Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.ydbio.2008.09.031
DC FieldValue
dc.titleTie2Cre-mediated inactivation of plexinD1 results in congenital heart, vascular and skeletal defects
dc.contributor.authorZhang, Ying
dc.contributor.authorSingh, Manvendra K
dc.contributor.authorDegenhardt, Karl R
dc.contributor.authorLu, Min Min
dc.contributor.authorBennett, Jean
dc.contributor.authorYoshida, Yutaka
dc.contributor.authorEpstein, Jonathan A
dc.date.accessioned2021-09-28T06:54:42Z
dc.date.available2021-09-28T06:54:42Z
dc.date.issued2009-01-01
dc.identifier.citationZhang, Ying, Singh, Manvendra K, Degenhardt, Karl R, Lu, Min Min, Bennett, Jean, Yoshida, Yutaka, Epstein, Jonathan A (2009-01-01). Tie2Cre-mediated inactivation of plexinD1 results in congenital heart, vascular and skeletal defects. DEVELOPMENTAL BIOLOGY 325 (1) : 82-93. ScholarBank@NUS Repository. https://doi.org/10.1016/j.ydbio.2008.09.031
dc.identifier.issn00121606
dc.identifier.issn1095564X
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/201390
dc.description.abstractPlexinD1 is a membrane-bound receptor that mediates signals derived from class 3 secreted semaphorins. Although semaphorin signaling in axon guidance in the nervous system has been extensively studied, functions outside the nervous system including important roles in vascular patterning have also been demonstrated. Inactivation of plexinD1 leads to neo-natal lethality, structural defects of the cardiac outflow tract, peripheral vascular abnormalities, and axial skeletal morphogenesis defects. PlexinD1 is expressed by vascular endothelial cells, but additional domains of expression have also been demonstrated including in lymphocytes, osteoblasts, neural crest and the central nervous system. Hence, the cell-type specific functions of plexinD1 have remained unclear. Here, we describe the results of tissue-specific gene inactivation of plexinD1 in Tie2 expressing precursors, which recapitulates the null phenotype with respect to congenital heart, vascular, and skeletal abnormalities resulting in neonatal lethality. Interestingly, these mutants also have myocardial defects not previously reported. In addition, we demonstrate functions for plexinD1 in post-natal retinal vasculogenesis and adult angiogenesis through the use of inducible cre-mediated deletion. These results demonstrate an important role for PlexinD1 in embryonic and adult vasculature. © 2008 Elsevier Inc. All rights reserved.
dc.language.isoen
dc.publisherACADEMIC PRESS INC ELSEVIER SCIENCE
dc.sourceElements
dc.subjectScience & Technology
dc.subjectLife Sciences & Biomedicine
dc.subjectDevelopmental Biology
dc.subjectplexinD1
dc.subjectTissue-specific gene inactivation
dc.subjectCongenital heart
dc.subjectVascular
dc.subjectSkeletal
dc.subjectMyocardial
dc.subjectCARDIAC NEURAL CREST
dc.subjectENDOTHELIAL-CELLS
dc.subjectAXON GUIDANCE
dc.subjectENDOCHONDRAL OSSIFICATION
dc.subjectTRANSGENIC MOUSE
dc.subjectLINEAGE ANALYSIS
dc.subjectSEMAPHORIN
dc.subjectANGIOGENESIS
dc.subjectEXPRESSION
dc.subjectRECEPTORS
dc.typeArticle
dc.date.updated2021-09-22T02:38:15Z
dc.contributor.departmentDUKE-NUS MEDICAL SCHOOL
dc.contributor.departmentInstitute of Data Science
dc.description.doi10.1016/j.ydbio.2008.09.031
dc.description.sourcetitleDEVELOPMENTAL BIOLOGY
dc.description.volume325
dc.description.issue1
dc.description.page82-93
dc.published.statePublished
Appears in Collections:Staff Publications
Elements

Show simple item record
Files in This Item:
There are no files associated with this item.

Google ScholarTM

Check

Altmetric


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