http://purl.uniprot.org/citations/16172397 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/16172397 | http://www.w3.org/2000/01/rdf-schema#comment | "VEGF receptor 1 (VEGFR-1/Flt-1) is a high-affinity tyrosine kinase (TK) receptor for VEGF and regulates angiogenesis as well as monocyte/macrophage functions. We previously showed that the osteoclast deficiency in osteopetrotic Csf1op/Csf1op (op/op) mice is gradually restored in an endogenous, VEGF-dependent manner. However, the molecular basis of the recovery is still not clear. To examine which VEGFR is important and to clarify how colony-stimulating factor 1 (CSF-1) and VEGF signals interact in osteoclastogenesis, we introduced a VEGFR-1 signaling deficiency (Flt1(TK)-/-) into op/op mice. The original Flt1(TK)-/-mice showed mild osteoclast reduction without bone marrow suppression. The double mutant (op/opFlt1(TK)-/-) mice, however, exhibited very severe osteoclast deficiency and did not have numbers of osteoclasts sufficient to form the bone marrow cavity. The narrow bone marrow cavity in the op/opFlt1(TK)-/-mice was gradually replaced with fibrous tissue, resulting in severe marrow hypoplasia and extramedullary hematopoiesis. In addition to osteoclasts, osteoblasts also decreased in number in the op/opFlt1(TK)-/-mice. These results strongly suggest that the interaction of signals by means of VEGFR-1 and the CSF-1 receptor plays a predominant role not only in osteoclastogenesis but also in the maintenance of bone marrow functions."xsd:string |
http://purl.uniprot.org/citations/16172397 | http://purl.org/dc/terms/identifier | "doi:10.1073/pnas.0503544102"xsd:string |
http://purl.uniprot.org/citations/16172397 | http://purl.uniprot.org/core/author | "Hayashi S."xsd:string |
http://purl.uniprot.org/citations/16172397 | http://purl.uniprot.org/core/author | "Ikeda K."xsd:string |
http://purl.uniprot.org/citations/16172397 | http://purl.uniprot.org/core/author | "Kondo T."xsd:string |
http://purl.uniprot.org/citations/16172397 | http://purl.uniprot.org/core/author | "Shibuya M."xsd:string |
http://purl.uniprot.org/citations/16172397 | http://purl.uniprot.org/core/author | "Noda T."xsd:string |
http://purl.uniprot.org/citations/16172397 | http://purl.uniprot.org/core/author | "Niida S."xsd:string |
http://purl.uniprot.org/citations/16172397 | http://purl.uniprot.org/core/author | "Hiratsuka S."xsd:string |
http://purl.uniprot.org/citations/16172397 | http://purl.uniprot.org/core/author | "Amizuka N."xsd:string |
http://purl.uniprot.org/citations/16172397 | http://purl.uniprot.org/core/date | "2005"xsd:gYear |
http://purl.uniprot.org/citations/16172397 | http://purl.uniprot.org/core/name | "Proc Natl Acad Sci U S A"xsd:string |
http://purl.uniprot.org/citations/16172397 | http://purl.uniprot.org/core/pages | "14016-14021"xsd:string |
http://purl.uniprot.org/citations/16172397 | http://purl.uniprot.org/core/title | "VEGF receptor 1 signaling is essential for osteoclast development and bone marrow formation in colony-stimulating factor 1-deficient mice."xsd:string |
http://purl.uniprot.org/citations/16172397 | http://purl.uniprot.org/core/volume | "102"xsd:string |
http://purl.uniprot.org/citations/16172397 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/16172397 |
http://purl.uniprot.org/citations/16172397 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/16172397 |
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http://purl.uniprot.org/uniprot/#_D3Z090-mappedCitation-16172397 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16172397 |
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