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• W2045247798 abstract "Blood vessels form either by the assembly and differentiation of mesodermal precursor cells (vasculogenesis) or by sprouting from preexisting vessels (angiogenesis) [1Risau W. Flamme I. Vasculogenesis.Annu. Rev. Cell Dev. Biol. 1995; 11: 73-91Crossref PubMed Scopus (1292) Google Scholar, 2Risau W. Mechanisms of angiogenesis.Nature. 1997; 386: 671-674Crossref PubMed Scopus (4671) Google Scholar, 3Carmeliet P. Mechanisms of angiogenesis and arteriogenesis.Nat. Med. 2000; 6: 389-395Crossref PubMed Scopus (3320) Google Scholar]. Endothelial-specific receptor tyrosine kinases and their ligands are known to be essential for these processes. Targeted disruption of vascular endothelial growth factor (VEGF) or its receptor kdr (flk1, VEGFR2) in mouse embryos results in a severe reduction of all blood vessels [4Carmeliet P. Ferreira V. Breier G. Pollefeyt S. Kieckens L. Gertsenstein M. Fahrig M. Vandenhoeck A. Harpal K. Eberhardt C. et al.Abnormal blood vessel development and lethality in embryos lacking a single VEGF allele.Nature. 1996; 380: 435-439Crossref PubMed Scopus (3364) Google Scholar, 5Ferrara N. Carver-Moore K. Chen H. Dowd M. Lu L. O'Shea K.S. Powell-Braxton L. Hilla K.J. Moore M.W. Heterozygous embryonic lethality induced by targeted inactivation of the VEGF gene.Nature. 1996; 380: 439-442Crossref PubMed Scopus (2964) Google Scholar, 6Shalaby F. Rossant J. Yamaguchi T.P. Gertsenstein M. Wu X.F. Breitman M.L. Schuh A.C. Failure of blood-island formation and vasculogenesis in Flk-1-deficient mice.Nature. 1995; 376: 62-66Crossref PubMed Scopus (3272) Google Scholar], while the complete loss of flt1 (VEGFR1) leads to an increased number of hemangioblasts and a disorganized vasculature [7Fong G.H. Rossant J. Gertsenstein M. Breitman M.L. Role of the Flt-1 receptor tyrosine kinase in regulating the assembly of vascular endothelium.Nature. 1995; 376: 66-70Crossref PubMed Scopus (2160) Google Scholar, 8Fong G.H. Zhang L. Bryce D.M. Peng J. Increased hemangioblast commitment, not vascular disorganization, is the primary defect in flt-1 knock-out mice.Development. 1999; 126: 3015-3025Crossref PubMed Google Scholar]. In a large-scale forward genetic screen, we identified two allelic zebrafish mutants in which the sprouting of blood vessels is specifically disrupted without affecting the assembly and differentiation of angioblasts. Molecular cloning revealed nonsense mutations in flk1. Analysis of mRNA expression in flk1 mutant embryos showed that flk1 expression was severely downregulated, while the expression of other genes (scl, gata1, and fli1) involved in vasculogenesis or hematopoiesis was unchanged. Overexpression of vegf121+165 led to the formation of additional vessels only in sibling larvae, not in flk1 mutants. We demonstrate that flk1 is not required for proper vasculogenesis and hematopoiesis in zebrafish embryos. However, the disruption of flk1 impairs the formation or function of vessels generated by sprouting angiogenesis." @default.
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• W2045247798 date "2002-08-01" @default.
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• W2045247798 title "Analysis of a Zebrafish VEGF Receptor Mutant Reveals Specific Disruption of Angiogenesis" @default.
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• W2045247798 doi "https://doi.org/10.1016/s0960-9822(02)01044-8" @default.
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