EGF–ERBB signalling: towards the systems level

By A. Citri, Y. Yarden. Nature reviews. Molecular cell biology, 2006

2,066 citations recorded by the source corpus.

Subfields: Computational Theory and Mathematics, Oncology, Radiology, Nuclear Medicine and Imaging

View Paper: https://www.semanticscholar.org/paper/4a474cca56d4614aeaeab109c3d0a498df5d866d

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Citations in the corpus

FDA-approved small-molecule kinase inhibitors. (2015, background): “The ErbB cascade is one of the most extensively studied signaling transduction pathways [49, 50], and the ErbB inhibitors gefitinib (Iressa®, AstraZeneca), erlotinib (Tarceva®, OSI Pharm.)”
Molecular mechanisms of cisplatin resistance (2012, background): “Mitsuuchi et al., 2000; Zhou et al., 2001; Ikeguchi and Kaibara, 2001; Citri and Yarden, 2006; Fijolek et al., 2006 HSPs Chaperones that exert prosurvival functions in response to a variety of stress conditions.”
Feedback regulation of EGFR signalling: decision making by early and delayed loops (2011, background): “The issue of signalling specificity, along with the existence of non-autonomous RTKs and the broad range of EGF-induced biological outcomes — which exceeds the number of signalling pathways — motivated a paradigm shift a decade ago; the view of simple pathways connecting ERBB proteins to enzymatic p”
ErbB receptors and signaling pathways in cancer. (2009, background): “Intracellular pathways downstream of ErbB receptors ErbB receptors control key intracellular pathways that govern fundamental cellular processes including proliferation, cell migration, metabolism, and survival [1,21].”
The MEK/ERK cascade: from signaling specificity to diverse functions. (2007, background): “The regulation of the kinetics of ERKs activation by extracellular signal has been extensively studied in the past decade, and was shown to involve several unrelated mechanisms that operate separately in each tier of the receptor-mediated pathways [86,95].”
Input–output behavior of ErbB signaling pathways as revealed by a mass action model trained against dynamic data (2009, methodology): “The ErbB1–4 receptor tyrosine kinases (RTKs) and the signaling pathways they activate, control cell division, motility and survival and are among the best studied of all signaltransduction networks (Citri and Yarden, 2006).”
Signaling pathways in cancer-associated fibroblasts and targeted therapy for cancer (2021, background): “ErbB family members can be activated by the following ligands: amphiregulin, betacellulin, EGF, heparin-binding EGF-like growth factor, TGF-α, epiregulin, epigen, and NRGs.(239,240) Structurally, EGFR family members share a common domain arrangement that comprises a cysteine-rich extracellular domai”
Human Epidermal Growth Factor Receptor 2 (HER2) in Cancers: Overexpression and Therapeutic Implications (2014, positive): “Moreover, HER2 dimerization promotes the mislocalization and rapid degradation of cell-cycle inhibitor p27Kip1 protein leading to cell-cycle progression [7, 10, 11].”
Targeting the EGFR signaling pathway in cancer therapy (2012, background): “ErbB family members can be activated by 13 known ligands, which include EGF, transforming growth factor alpha (TGF-a), amphiregulin (AR), betacellulin (BTC), heparin-binding EGF-like growth factor (HB-EGF), epiregulin (EPR), epigen (EPG) and neuregulins 1 -- 6 (NRG) [10,11].”
Thresholds for therapies: highlights of the St Gallen International Expert Consensus on the Primary Therapy of Early Breast Cancer 2009 (2009, background): “Success is more likely to occur if two or more perturbations can be introduced, preferably at crucial early parts of the network [14].”
Survivin, cancer networks and pathway-directed drug discovery (2008, background): “For instance, signalling through the epidermal growth factor receptor ( EGFR ) functions as a node, integrating extracellular cues with a panoply of downstream signalling responses, affecting cell proliferation, cell survival, differentiation and migratio”
Predicting ligand-dependent tumors from multi-dimensional signaling features (2017, background): “It is not intended to be a complete compendium of all the known molecular interactions.(33,36,37) Size and complexity of the computational model were chosen to reflect the available experimental data, and to facilitate efficient computation.”