R. Ferreira

The paper shows that nucleotide depletion and DNA replication stress drive cell fate transitions in hematopoietic systems by activating lineage-specific maturation genes.

This study identifies hypoxia and glucose deprivation as drivers of aggressiveness in bladder cancer through metabolic adaptation and altered glycosylation.

This study develops a CRISPR-dCas9 platform to enhance malonyl-CoA production in yeast through laboratory evolution.

The paper screens compounds targeting metabolism in serum-derived medium to identify differential responses in cancer cells, aiming to improve drug response prediction.

This study identifies naphthoquinone derivatives as inhibitors of SARS-CoV-2 proteases Mpro and PLpro through virtual screening and biochemical assays.

This study shows that bladder cancer cells become more aggressive under hypoxia and glucose deprivation through metabolic and glycosylation changes.

This study identifies the nucleolar surveillance pathway (NSP) as a central regulator of p53 stability, showing its role in integrating various cellular stresses and its potential as a therapeutic target in cancer.

The paper uses isotope tracing to compare metabolism between cancer cells and fibroblasts in pancreatic tumors, identifying key metabolic dependencies in cancer cells.

This study identifies DDAs as compounds that upregulate DR5 in cancer cells, leading to apoptosis and synergy with TRAIL, with selectivity for oncogene-transformed cells.

The paper challenges the validity of an occluded conformation of human P-glycoprotein, suggesting it may be an artifact from nanodisc size limitations.

This paper develops an immunoassay for sSIGLEC-1, showing its association with IFN signature, ancestry, and renal disease in SLE.