{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["5"],"submitter":["Li L"],"pubmed_abstract":["Excessive activation of inflammation and the accompanying lung vascular endothelial barrier disruption are primary pathogenic features of acute lung injury (ALI). Microtubule-associated protein 4 (MAP4), a tubulin assembly-promoting protein, is important for maintaining the microtubule (MT) cytoskeleton and cell-cell junctional structures. However, both the involvement and exact mechanism of MAP4 in the development of endothelial barrier disruption in ALI remains unknown. In this study, lipopolysaccharide (LPS) and tumour necrosis factor-α (TNF-α) were applied to human pulmonary microvascular endothelial cells (HPMECs) to mimic the endothelial damage during inflammation in vitro. We demonstrated that the MAP4 (Ser696 and Ser787) phosphorylation increased concomitantly with the p38/MAPK pat"],"journal":["Scientific reports"],"pagination":["8895"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4352893"],"repository":["biostudies-literature"],"pubmed_title":["P38/MAPK contributes to endothelial barrier dysfunction via MAP4 phosphorylation-dependent microtubule disassembly in inflammation-induced acute lung injury."],"pmcid":["PMC4352893"],"pubmed_authors":["Yang X","He T","Zhang D","Huang Y","Hu J","Mei H","Li L","Lan X","Chen B","Zhang Q"],"additional_accession":[]},"is_claimable":false,"name":"P38/MAPK contributes to endothelial barrier dysfunction via MAP4 phosphorylation-dependent microtubule disassembly in inflammation-induced acute lung injury.","description":"Excessive activation of inflammation and the accompanying lung vascular endothelial barrier disruption are primary pathogenic features of acute lung injury (ALI). Microtubule-associated protein 4 (MAP4), a tubulin assembly-promoting protein, is important for maintaining the microtubule (MT) cytoskeleton and cell-cell junctional structures. However, both the involvement and exact mechanism of MAP4 in the development of endothelial barrier disruption in ALI remains unknown. In this study, lipopolysaccharide (LPS) and tumour necrosis factor-α (TNF-α) were applied to human pulmonary microvascular endothelial cells (HPMECs) to mimic the endothelial damage during inflammation in vitro. We demonstrated that the MAP4 (Ser696 and Ser787) phosphorylation increased concomitantly with the p38/MAPK pat","dates":{"release":"2015-01-01T00:00:00Z","publication":"2015 Mar","modification":"2025-04-18T15:30:44.129Z","creation":"2019-03-27T01:47:47Z"},"accession":"S-EPMC4352893","cross_references":{"pubmed":["25746230"],"doi":["10.1038/srep08895"]}}