Ligand-induced, receptor-mediated dimerization and activation of EGF receptor.

By Joseph Schlessinger. Cell, 2002

998 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Radiology, Nuclear Medicine and Imaging

View Paper: https://www.semanticscholar.org/paper/7ae439326f93e5cfec115ac401865d5bbf06d8bb

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Citations in the corpus

Dynamic multiple-target tracing to probe spatiotemporal cartography of cell membranes (2008, methodology): “We tested MTT by analyzing the membrane dynamics of EGF”
Erlotinib in lung cancer - molecular and clinical predictors of outcome. (2005, background): “High trisomy (3 gene copies in ≥40% of cells) 3 (2)”
ADAMs: key components in EGFR signalling and development (2005, background): “Recent structural studies that have uncovered an unusual mechanism of EGFR dimerization (reviewed in Ref”
EGFR and EphA2 are host factors for hepatitis C virus entry and possible targets for antiviral therapy (2011, neutral): “Epidermal growth factor (EGF) and transforming growth factor-α (TGF-α) are well-characterized EGFR ligands whose binding promotes receptor dimerization and subsequent phosphorylation of the intracytoplasmic kinase domai”
The ErbB/HER family of protein-tyrosine kinases and cancer. (2014, background): “Moreover, ErbB1/2/4 each possess a C-terminal GG4-like signature, which is lacking in kinase-impaired ErbB3.”
Mechanism for activation of the EGF receptor catalytic domain by the juxtamembrane segment (2009, neutral): “…of these receptors includes the epidermal growth factor receptor (EGFR, also known as ErbB1 or Her1) and its three homologs in humans: ErbB2/Her2 and ErbB4/ Her4, which are kinase active, and ErbB3/Her3, which is not (Landau and Ben-Tal, 2008; Schlessinger, 2002; Yarden and Sliwkowski, 2001).”
Clathrin- and non-clathrin-mediated endocytic regulation of cell signalling (2005, methodology): “In this system, EGF binding induces the dimerization of EGF”
An allosteric mechanism for activation of the kinase domain of epidermal growth factor receptor. (2006, background): “The structural basis for ligand-induced dimerization of the extracellular region of EGFR family members is now well understood (Cho and Leahy, 2002; Ferguson et al., 2003; Garrett et al., 2002; Ogiso et al., 2002; Schlessinger, 2002).”
EGF activates its receptor by removing interactions that autoinhibit ectodomain dimerization. (2003, background): “additional contributions from domain IV (Berezov et al., 2002; Schlessinger, 2002).”
Prediction and validation of the distinct dynamics of transient and sustained ERK activation (2005, methodology): “(e) Rap1 activation at steady state derived from equation (1), where pR is given by a constant, α.”
Quantum dot ligands provide new insights into erbB/HER receptor–mediated signal transduction (2004, background): “Ligand binding leads to auto- and transactivation of cytoplasmic protein kinase domains in response to the formatio”