G. Superti-Furga

This study identifies orpinolide as a compound that disrupts cholesterol transport in leukemia by targeting OSBP, revealing a therapeutic strategy for leukemic dependencies.

This study identifies LRP8 as a targetable vulnerability in MYCN-amplified neuroblastoma by showing its role in selenocysteine import and resistance to ferroptosis.

This study uses gain-of-function genetic screens in human cells to identify SLC transporters that overcome nutrient limitations by enhancing uptake of essential amino acids.

This study identifies phosphatidic acid as critical for double membrane vesicle formation in HCV and SARS-CoV-2 replication, suggesting host-targeted PA synthesis inhibition as a therapeutic strategy.

This study analyzes SARS-CoV-2 superspreading events in Austria using genomic and epidemiological data to understand viral transmission and mutation dynamics.

The paper systematically maps genetic interactions among human solute carriers, identifying SLC25A51/MCART1 as a mitochondrial NAD(H) transporter.

The paper shows that mutations increasing efflux pump activity are more effective than inhibiting uptake transporters in reducing antibiotic internal concentrations, suggesting efflux inhibition as a better strategy for combating resistance.

This study identifies SLC transporters critical for drug resistance using CRISPR screens in human cells, revealing widespread roles of SLCs in drug uptake and activity.

This study identifies SLC35A1 and SLC30A1 as host factors influencing cell survival during VSV infection through genetic screens and apoptosis analysis.

This study identifies critical host-virus interaction nodes through network analysis and drug re-purposing, revealing key targets for antiviral therapies.

The paper uses pharmacogenomics data and regression models to identify drug-transporter relationships, uncovering both known and novel associations.

The paper uses genetic screens to identify SLC39A7 as a modulator of necroptosis by affecting TNF receptor trafficking and ER homeostasis.