Nerve growth factor-mediated activation of p53-depedent transcription represents an unusual example of receptor-mediated, non-genotoxic p53 activation.
The initial skepticism is now subsiding as more and more examples of receptor oligomerization are identified.
Examples of receptor tyrosine kinases (RTKs) include vascular endothelial growth factor receptor (VEGFR), nerve growth factor (NGF /neurotrophin receptor TrkA, Axl, Tie2, epidermal growth factor receptor (EGFR, ErbB), stem cell factor receptor KIT c-KIT), and platelet-derived growth factor receptors (PDGFR) α and β.
For example, endocytosis of receptor tyrosine kinases (RTKs) requires tyrosine phosphorylation and monoubiquitination of the receptor and downstream components to sort endocytosed cargo for subsequent degradation (down regulation) or recycling to the cell surface [2], [3], [4].
For example, activation of receptor tyrosine kinases such as the EGFR [EGF (epidermal growth factor) receptor] family and the VEGFR (vascular EGFR) family is frequently observed in EOC and regulates cell proliferation, survival, motility and metastasis [ 17, 18].
With specific targets for new agents, demonstration that the target has been appropriately modified, for example, inhibition of receptor signalling either in the tumour or surrogate tissue is now an early decision point in drug development.
CCR5 and CXCR3 are classical examples of receptors for inflammatory chemokines [ 5].
Although many chemicals and endogenous hormones require receptor interactions as a necessary event in their carcinogenic activity, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and its structural analogs are the most visible examples of receptor-mediated carcinogens.
Examples of receptors known to regulate RasGRF1 and expressed in RA synovial tissue include those for lysophosphatidic acid and muscarinic acid, N-methyl-D-aspartic acid, and nerve growth factor [ 50- 53].
