| http://purl.uniprot.org/citations/20371769 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/20371769 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/20371769 | http://www.w3.org/2000/01/rdf-schema#comment | "Cerebral cavernous malformations (CCMs) are human vascular malformations caused by mutations in three genes of unknown function: CCM1, CCM2, and CCM3. CCM3, also known as PDCD10 (programmed cell death 10), was initially identified as a messenger RNA whose abundance was induced by apoptotic stimuli in vitro. However, the in vivo function of CCM3 has not been determined. Here, we describe mice with a deletion of the CCM3 gene either ubiquitously or specifically in the vascular endothelium, smooth muscle cells, or neurons. Mice with global or endothelial cell-specific deletion of CCM3 exhibited defects in embryonic angiogenesis and died at an early embryonic stage. CCM3 deletion reduced vascular endothelial growth factor receptor 2 (VEGFR2) signaling in embryos and endothelial cells. In response to VEGF stimulation, CCM3 was recruited to and stabilized VEGFR2, and the carboxyl-terminal domain of CCM3 was required for the stabilization of VEGFR2. Indeed, the CCM3 mutants found in human patients lacking the carboxyl-terminal domain were labile and were unable to stabilize and activate VEGFR2. These results demonstrate that CCM3 promotes VEGFR2 signaling during vascular development."xsd:string |
| http://purl.uniprot.org/citations/20371769 | http://purl.org/dc/terms/identifier | "doi:10.1126/scisignal.2000722"xsd:string |
| http://purl.uniprot.org/citations/20371769 | http://purl.org/dc/terms/identifier | "doi:10.1126/scisignal.2000722"xsd:string |
| http://purl.uniprot.org/citations/20371769 | http://purl.uniprot.org/core/author | "Chen H."xsd:string |
| http://purl.uniprot.org/citations/20371769 | http://purl.uniprot.org/core/author | "Chen H."xsd:string |
| http://purl.uniprot.org/citations/20371769 | http://purl.uniprot.org/core/author | "He Y."xsd:string |
| http://purl.uniprot.org/citations/20371769 | http://purl.uniprot.org/core/author | "He Y."xsd:string |
| http://purl.uniprot.org/citations/20371769 | http://purl.uniprot.org/core/author | "Zhang H."xsd:string |
| http://purl.uniprot.org/citations/20371769 | http://purl.uniprot.org/core/author | "Zhang H."xsd:string |
| http://purl.uniprot.org/citations/20371769 | http://purl.uniprot.org/core/author | "Yu L."xsd:string |
| http://purl.uniprot.org/citations/20371769 | http://purl.uniprot.org/core/author | "Yu L."xsd:string |
| http://purl.uniprot.org/citations/20371769 | http://purl.uniprot.org/core/author | "Min W."xsd:string |
| http://purl.uniprot.org/citations/20371769 | http://purl.uniprot.org/core/author | "Min W."xsd:string |
| http://purl.uniprot.org/citations/20371769 | http://purl.uniprot.org/core/author | "Gunel M."xsd:string |
| http://purl.uniprot.org/citations/20371769 | http://purl.uniprot.org/core/author | "Gunel M."xsd:string |
| http://purl.uniprot.org/citations/20371769 | http://purl.uniprot.org/core/author | "Boggon T.J."xsd:string |
| http://purl.uniprot.org/citations/20371769 | http://purl.uniprot.org/core/author | "Boggon T.J."xsd:string |
| http://purl.uniprot.org/citations/20371769 | http://purl.uniprot.org/core/date | "2010"xsd:gYear |
| http://purl.uniprot.org/citations/20371769 | http://purl.uniprot.org/core/date | "2010"xsd:gYear |
| http://purl.uniprot.org/citations/20371769 | http://purl.uniprot.org/core/name | "Sci. Signal."xsd:string |
| http://purl.uniprot.org/citations/20371769 | http://purl.uniprot.org/core/name | "Sci. Signal."xsd:string |
| http://purl.uniprot.org/citations/20371769 | http://purl.uniprot.org/core/pages | "RA26"xsd:string |
| http://purl.uniprot.org/citations/20371769 | http://purl.uniprot.org/core/pages | "RA26"xsd:string |