Giulio Superti‐Furga

The paper analyzes physicochemical features of transmembrane protein-protein interfaces to determine their topology, finding that amino acid composition and secondary structure are key predictors.

This study identifies ARID5B as a chromatin repressor that interacts with HDAC1/2 to repress B cell-specific genes, linking its germline variants to B-ALL risk.

This study identifies small molecule inhibitors of the NaCT transporter by targeting an allosteric site, revealing a chemically distinct series with improved potency.

The paper identifies SAGA CORE subunits as essential for KAT2A stability, showing that their disruption leads to proteasomal degradation of KAT2A and reduced H3K9 acetylation.

The paper identifies genetic modules regulating KRAS proteostasis and shows that the oncogenic KRAS G12D mutant is less regulated by CRL3LZTR1, contributing to cancer progression.

The paper identifies inhibitor-induced kinase destabilization as a common phenomenon and reveals that it occurs through endogenous proteolytic mechanisms rather than classical ubiquitination.

This study identifies purine nucleobases as immunometabolites that enhance CD8+ T cell effector function by enabling a metabolic switch from de novo synthesis to salvage pathway.

The paper maps protein-protein interactions of 396 SLC transporters using interaction proteomics and functional assays, providing a resource for understanding SLC function and drug targeting.

The paper systematically identifies genetic interactions among human solute carrier proteins using CRISPR-Cas12a and -Cas9, revealing 1,236 interactions with growth phenotypes and highlighting SLC39A1's role in metabolic reprogramming.

The paper systematically evaluates the metabolic and transcriptional effects of SLC superfamily members, identifying new substrates and functional groups.

The paper creates a functional landscape of human solute carriers by integrating multi-omics data and curated knowledge, assigning functions to each SLC and providing a web-accessible resource.

The paper performs a genome-wide CRISPR/Cas9 knock-out screen to identify genes involved in phagocytosis, validates key complexes, and maps their functional roles in human cells.

This study identifies PCYT2 as critical for muscle health and aging, showing its deficiency causes muscle weakness and aging, and demonstrates therapeutic potential through AAV-based delivery.