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Copyright ©2006 Baishideng Publishing Group Co.
World J Gastroenterol. Dec 14, 2006; 12(46): 7440-7450
Published online Dec 14, 2006. doi: 10.3748/wjg.v12.i46.7440
Figure 1
Figure 1 Schematic representation of the four ErbB family members and their respective ligands. The numbers depict percentage homology of each domain relative to EGFR/ErbB-1. There are no known ligands for ErbB-2 and the tyrosine kinase domain is non-functional in ErbB-3, as marked with a cross.
Figure 2
Figure 2 Schematic representations of different ErbBs/EGFRs ligand-induced signaling pathways leading to development and progression of tumors. BTC: betacellulin; EGF: Epidermal growth factor; EGFR: Epidermal growth factor receptor; ERK: Extracellular signal regulated protein kinase; HB-EGF: heparin binding-EGF; Grb: Growth factor receptor receptor binding protein; JNK: c-Jun N-Terminal kinase; MEK: Mitogen activated protein kinase kinase; NDF: neu differentiation factors (also called neuregulins); PI3K: Phosphoinositide-3-kinase; PKB: Protein kinase B; SOS: Son of sevenless;TGF-α: transforming growth factor α.
Figure 3
Figure 3 Different strategies to inhibit EGFRs signaling. mAbs: monoclonal antibodies; siRNA: small interfering ribonucleic acid.
Figure 4
Figure 4 Schematic representation of the comparison of ERRP structure with EGFR (A) and hypothetical mechanism of action of ERRP (B). EGFR: Epidermal growth factor receptor; ERRP: Epidermal growth factor receptor-related protein.