Multiple antiapoptotic pathways from IGF-1R signaling lead to BAD phosphorylation
| PAG Title | Multiple antiapoptotic pathways from IGF-1R signaling lead to BAD phosphorylation |
| PAG ID | WIG000346 |
| Type | P |
| Source Link |  MSigDB |
| Publication Reference | NA |
| PAG Description | IGF-1R, the type 1 receptor for insulin-like growth factor, mediates cell survival and growth in response to its ligands IGF-1 and IGF-2. This tyrosine kinase receptor is widely expressed in many cell types and is a key mediator of growth. Overexpression or activation of IGF-1R may be involved in the proliferation of transformed cells, making inhibition of IGF-1R signaling a strategy for the development of cancer drugs. IGF-1R activates three signaling pathways that converge to phosphorylate BAD protein and block apoptosis. The first pathway activated by IGF-1R stimulates PI3-kinase and the AKT pathway to phosphorylate BAD and block apoptosis. A second pathway activated by IGF-1R involves ras mediated activation of the map kinase pathway to block apoptosis. A third pathway involves interaction of raf with mitochondria in response to IGF-1R activation. The convergence of these pathways to block apoptosis may enhance the IGF-1R response. |
| Species | Homo sapiens |
| nCoCo Score | 3,461 |
| Base PAG ID | WIG000346 |
| Human Phenotyte Annotation | |
| Curator | PAGER curation team |
| Curator Contact | PAGER-contact@googlegroups.com |
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