Bio

TAK1 (MAP3K7) lab  mediates inflammation leading to many age-related chronic inflammatory diseases such as neurodegenerative diseases. Environmental stressors, pathogens, as well as metabolic changes are potential activator of TAK1. We are working on the mechanisms of TAK1 activation, and exploring the possibility of targeting TAK in chronic inflammatory diseases.

Awards

2021, The Research Leadership Academy

Publications

• TAK1 inhibition activates pore-forming proteins to block intracellular bacterial growth through modulating mitochondria , Cell Death and Disease (2025)
• Abstract 1191 TAK1 inhibition translocates pore-forming proteins, MLKL and gasdermins into mitochondria to generate reactive oxygen species , Journal of Biological Chemistry (2024)
• Abstract 1192 The Mechanism and Roles of TAK1 hyperactivation in the Alzheimer's Disease Mouse Model , Journal of Biological Chemistry (2024)
• Modulation of iron metabolism by new chemicals interacting with the iron regulatory system , Redox Biology (2024)
• Aberrantly activated TAK1 links neuroinflammation and neuronal loss in Alzheimer's disease mouse models , Journal of Cell Science (2023)
• TAK1 inhibition elicits mitochondrial ROS to block intracellular bacterial colonization , Proceedings of the National Academy of Sciences (2021)
• Coordinating Tissue Regeneration Through Transforming Growth Factor-β Activated Kinase 1 Inactivation and Reactivation , Stem Cells (2019)
• Necroptosis mediators RIPK3 and MLKL suppress intracellular Listeria replication independently of host cell killing , The Journal of Cell Biology (2019)
• Compound mutations in Bmpr1a and Tak1 synergize facial deformities via increased cell death , genesis (2018)
• Erratum: Noncanonical cell death program independent of caspase activation cascade and necroptotic modules is elicited by loss of TGFβ-activated kinase 1 , Scientific Reports (2017)