Gene Set: BIOCARTA_IGF1R_PATHWAY

Standard name BIOCARTA_IGF1R_PATHWAY
Systematic name M19613
Brief description Multiple antiapoptotic pathways from IGF-1R signaling lead to BAD phosphorylation
Full description or abstract 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.
Collection C2: curated gene sets
      CP:BIOCARTA: BioCarta gene sets
Source publication  
Exact source  
Related gene sets  
External links http://cgap.nci.nih.gov/Pathways/BioCarta/h_igf1rPathway
http://cgap.nci.nih.gov/Genes/PathGeneQuery?PAGE=1&ORG=Hs&PATH=h_igf1rPathway
Organism Homo sapiens
Contributed by BioCarta
Source platform EntrezGeneIds
Dataset references  
Download gene set format: grp | text | gmt | gmx | xml
Compute overlaps (show collections to investigate for overlap with this gene set)
Compendia expression profiles Human tissue compendium (Novartis)
NCI-60 cell lines (National Cancer Institute)
Advanced query Further investigate these 23 genes
Gene families Categorize these 23 genes by gene family
Show members (show 23 members mapped to 23 genes)
Version history  

See MSigDB license terms here. Please note that certain gene sets have special access terms.