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. 2012 Jul 10;7(7):e40671. doi: 10.1371/journal.pone.0040671

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Steinestel et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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Ligand-binding to membrane-associated receptor tyrosine kinase (RTK) leads to an activation of RAS, which is constitutively activated in mutant KRAS (*). Activated KRAS activates - among others - both the B1 Rapidly accelerated fibrosarcoma (BRAF)- and Phosphatidylinositol-3-kinase (PI3K)-pathway, only the latter leading to activation of the Abi1/Sos1/Eps8 complex. Via activation of the small GTPase Rac, this leads to reorganization of the actin cytoskeleton and to a change in cellular shape. RTK: receptor tyrosine kinase; KRAS: Kirsten rat sarcoma; BRAF: B1 Rapidly accelerated fibrosarcoma; PI3K: Phosphatidylinositol-3-kinase; Abi1: Abelson interactor 1; Eps8: Epidermal growth factor receptor kinase substrate; Sos1: Son of sevenless homolog 1; Rac: Ras-related C3 botulinum toxin substrate.