Endothelial ERK1/2 signaling maintains integrity of the quiescent endothelium

Autor:	Jeffrey R. Gulcher, Nicholas A. Cilfone, Carmen J. Booth, Heino Velazquez, Nicolas Ricard, Susan E. Quaggin, Michael Simons, Rizaldy P. Scott, Thomas Chittenden, Javier L. Baylon
Rok vydání:	2019
Předmět:	0301 basic medicine Epithelial-Mesenchymal Transition Nitric Oxide Synthase Type III Endothelium MAP Kinase Signaling System Immunology News Biology Transfection Insights Mice 03 medical and health sciences Deep Learning 0302 clinical medicine Transforming Growth Factor beta Fibrosis In vivo Enos Human Umbilical Vein Endothelial Cells medicine Animals Humans Immunology and Allergy RNA-Seq Mice Knockout Mitogen-Activated Protein Kinase 1 Mitogen-Activated Protein Kinase 3 Endothelin-1 medicine.disease biology.organism_classification Endothelin 1 3. Good health Cell biology Mice Inbred C57BL Nitric oxide synthase Disease Models Animal 030104 developmental biology medicine.anatomical_structure 030220 oncology & carcinogenesis Hypertension biology.protein Signal transduction Immunostaining
Zdroj:	The Journal of Experimental Medicine
ISSN:	1540-9538 0022-1007
Popis:	Suppression of endothelial ERK1/1 pathways results in multi-organ failure, similar to what is observed in patients treated with anti-VEGF therapies. The mechanism of maintaining vascular endothelial identity and integrity is largely unknown. In this issue of JEM, Ricard et al. (https://doi.org/10.1084/jem.20182151) discover essential roles of ERK1/2 in maintaining endothelial homeostasis and its deletion-related serious defects in multiple tissues and organs.
Databáze:	OpenAIRE
Externí odkaz:	https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ef7fd10672deaac9dd1c195793c1bcd0 https://doi.org/10.1084/jem.20182151 Zobrazit plný text záznamu