Jun Ninomiya-Tsuji

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.

Publications

• Modulation of iron metabolism by new chemicals interacting with the iron regulatory system , REDOX BIOLOGY (2024)
• TAK1 inhibition translocates pore-forming proteins, MLKL and gasdermins into mitochondria to generate reactive oxygen species , JOURNAL OF BIOLOGICAL CHEMISTRY (2024)
• The Mechanism and Roles of TAK1 hyperactivation in the Alzheimer's Disease Mouse Model , JOURNAL OF BIOLOGICAL CHEMISTRY (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 OF THE UNITED STATES OF AMERICA (2021)
• Coordinating Tissue Regeneration Through Transforming Growth Factor-beta Activated Kinase 1 Inactivation and Reactivation , STEM CELLS (2019)
• Necroptosis mediators RIPK3 and MLKL suppress intracellular Listeria replication independently of host cell killing , 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)
• Noncanocial cell death program independent of caspase activation cascade and necroptotic modules is elicited by loss of TGF beta-activated kinase 1 , SCIENTIFIC REPORTS (2017)