| http://purl.uniprot.org/citations/12819200 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/12819200 | http://www.w3.org/2000/01/rdf-schema#comment | "Endothelial cell-selective adhesion molecule (ESAM) is a member of the immunoglobulin receptor family that mediates homophilic interactions between endothelial cells. To address potential in vivo angiogenic functions of this molecule, mice lacking ESAM (ESAM-/-) were generated by gene-targeted deletion. ESAM-/-mice did not show overt morphological defects in the vasculature. To evaluate the role of ESAM in pathological angiogenesis, wild type (WT) and ESAM-/-mice were injected with melanoma and Lewis lung carcinoma cells. By 14 days after injection, tumor volumes of B16F10 and LL/2 in ESAM-/-mice were 48 and 37% smaller, respectively, compared with WT mice. Vascular density of the tumors, as determined by CD31 staining, was also decreased in the ESAM null animals. Matrigel plug assays showed less neovascularization in ESAM-/- mice than in WT mice. ESAM-/-endothelial cells exhibited less in vitro tube formation and decreased migration in response to basic fibroblast growth factor when compared with WT cells, and endothelial-like yolk sac cells engineered to overexpress ESAM showed accelerated tube formation in vitro. These in vitro and in vivo studies suggest that ESAM has a redundant functional role in physiological angiogenesis but serves a unique and essential role in pathological angiogenic processes such as tumor growth."xsd:string |
| http://purl.uniprot.org/citations/12819200 | http://purl.org/dc/terms/identifier | "doi:10.1074/jbc.m304890200"xsd:string |
| http://purl.uniprot.org/citations/12819200 | http://purl.uniprot.org/core/author | "Ishida T."xsd:string |
| http://purl.uniprot.org/citations/12819200 | http://purl.uniprot.org/core/author | "Yang E."xsd:string |
| http://purl.uniprot.org/citations/12819200 | http://purl.uniprot.org/core/author | "Hirata K."xsd:string |
| http://purl.uniprot.org/citations/12819200 | http://purl.uniprot.org/core/author | "Quertermous T."xsd:string |
| http://purl.uniprot.org/citations/12819200 | http://purl.uniprot.org/core/author | "Kundu R.K."xsd:string |
| http://purl.uniprot.org/citations/12819200 | http://purl.uniprot.org/core/author | "Ho Y.D."xsd:string |
| http://purl.uniprot.org/citations/12819200 | http://purl.uniprot.org/core/date | "2003"xsd:gYear |
| http://purl.uniprot.org/citations/12819200 | http://purl.uniprot.org/core/name | "J Biol Chem"xsd:string |
| http://purl.uniprot.org/citations/12819200 | http://purl.uniprot.org/core/pages | "34598-34604"xsd:string |
| http://purl.uniprot.org/citations/12819200 | http://purl.uniprot.org/core/title | "Targeted disruption of endothelial cell-selective adhesion molecule inhibits angiogenic processes in vitro and in vivo."xsd:string |
| http://purl.uniprot.org/citations/12819200 | http://purl.uniprot.org/core/volume | "278"xsd:string |
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