Frontier Research Institute for Interdisciplinary Sciences
Tohoku University

Researcher

Kyoko Chiba

Assistant Professor Life and Environments

Mentor Information
Professor
Shoichiro Kurata (Graduate School of Pharmaceutical Sciences)
Research Fields Biochemistry
Research Subjects
  • Regulation of Intracellular Transport
  • Mechanisms of Kinesin Activation
  • How motor proteins select their cargoes
  • How dysfunction of motor activity is related to human diseases
Academic Society Membership The Molecular Biology Society of Japan, The Japanese Biochemical Society, American Society for Cell Biology
Research Outline  

Our lives are supported by various logistics systems. Trains that carry people, trucks that carry luggage at convenience stores, tankers that carry oil ... Modern life is made up of these logistics systems. Similarly, there is a mechanism to transport luggage in our body. I am studying this mechanism called intracellular transport.

The protein I am focusing on is kinesin, which carries mitochondria and synaptic vesicles inside cells. In our society, kinesin is equivalent to a freight truck. Kinesin is normally in the garage (inactive state) to prevent waste of energy, but the engine is started by some switch and transportation starts (active state). The mechanism of this switching is not yet well understood.

I will work on elucidating the molecular mechanism by which kinesin is activated using a single-molecule observation method that allows direct observation of the movement of kinesin. By incorporating biological factors such as lipids into single molecule observation, I will construct an in vitro reconstitution system that reproduces intracellular transport.

Kinesin is the cause of neurodegenerative diseases. It is necessary to clarify how kinesin is controlled for the development of treatment methods. By clarifying the mechanism of kinesin activation, I would like to establish a new treatment strategy. When a pathogenic microorganism invades the cell, the protein derived from the microorganism hijacks kinesin-dependent transport instead of the endogenous mechanism. I would also like to clarify the reason why such a takeover occurs.

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