| http://purl.uniprot.org/citations/18070883 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/18070883 | http://www.w3.org/2000/01/rdf-schema#comment | "Sprouty (SPRY) proteins modulate receptor-tyrosine kinase signaling and, thereby, regulate cell migration and proliferation. Here, we have examined the role of endogenous human SPRY2 (hSPRY2) in the regulation of cellular apoptosis. Small inhibitory RNA-mediated silencing of hSPRY2 abolished the anti-apoptotic action of serum in adrenal cortex adenocarcinoma (SW13) cells. Silencing of hSPRY2 decreased serum- or epidermal growth factor (EGF)-elicited activation of AKT and ERK1/2 and reduced the levels of EGF receptor. Silencing of hSPRY2 also inhibited serum-induced activation of p90RSK and decreased phosphorylation of pro-apoptotic protein BAD (BCL2-antagonist of cell death) by p90RSK. Inhibiting both the ERK1/2 and AKT pathways abolished the ability of serum to protect against apoptosis, mimicking the effects of silencing hSPRY2. Serum transactivated the EGF receptor (EGFR), and inhibition of the EGFR by a neutralizing antibody attenuated the anti-apoptotic actions of serum. Consistent with the role of EGFR and perhaps other growth factor receptors in the anti-apoptotic actions of serum, the tyrosine kinase binding domain of c-Cbl (Cbl-TKB) protected against down-regulation of the growth factor receptors such as EGFR and preserved the anti-apoptotic actions of serum when hSpry2 was silenced. Additionally, silencing of Spry2 in c-Cbl null cells did not alter the ability of serum to promote cell survival. Moreover, reintroduction of wild type hSPRY2, but not its mutants that do not bind c-Cbl or CIN85 into SW13 cells after endogenous hSPRY2 had been silenced, restored the anti-apoptotic actions of serum. Overall, we conclude that endogenous hSPRY2-mediated regulation of apoptosis requires c-Cbl and is manifested by the ability of hSPRY2 to sequester c-Cbl and thereby augment signaling via growth factor receptors."xsd:string |
| http://purl.uniprot.org/citations/18070883 | http://purl.org/dc/terms/identifier | "doi:10.1074/jbc.m706567200"xsd:string |
| http://purl.uniprot.org/citations/18070883 | http://purl.uniprot.org/core/author | "Patel T.B."xsd:string |
| http://purl.uniprot.org/citations/18070883 | http://purl.uniprot.org/core/author | "Edwin F."xsd:string |
| http://purl.uniprot.org/citations/18070883 | http://purl.uniprot.org/core/date | "2008"xsd:gYear |
| http://purl.uniprot.org/citations/18070883 | http://purl.uniprot.org/core/name | "J Biol Chem"xsd:string |
| http://purl.uniprot.org/citations/18070883 | http://purl.uniprot.org/core/pages | "3181-3190"xsd:string |
| http://purl.uniprot.org/citations/18070883 | http://purl.uniprot.org/core/title | "A novel role of Sprouty 2 in regulating cellular apoptosis."xsd:string |
| http://purl.uniprot.org/citations/18070883 | http://purl.uniprot.org/core/volume | "283"xsd:string |
| http://purl.uniprot.org/citations/18070883 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/18070883 |
| http://purl.uniprot.org/citations/18070883 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/18070883 |
| http://purl.uniprot.org/uniprot/P22681#attribution-769CE581826149821F0848733E059AC2 | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/18070883 |
| http://purl.uniprot.org/uniprot/P00533#attribution-769CE581826149821F0848733E059AC2 | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/18070883 |
| http://purl.uniprot.org/uniprot/Q9QXV8#attribution-769CE581826149821F0848733E059AC2 | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/18070883 |
| http://purl.uniprot.org/uniprot/O43597#attribution-769CE581826149821F0848733E059AC2 | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/18070883 |
| http://purl.uniprot.org/uniprot/#_A0A0U1RP17-mappedCitation-18070883 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/18070883 |
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| http://purl.uniprot.org/uniprot/#_A0A0X1KG61-mappedCitation-18070883 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/18070883 |
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| http://purl.uniprot.org/uniprot/#_B1NE42-mappedCitation-18070883 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/18070883 |
| http://purl.uniprot.org/uniprot/#_B2RS85-mappedCitation-18070883 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/18070883 |