Tom H. Cheung

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 age- and sex-related changes in the mouse myelin proteome, revealing increased structural proteins and decreased cytoskeletal and synaptic proteins with aging.

The paper identifies neuronal proteins that degrade slower with aging and accumulate in microglia, linking impaired synaptic protein turnover to age-related cognitive decline.

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 identifies a microglia population that takes up circulatory proteins, enhancing phagocytosis and innate immunity through ApoA-I uptake.