Alexandre R. Colas

This study identifies SAA1-TLR4 signaling as a tumor-derived pathway driving muscle wasting in pancreatic cancer, showing that targeting this pathway can preserve muscle mass and improve survival without affecting tumor growth.

The paper identifies ribosomal protein genes as contributors to hypoplastic left heart syndrome through functional analysis across multiple model systems.

This study identifies Tenascin-C as a key factor promoting muscle stem cell self-renewal through Annexin A2 signaling, showing its role in muscle repair and aging.

The paper shows that reduced nucleosome stability impairs cell identity, stress resilience, and healthy aging across species.

The paper identifies mitochondrial MICOS complex genes, CHCHD3 and CHCHD6, as contributors to hypoplastic left heart syndrome through functional studies in Drosophila and genetic analysis of patient cohorts.

The paper identifies genetic networks and regulatory elements associated with cardiac performance variation in Drosophila and finds conserved genetic architecture between flies and humans.

This study identifies NAC and SRP as novel regulators of cardiac development and remodeling in Drosophila and human cardiac progenitors, showing their spatial and temporal regulation in heart formation.

This study identifies PGC1/PPAR signaling and its regulators Yap1 and SF3B2 as key drivers of cardiomyocyte maturation through single-cell transcriptomic analysis across neonatal to adult hearts.

The paper identifies LRP2 as a novel genetic driver of hypoplastic left heart syndrome using whole genome sequencing and multi-model systems.