Jaideep Singh Rose Hills
Investigating Rad23b as a Mediator of Copper Homeostasis in the Liver
In humans, copper (Cu) regulates cellular respiration, antioxidant defense, cell proliferation, and apoptosis as a redox-active cofactor and signaling molecule. While vital, Cu is toxic when misregulated. Cu misregulation can lead to genetic disorders such as Wilson’s disease, characterized by excessive copper accumulation, and Menkes disease, marked by severe copper deficiency. Both cause neurodegeneration and developmental issues, underscoring the need to study Cu transport for better treatments. Recent findings from Chang Lab revealed a novel connection in the Cu homeostasis pathway, identifying RAD homolog B (Rad23b) as a potential metalloadapter linking Cu uptake to intracellular distribution. However, the mechanism by which it regulates Cu homeostasis and liver metabolism in vivo is unclear. The goal of my project is to characterize the effects of Rad23b knockout in mouse liver cells, where Cu metabolism is highest. Understanding how Rad23b regulates liver physiology may reveal a novel therapeutic target for diseases of Cu imbalance, paving the way for effective treatments that could improve the quality of life for thousands affected.
Message To Sponsor
Thank you for your kind donation to support my summer research and provide me with this opportunity to grow as a researcher. Within this project, I hope to discover a new function of RAD23B and make possible contributions to the copper-related disease treatments in the future. I am deeply grateful for your support enabling me to explore my research interests!