RAStoERK: A reference interaction atlas for insights into signaling and disease
The RAS/RAF/MEK/ERK pathway has been extensively studied for its roles in physiology and disease, yet a systems-level view of its interplay with the broader cellular context is lacking, limiting insight into paralog-specific roles, mutation-driven rewiring, and cross-pathway integration. To address this, we simultaneously mapped the interactomes of all pathway components and their activating and inactivating mutations, identifying 2,500 high-confidence interactors, 88% of which previously unreported, and generating a high-confidence, comprehensive reference map of the pathway in resting and activated states. The pathway behaves like a "molecular organism" that connects to other signaling complexes, operates from distinct subcellular sites, and integrates into networks relevant to physiology and disease. Dataset exploration uncovers paralog- and mutation-specific interaction signatures and pathway-level crosstalk, including previously unknown connections to mRNA metabolism and WNT signaling. The interactomes available at RAStoERK.univie.ac.at provide a foundational community resource for unbiased discovery, targeted mechanistic studies, and potential therapeutic exploration.
Authors
- Sebastian Didusch (ORCID: https://orcid.org/0000-0003-2511-834X)
- Georg Vucak (ORCID: https://orcid.org/0009-0004-4224-9151)
- Manuela Baccarini (ORCID: https://orcid.org/0000-0002-3033-391X)
- Markus Hartl (ORCID: https://orcid.org/0000-0002-4970-7336)
- Leandro Cannizzaro
- Ana Santiago
- Jörg Menche
Institutions
- University of Vienna (AT)
- Austrian Academy of Sciences (AT)
- Max Perutz Labs (AT)
- CeMM Research Center for Molecular Medicine (AT)
- Vienna Biocenter (AT)
- Ludwig Boltzmann Institute for Network Medicine at the University of Vienna (AT)
- Medical University of Vienna (AT)
Publication Details
- Journal
- Cell Reports
- Published
- 2026-10-26
- DOI
- https://doi.org/10.1016/j.celrep.2026.118201
- Primary Topic
- Protein Kinase Regulation and GTPase Signaling
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- Austrian Science Fund