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• W2125151502 abstract "Endothelial barrier function is critical for tissue fluid homeostasis, and its disruption contributes to various pathologies, including inflammation and sepsis. Thrombin is an endogenous agonist that impairs endothelial barrier function. We showed that the thrombin-induced decrease in transendothelial electric resistance of cultured human endothelial cells required the endoplasmic reticulum-localized, calcium-sensing protein stromal interacting molecule 1 (STIM1), but was independent of Ca2+ entry across the plasma membrane and the Ca2+ release-activated Ca2+ channel protein Orai1, which is the target of STIM1 in the store-operated calcium entry pathway. We found that STIM1 coupled the thrombin receptor to activation of the guanosine triphosphatase RhoA, stimulation of myosin light chain phosphorylation, formation of actin stress fibers, and loss of cell-cell adhesion. Thus, STIM1 functions in pathways that are dependent on and independent of Ca2+ entry." @default.
• W2125151502 created "2016-06-24" @default.
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• W2125151502 creator A5081068429 @default.
• W2125151502 creator A5083383869 @default.
• W2125151502 creator A5091353622 @default.
• W2125151502 date "2013-03-19" @default.
• W2125151502 modified "2023-10-15" @default.
• W2125151502 title "STIM1 Controls Endothelial Barrier Function Independently of Orai1 and Ca ²⁺ Entry" @default.
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• W2125151502 doi "https://doi.org/10.1126/scisignal.2003425" @default.
• W2125151502 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4030669" @default.
• W2125151502 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23512989" @default.
• W2125151502 hasPublicationYear "2013" @default.
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