MDM4 exon skipping upon dysfunctional ribosome assembly
Recent studies revealed how nucleolar stress enhances MDM4 exon skipping and activates p53 via the ribosomal protein L22 (RPL22; eL22). Tumor-associated L22 mutations lead to full-length MDM4 synthesis, overcoming tumor suppression by p53. This forum article explores how MDM4 splicing patterns integrate stress signaling to take p53-dependent cell fate decisions.
Authors
- Matthias Dobbelstein (ORCID: https://orcid.org/0000-0001-5052-3967)
- Jennifer Jansen (ORCID: https://orcid.org/0000-0001-6993-3069)
Institutions
- Max Planck Institute for Biophysical Chemistry (DE)
- Max Planck Institute of Experimental Medicine (DE)
- University of Göttingen (DE)
Publication Details
- Journal
- Trends in Cell Biology
- Published
- 2024-11-07
- DOI
- https://doi.org/10.1016/j.tcb.2024.10.006
- Citations
- 4
- Primary Topic
- Cancer-related Molecular Pathways
- Type
- article
- Field-Weighted Citation Impact
- 1.13
Funders
- Deutsche Forschungsgemeinschaft
- Studienstiftung des Deutschen Volkes