Please use this identifier to cite or link to this item: https://scholarhub.balamand.edu.lb/handle/uob/2629
DC FieldValueLanguage
dc.contributor.authorDeleuze, Virginieen_US
dc.contributor.authorChalhoub, Eliasen_US
dc.contributor.authorHajj, Rawan Elen_US
dc.contributor.authorDohet, Christianeen_US
dc.contributor.authorLe Clech, Mikaëlen_US
dc.contributor.authorCouraud, Pierre-Olivieren_US
dc.contributor.authorHuber, Philippeen_US
dc.contributor.authorMathieu, Danièleen_US
dc.date.accessioned2020-12-23T09:17:04Z-
dc.date.available2020-12-23T09:17:04Z-
dc.date.issued2007-
dc.identifier.urihttps://scholarhub.balamand.edu.lb/handle/uob/2629-
dc.description.abstractThe basic helix-loop-helix TAL-1/SCL essential for hematopoietic development is also required during vascular development for embryonic angiogenesis. We reported that TAL-1 acts positively on postnatal angiogenesis by stimulating endothelial morphogenesis. Here, we investigated the functional consequences of TAL-1 silencing in human primary endothelial cells. We found that TAL-1 knockdown caused the inhibition of in vitro tubulomorphogenesis, which was associated with a dramatic reduction in vascular endothelial cadherin (VE-cadherin) at intercellular junctions. Consistently, silencing of TAL-1 as well as of its cofactors E47 and LMO2 down-regulated VE-cadherin at both the mRNA and the protein level. Endogenous VE-cadherin transcription could be activated in nonendothelial HEK-293 cells by the sole concomitant ectopic expression of TAL-1, E47, and LMO2. Transient transfections in human primary endothelial cells derived from umbilical vein (HUVECs) demonstrated that VE-cadherin promoter activity was dependent on the integrity of a specialized E-box associated with a GATA motif and was maximal with the coexpression of the different components of the TAL-1 complex. Finally, chromatin immunoprecipitation assays showed that TAL-1 and its cofactors occupied the VE-cadherin promoter in HUVECs. Together, these data identify VE-cadherin as a bona fide target gene of the TAL-1 complex in the endothelial lineage, providing a first clue to TAL-1 function in angiogenesis.en_US
dc.format.extent11 p.en_US
dc.language.isoengen_US
dc.titleTAL-1/SCL and Its Partners E47 and LMO2 Up-Regulate VE-Cadherin Expression in Endothelial Cellsen_US
dc.typeJournal Articleen_US
dc.contributor.affiliationDepartment of Medical Laboratory Sciencesen_US
dc.description.volume27en_US
dc.description.issue7en_US
dc.description.startpage2687en_US
dc.description.endpage2697en_US
dc.date.catalogued2017-12-12-
dc.description.statusPublisheden_US
dc.identifier.OlibID175531-
dc.relation.ispartoftextJournal of molecular and cellular biologyen_US
dc.provenance.recordsourceOliben_US
Appears in Collections:Department of Medical Laboratory Sciences
Show simple item record

Google ScholarTM

Check


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.