Jimmy Massenet

This study shows that Ctcf deficiency in myofibers leads to genome reprogramming and myopathy by disrupting 3D genome structure and gene regulation.

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 3D chromatin changes during human muscle stem cell state transition, showing increased CTCF binding at PAX7 enhancers stabilizes the stem cell state.

This paper identifies a new function of MYOD as a transcriptional repressor through E-box-independent chromatin binding, revealing a mechanism to repress gene expression and maintain cell identity during myogenesis.

The paper investigates how epigenetic changes in muscle stem cells from Duchenne Muscular Dystrophy patients lead to loss of myogenic identity and identifies MEF2B as a key mediator.