ArticleJournal of cell science2015
Segregation of VE-cadherin from the LBRC depends on the ectodomain sequence required for homophilic adhesion.
Article in Journal of cell science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed.
- An Intriguing Structural Modification in Neutrophil Migration Across Blood Vessels to Inflammatory Sites: Progress in the Core Mechanisms.Cell biochemistry and biophysics · 2024Review
- Mechanotransduction via endothelial adhesion molecule CD31 initiates transmigration and reveals a role for VEGFR2 in diapedesis.Immunity · 2023Article
- Human CD99L2 Regulates a Unique Step in Leukocyte Transmigration.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- The rs7404339 AA Genotype inFrontiers in cardiovascular medicine · 2022Article
- SARS-CoV-2 Spike Protein Induces Degradation of Junctional Proteins That Maintain Endothelial Barrier Integrity.Frontiers in cardiovascular medicine · 2021Article
- Endothelial IQGAP1 regulates leukocyte transmigration by directing the LBRC to the site of diapedesis.The Journal of experimental medicine · 2019Article
- Endothelial Cell Junctional Adhesion Molecules: Role and Regulation of Expression in Inflammation.Arteriosclerosis, thrombosis, and vascular biology · 2016Review
- Transendothelial migration: unifying principles from the endothelial perspective.Immunological reviews · 2016Review
- Targeted Recycling of the Lateral Border Recycling Compartment Precedes Adherens Junction Dissociation during Transendothelial Migration.The American journal of pathology · 2016Article
- A Unique Role for Endothelial Cell Kinesin Light Chain 1, Variant 1 in Leukocyte Transendothelial Migration.The American journal of pathology · 2016Article
- Localized signals that regulate transendothelial migration.Current opinion in immunology · 2016Review
- Dephosphorylation of Y685-VE-Cadherin Involved in Pulmonary Microvascular Endothelial Barrier Injury Induced by Angiotensin II.Mediators of inflammation · 2016Article
- The regulation of transendothelial migration: new knowledge and new questions.Cardiovascular research · 2015Review
- Endothelial CD99 signals through soluble adenylyl cyclase and PKA to regulate leukocyte transendothelial migration.The Journal of experimental medicine · 2015Article
- Septin and actin contributions to endothelial cell-cell junctions and monolayer integrity.Cytoskeleton (Hoboken, N.J.)Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
The lateral border recycling compartment (LBRC) is a reticulum ofperijunctional tubulovesicular membrane that is continuous with the plasmalemma of endothelial cells and is essential for efficient transendothelial migration (TEM) of leukocytes. The LBRC contains molecules involved in TEM, such as PECAM, PVR and CD99, but not VE-cadherin. Despite its importance, how membrane proteins are included in or excluded from the LBRC is not known. Immunoelectronmicroscopy and biochemical approaches demonstrate that inclusion into the LBRC is the default pathway for transmembrane molecules present at endothelial cell borders. A chimeric molecule composed of the extracellular domain of VE-cadherin and cytoplasmic tail of PECAM (VE-CAD/PECAM) did not enter the LBRC, suggesting that VE-cadherin was excluded by a mechanism involving its extracellular domain. Deletion of the homophilic interaction domain EC1 or the homophilic interaction motif RVDAE allowed VE-CAD/PECAM and even native VE-cadherin to enter the LBRC. Similarly, treatment with RVDAE peptide to block homophilic VE-cadherin interactions allowed endogenous VE-cadherin to enter the LBRC. This suggests that homophilic interactions of VE-cadherin stabilize it at cell borders and prevent entry into the LBRC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.