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Cited by 277

The DOI matches its Crossref record; 52 of the 52 references it cites were found in a registry or an index.

Expression of tie-2, a member of a novel family of receptor tyrosine kinases, in the endothelial cell lineage

Schnürch, Harald, Risau, Werner·1993·Development

Abstract

We are interested in the molecular mechanisms that are involved in the development of the vascular system. In order to respond to morphogenetic and mitogenic signals, endothelial cells must express appropriate receptors. To characterize endothelial cell-specific receptors, we have concentrated on receptor tyrosine kinases, because several lines of evidence suggested the importance of controlled phosphotyrosine levels in endothelial cells. A strategy based on PCR amplification using degenerate oligonucleotides and mouse brain capillaries as mRNA source, led to the identification of a novel receptor tyrosine kinase, which we designated tie-2. In situ hybridization using a tie-2-specific probe revealed an interesting spatial and temporal expression pattern. The gene was expressed specifically in the endothelial lineage. tie-2 transcripts were present in endothelial cell precursors (angioblasts) and also in endothelial cells of sprouting blood vessels throughout development and in all organs and tissues so far examined. tie-2 was down-regulated in the adult. Because of the unusual combination of immunoglobulin, EGF-like and fibronectin type III domains in the extracellular portion of tie-2 which is shared by TEK and tie, these molecules may be considered members of a new family of receptor tyrosine kinases. Signal transduction via this new class of tyrosine kinases could lead to a better understanding of the molecular mechanisms of blood vessel formation.

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Crossref · 10.1242/dev.119.3.957

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Metadata

Authors
Schnürch, H., & Risau, W.
Venue
Development
Published
1993-11-01
Volume
119
Issue
3
Pages
957-968
ISSN
  • 0950-1991 (ISSN-L)
  • 1477-9129
OpenAlex
W1895421323
Cited by
277
References
52
FWCI
2.62
Type
journal article
Language
en
Open access
closed

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