-coupled protein receptors (GPCRs) comprise the largest class of druggable targets. Signaling by GPCRs is initiated from subcellular hot spots including the plasma membrane, signalosomes and endosomes to contribute to vascular inflammation. GPCR-G protein signaling at the plasma membrane causes endothelial barrier disruption and also cross-talks with growth factor receptors to promote proinflammatory signaling. A second surge of GPCR signaling is initiated by cytoplasmic NFκB activation mediated by β-arrestins and CARMA-Bcl10-MALT1 signalosomes. Once internalized, ubiquitinated GPCRs initiate signaling from endosomes via assembly of the transforming growth factor-β-activated kinase binding protein-1 (TAB1)-TAB2-p38 MAPK complex to promote vascular inflammation. 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