Ken Inoki

Our Research

In response to growth factors and nutrients, target of rapamycin (TOR) plays essential roles in a wide array of cellular processes including protein translation, gene transcription, apoptosis and autophagy. Dysregulation of mammalian TOR (mTOR) signaling pathway is involved in the development of diseases including cancer and metabolic diseases.

Using biochemical and genetic approaches,we are investigating the function and regulation of the mTOR signaling pathway and the role of mTOR signaling in disease.

About Ken Inoki

Specialties:
  • Metabolism
  • Nephrology
  • mTOR pathway signalling

Ken Inoki is investigating the function and regulation of the mTOR signaling pathway. Disregulation of this pathway is involved in development of a number of human diseases. His research interests include both physiological and pathological roles of TSC-mTOR signaling in human health and their implication in diabetes, aging and cancer.

Highlight: Switching between anabolic and catabolic

The Inoki lab found that disrupting the interaction between a protein called AMPK - a key part of regulating the balance between consuming and producing energy in cells - and a molecule called GSK3 can help restore the energy consumption-production balance. In metabolic disorders like obesity, this balance is tipped away from consuming energy, making enhancement of AMPK activity is a promising therapeutic strategy.

The research was published April 25 in Molecular Cell.

Recent Publications

Suzuki T, Bridges D, Nakada D, Skiniotis G, Morrison SJ, Lin J, Saltiel AR, Inoki K. (2013) Inhibition of AMPK catabolic action by GSK3. Mol Cell. (In Press)

Henry FE, McCartney AJ, Neely R, Perez AS, Carruthers CJ, Stuenkel EL, Inoki K, Sutton MA. (2012) Retrograde changes in presynaptic function driven by dendritic mTORC1. J Neurosci. 32(48):17128-42.

Fukuda A, Chowdhury MA, Venkatareddy MP, Wang SQ, Nishizono R, Suzuki T, Wickman LT, Wiggins JE, Muchayi T, Fingar D, Shedden KA, Inoki K, Wiggins RC. (2012) Growth-dependent podocyte failure causes glomerulosclerosis. J Am Soc Nephrol. 23(8):1351-63.