Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
19
pubmed:dateCreated
2001-10-4
pubmed:abstractText
Recent evidence indicates that acquisition of artery or vein identity during vascular development is governed, in part, by genetic mechanisms. The artery-specific expression of a number of Notch signaling genes in mouse and zebrafish suggests that this pathway may play a role in arterial-venous cell fate determination during vascular development. We show that loss of Notch signaling in zebrafish embryos leads to molecular defects in arterial-venous differentiation, including loss of artery-specific markers and ectopic expression of venous markers within the dorsal aorta. Conversely, we find that ectopic activation of Notch signaling leads to repression of venous cell fate. Finally, embryos lacking Notch function exhibit defects in blood vessel formation similar to those associated with improper arterial-venous specification. Our results suggest that Notch signaling is required for the proper development of arterial and venous blood vessels, and that a major role of Notch signaling in blood vessels is to repress venous differentiation within developing arteries. Movies available on-line
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Basic Helix-Loop-Helix..., http://linkedlifedata.com/resource/pubmed/chemical/Biological Markers, http://linkedlifedata.com/resource/pubmed/chemical/Ephrin-B2, http://linkedlifedata.com/resource/pubmed/chemical/Intracellular Signaling Peptides..., http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Receptor Protein-Tyrosine Kinases, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cell Surface, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Growth Factor, http://linkedlifedata.com/resource/pubmed/chemical/Vascular Endothelial Growth Factor..., http://linkedlifedata.com/resource/pubmed/chemical/Zebrafish Proteins, http://linkedlifedata.com/resource/pubmed/chemical/delta protein, http://linkedlifedata.com/resource/pubmed/chemical/hey2 protein, zebrafish
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0950-1991
pubmed:author
pubmed:issnType
Print
pubmed:volume
128
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3675-83
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:11585794-Animals, pubmed-meshheading:11585794-Arteries, pubmed-meshheading:11585794-Base Sequence, pubmed-meshheading:11585794-Basic Helix-Loop-Helix Transcription Factors, pubmed-meshheading:11585794-Biological Markers, pubmed-meshheading:11585794-Cell Differentiation, pubmed-meshheading:11585794-Embryonic Induction, pubmed-meshheading:11585794-Ephrin-B2, pubmed-meshheading:11585794-Female, pubmed-meshheading:11585794-Gene Expression Regulation, Developmental, pubmed-meshheading:11585794-Intracellular Signaling Peptides and Proteins, pubmed-meshheading:11585794-Membrane Proteins, pubmed-meshheading:11585794-Microinjections, pubmed-meshheading:11585794-Molecular Sequence Data, pubmed-meshheading:11585794-Mutation, pubmed-meshheading:11585794-Proteins, pubmed-meshheading:11585794-Proto-Oncogene Proteins, pubmed-meshheading:11585794-Receptor Protein-Tyrosine Kinases, pubmed-meshheading:11585794-Receptors, Cell Surface, pubmed-meshheading:11585794-Receptors, Growth Factor, pubmed-meshheading:11585794-Signal Transduction, pubmed-meshheading:11585794-Vascular Endothelial Growth Factor Receptor-3, pubmed-meshheading:11585794-Veins, pubmed-meshheading:11585794-Zebrafish, pubmed-meshheading:11585794-Zebrafish Proteins
pubmed:year
2001
pubmed:articleTitle
Notch signaling is required for arterial-venous differentiation during embryonic vascular development.
pubmed:affiliation
Laboratory of Molecular Genetics, NICHD, NIH, Bethesda, MD 20892, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't