Christopher J. Chang

This study shows that CTR1-mediated copper uptake is essential for pTH17 cell differentiation and function in autoimmune disease by linking copper homeostasis to metabolic and epigenetic regulation.

The paper develops membrane-targeted TurboID variants for in vivo proteomics in neuronal circuits, identifying subcellular proteins and their changes during acute drug exposure.

This study shows that copper import via CTR1 supports the β3-adrenergic thermogenic program by enhancing mitochondrial oxidation and thermogenic capacity in adipose tissues.

The paper shows liver-targeted copper supplementation reduces steatosis by enhancing lipolysis and fatty acid oxidation through copper-dependent metabolic pathways.

This study shows that reduced hepatic phosphatidylcholine biosynthesis leads to copper deficiency, which promotes MASH through disrupted copper distribution and fibrogenesis.

The paper develops chiral reagents to identify stereospecific methionine oxidation sites and shows their functional impact on protein activity in oxidative stress models.

The paper shows that lysosomes in C. elegans expand to store zinc, copper, and manganese, with metal transporters localizing to both acidified and expansion compartments.

The paper shows that the PBAF chromatin remodeling complex regulates metal homeostasis in myoblasts via Mtf1, with metal supplementation compensating for some complex deficiencies.

This paper evaluates melatonin as a dual-function therapeutic for Wilson disease, showing it reduces copper toxicity and oxidative stress in vitro and in vivo.

This study shows that endothelial CTR1 senses disturbed flow by increasing mitochondrial copper, leading to cuproptosis and atherosclerosis, and identifies a therapeutic target.

This study identifies mCrip2 as a copper-responsive regulator of skeletal muscle differentiation through functional and biochemical analyses in murine myoblasts.

This paper identifies swip-10's role in systemic copper homeostasis in C. elegans, linking it to mitochondrial function, oxidative stress, and neurodegeneration.

The paper identifies a mechanism where post-synaptic mushroom body neurons generate carbon monoxide to induce localized dopamine release from presynaptic terminals, facilitating memory-related plasticity.