{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1362825894533504384.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1073/pnas.95.16.9349"}},{"identifier":{"@type":"URI","@value":"https://pnas.org/doi/pdf/10.1073/pnas.95.16.9349"}},{"identifier":{"@type":"PMID","@value":"9689083"}},{"identifier":{"@type":"NAID","@value":"80010499845"}}],"dc:title":[{"@value":"Flt-1 lacking the tyrosine kinase domain is sufficient for normal development and angiogenesis in mice"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:p>\n            Receptor tyrosine kinases Flt-1 and Flk-1/KDR, and their ligand, the vascular endothelial growth factor (VEGF), were shown to be essential for angiogenesis in the mouse embryo by gene targeting. Flk-1/KDR null mutant mice exhibited impaired endothelial and hematopoietic cell development. On the other hand, Flt-1 null mutation resulted in early embryonic death at embryonic day 8.5, showing disorganization of blood vessels, such as overgrowth of endothelial cells. Flt-1 differs from Flk-1 in that it displays a higher affinity for VEGF but lower kinase activity, suggesting the importance of its extracellular domain. To examine the biological role of Flt-1 in embryonic development and vascular formation, we deleted the kinase domain without affecting the ligand binding region. Flt-1 tyrosine kinase-deficient homozygous mice (\n            <jats:italic>\n              flt-1\n              <jats:sup>TK−/−</jats:sup>\n            </jats:italic>\n            ) developed normal vessels and survived. However, VEGF-induced macrophage migration was strongly suppressed in\n            <jats:italic>\n              flt-1\n              <jats:sup>TK−/−</jats:sup>\n            </jats:italic>\n            mice. These results indicate that Flt-1 without tyrosine kinase domain is sufficient to allow embryonic development with normal angiogenesis, and that a receptor tyrosine kinase plays a main biological role as a ligand-binding molecule.\n          </jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1382825894533504388","@type":"Researcher","foaf:name":[{"@value":"Sachie Hiratsuka"}],"jpcoar:affiliationName":[{"@value":"Department of Genetics, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan; and Department of Cell Biology, Cancer Institute, 1-37-1 Kami-Ikebukuro, Toshima-ku, Tokyo 170-0012, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1420845751157015168","@type":"Researcher","personIdentifier":[{"@type":"KAKEN_RESEARCHERS","@value":"00181967"},{"@type":"NRID","@value":"1000000181967"},{"@type":"NRID","@value":"9000391636397"},{"@type":"NRID","@value":"9000253204534"},{"@type":"NRID","@value":"9000391636390"},{"@type":"NRID","@value":"9000008107938"},{"@type":"NRID","@value":"9000253204004"},{"@type":"NRID","@value":"9000253163805"},{"@type":"NRID","@value":"9000321623803"},{"@type":"NRID","@value":"9000252810795"},{"@type":"NRID","@value":"9000391641590"},{"@type":"NRID","@value":"9000391627487"},{"@type":"NRID","@value":"9000253206364"},{"@type":"NRID","@value":"9000004694223"},{"@type":"NRID","@value":"9000391619106"},{"@type":"NRID","@value":"9000391614471"},{"@type":"NRID","@value":"9000253168721"},{"@type":"NRID","@value":"9000253163808"},{"@type":"NRID","@value":"9000000190461"},{"@type":"NRID","@value":"9000391630277"},{"@type":"NRID","@value":"9000391620335"},{"@type":"NRID","@value":"9000021215715"},{"@type":"NRID","@value":"9000253164088"},{"@type":"NRID","@value":"9000391620333"},{"@type":"NRID","@value":"9000253204684"},{"@type":"NRID","@value":"9000391605720"},{"@type":"NRID","@value":"9000253205733"},{"@type":"NRID","@value":"9000253106779"},{"@type":"RESEARCHMAP","@value":"https://researchmap.jp/leo"}],"foaf:name":[{"@value":"Osamu Minowa"}],"jpcoar:affiliationName":[{"@value":"Department of Genetics, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan; and Department of Cell Biology, Cancer Institute, 1-37-1 Kami-Ikebukuro, Toshima-ku, Tokyo 170-0012, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1382825894533504384","@type":"Researcher","foaf:name":[{"@value":"Junko Kuno"}],"jpcoar:affiliationName":[{"@value":"Department of Genetics, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan; and Department of Cell Biology, Cancer Institute, 1-37-1 Kami-Ikebukuro, Toshima-ku, Tokyo 170-0012, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1382825894533504385","@type":"Researcher","foaf:name":[{"@value":"Tetsuo Noda"}],"jpcoar:affiliationName":[{"@value":"Department of Genetics, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan; and Department of Cell Biology, Cancer Institute, 1-37-1 Kami-Ikebukuro, Toshima-ku, Tokyo 170-0012, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1382825894533504386","@type":"Researcher","foaf:name":[{"@value":"Masabumi Shibuya"}],"jpcoar:affiliationName":[{"@value":"Department of Genetics, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan; and Department of Cell Biology, Cancer Institute, 1-37-1 Kami-Ikebukuro, Toshima-ku, Tokyo 170-0012, Japan"}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"00278424"},{"@type":"EISSN","@value":"10916490"},{"@type":"PISSN","@value":"https://id.crossref.org/issn/00278424"}],"prism:publicationName":[{"@value":"Proceedings of the National Academy of Sciences"}],"dc:publisher":[{"@value":"Proceedings of the National Academy of Sciences"}],"prism:publicationDate":"1998-08-04","prism:volume":"95","prism:number":"16","prism:startingPage":"9349","prism:endingPage":"9354"},"reviewed":"false","dcterms:accessRights":"http://purl.org/coar/access_right/c_abf2","url":[{"@id":"https://pnas.org/doi/pdf/10.1073/pnas.95.16.9349"}],"createdAt":"2002-07-26","modifiedAt":"2022-04-13","foaf:topic":[{"@id":"https://cir.nii.ac.jp/all?q=Vascular%20Endothelial%20Growth%20Factor%20A","dc:title":"Vascular Endothelial Growth Factor A"},{"@id":"https://cir.nii.ac.jp/all?q=Lymphokines","dc:title":"Lymphokines"},{"@id":"https://cir.nii.ac.jp/all?q=Vascular%20Endothelial%20Growth%20Factor%20Receptor-1","dc:title":"Vascular Endothelial Growth Factor Receptor-1"},{"@id":"https://cir.nii.ac.jp/all?q=Base%20Sequence","dc:title":"Base Sequence"},{"@id":"https://cir.nii.ac.jp/all?q=Vascular%20Endothelial%20Growth%20Factors","dc:title":"Vascular Endothelial Growth Factors"},{"@id":"https://cir.nii.ac.jp/all?q=Macrophages","dc:title":"Macrophages"},{"@id":"https://cir.nii.ac.jp/all?q=Neovascularization,%20Physiologic","dc:title":"Neovascularization, Physiologic"},{"@id":"https://cir.nii.ac.jp/all?q=Receptor%20Protein-Tyrosine%20Kinases","dc:title":"Receptor Protein-Tyrosine Kinases"},{"@id":"https://cir.nii.ac.jp/all?q=Endothelial%20Growth%20Factors","dc:title":"Endothelial Growth Factors"},{"@id":"https://cir.nii.ac.jp/all?q=Capillary%20Permeability","dc:title":"Capillary Permeability"},{"@id":"https://cir.nii.ac.jp/all?q=Embryonic%20and%20Fetal%20Development","dc:title":"Embryonic and Fetal Development"},{"@id":"https://cir.nii.ac.jp/all?q=Mice","dc:title":"Mice"},{"@id":"https://cir.nii.ac.jp/all?q=Proto-Oncogene%20Proteins","dc:title":"Proto-Oncogene Proteins"},{"@id":"https://cir.nii.ac.jp/all?q=Gene%20Targeting","dc:title":"Gene 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