Nils Helge Schebb

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.

Information & Authors Information Published In Science Signaling Volume 18 | Issue 887 May 2025 Copyright Copyright © 2025 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. This is an article distributed under the terms of the Science Journals Default License. Article versions Submission history Received: 20 January 2025 Accepted: 24 April 2025 Permissions Request permissions for this article.

Editor’s summary Pseudohypoparathyroidism type Ic is caused by maternally inherited loss-of-function mutations in the gene that encodes the Gαs subunit (GNAS), which is activated by G protein–coupled receptors (GPCRs). Redfern-Nichols et al. investigated how two of these Gαs variants, L388R and E392K, affected GPCR signaling in the kidney, where only the maternal copy of GNAS is expressed.