The research of Joseph Huang’s group is directed toward unraveling the signaling events that direct protein trafficking in co-translational protein folding as well as toward understanding the role that protein misfolding plays in neuron degenerative diseases. It is now well known that the synthesis and correct folding of proteins within the living cell is regulated by various chaperones. The failure of this process may lead to protein aggregation and cause many different neuron degenerative disorders. Dr. Huang’s team and collaborators are developing novel biophysical/chemical techniques to investigate interactions between the chaperones and the ribosome during the protein translation process. At the moment, this group is focusing on the TAR (trans-activation response element) DNA binding protein (TDP-43) in Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal Lobar Dementia (FTLD). Studies are in progress to elucidate the participation of the chaperones in preventing protein aggregation in this system. From these studies, this group hopes to eventually develop new therapeutic strategies against different neurodegenerative disorders. As a member of the NPAS (Neuroscience Program in Academia Sinica, Link to the Website), Dr. Huang’s team is also investigating the proteinopathy of misfolded proteins in human diseases in general.
Current specific interests are listed below: