B. Ghesquiere

Integrating multiple omics levels using the human protein complexome as a framework, a multi-omics study of inborn errors of metabolism

This study integrates proteomics, transcriptomics, and metabolomics data from IEM patients to identify perturbed protein complexes and pathways, highlighting mitochondrial oxidative phosphorylation and histone acetylation dysregulation.

Ancient genomic linkage couples metabolism with erythroid development

This study identifies Nprl3 as a key regulator of erythroid metabolism, showing its role in coupling metabolic and developmental processes during erythropoiesis.

HIF-1α-mediated mitochondrial-glycolytic reprogramming controls the transition of precursor to terminally exhausted T cells

This study identifies HIF-1α-mediated metabolic reprogramming as a mechanism controlling the transition of precursor T cells to terminally exhausted T cells in chronic infections and cancer.

13C tracer analysis reveals the landscape of metabolic checkpoints in human CD8+ T cell differentiation

This study uses 13C metabolomics and transcriptomics to analyze metabolic changes in CD8+ T cells during differentiation, identifying key metabolic checkpoints and their role in exhaustion.

Intracellular BAPTA directly inhibits PFKFB3, thereby impeding mTORC1-driven Mcl-1 translation and killing Mcl-1-addicted cancer cells

This paper shows that BAPTAi inhibits PFKFB3, reducing mTORC1-driven Mcl-1 translation and killing Mcl-1-dependent cancer cells, independent of Ca2+ signaling.

ANTIMETABOLIC COOPERATIVITY WITH THE CLINICALLY APPROVED KIDROLASE AND TYROSINE KINASE INHIBITORS TO ERADICATE CML STEM CELLS

This study shows that combining tyrosine kinase inhibitors with Kidrolase targets glutamine metabolism and enhances CML stem cell eradication.

Exostosin-1 Glycosyltransferase Regulates Endoplasmic Reticulum Architecture and Dynamics

This study shows that Exostosin-1 glycosyltransferase regulates ER morphology and dynamics, affecting cell size and metabolic processes in mammalian cells.