Óscar Fernández-Capetillo

The paper identifies RUVBL1/2-RPAP3 interface as a vulnerability and develops de novo protein binders that selectively disrupt R2TP, reducing PIKK levels without affecting other RUVBL1/2 complexes.

This study shows that ARC acts as a retroviral-like capsid for TDP-43 spreading in ALS and FTD, and that Lenacapavir blocks this process.

This study identifies the accumulation of orphan ribosomal proteins as a molecular hallmark of ALS, linking it to various ALS-related mutations and neurotoxins.

The paper identifies 70 antiviral compounds against Puumala Orthohantavirus through a drug repurposing screen in human cell lines.

The paper identifies a chemical inducer of ribophagy, SALSa, that reduces toxicity of ALS-related arginine-rich peptides and extends lifespan in a Drosophila model.

The paper identifies genetic factors that influence cancer cells' sensitivity to nucleolar stress-inducing drugs through CRISPR screens, revealing roles for P53, RB1, and PI3K/mTOR signaling.

This study identifies GNF-7 as a senolytic drug that activates GCN2 to kill senescent cells, showing synergy with CDK4/6 inhibitors in preclinical models.

This study identifies novel SETD8 inhibitors and shows their toxicity correlates with ribosome biogenesis regulators, suggesting a biomarker for targeted cancer therapy.

The paper identifies clofazimine as a drug that reduces polyQ toxicity by activating PPARγ, improving mitochondrial function in models of polyQ diseases.

This study shows that arginine-rich peptides cause nucleolar stress, leading to ribosomopathy and accelerated ageing in mice, with mTOR inhibition alleviating lifespan reduction.

The paper introduces DRE, a web server that enables drug repurposing analyses across 20 organisms using 198 million drug-signature associations.

This paper introduces a high-throughput platform for identifying host binding factors and antiviral drug targets by overcoming limitations in host plasma membrane complexity.

The paper identifies chemical and genetic regulators of the tetracycline-inducible gene expression system in mammalian cells, showing that FDA-approved drugs and genetic modifiers inhibit the system rather than alleviate TDP-43 toxicity.

This study identifies SPHK inhibitors as a new class of translation suppressors independent of mTOR, linking lipid metabolism to mRNA translation.

This study shows arginine-rich CPPs like (PR)n displace DNA- and RNA-binding factors, impairing nucleic acid processes and causing toxicity, similar to PROTAMINE's effects.