Justine M Keth

Editor’s summary In response to a specific type of anticancer kinase inhibitors, a gain-of-function mutation in the small GTPase Rac1 results in the persistent formation of subcellular protrusions called lamellipodia, which are linked to inactivation of the tumor suppressor merlin and cellular proliferation. Weiss et al. found that mutant Rac1 activity and merlin inactivation were localized to a microdomain within lamellipodia in cancer cells treated with one of these kinase inhibitors.

Authors Carolina Franco Nitta, Department of Pathology, University of New Mexico, Albuquerque, United States Ellen W. Green, Department of Pathology, University of New Mexico, Albuquerque, United States Elton D. Jhamba, Department of Pathology, University of New Mexico, Albuquerque, United States Justine M. Keth, Department of Pathology, University of New Mexico, Albuquerque, United States Iraís Ortiz-Caraveo, Department of Pathology, University of New Mexico, Albuquerque, United States Rachel M.

Abstract Crosstalk between different receptor tyrosine kinases (RTKs) is thought to drive oncogenic signaling and allow therapeutic escape. EGFR and RON are two such RTKs from different subfamilies, which engage in crosstalk through unknown mechanisms. We combined high-resolution imaging with biochemical and mutational studies to ask how EGFR and RON communicate.