KAMADA, Shinji, Ph.D.

Professor, Division of Biosignal Transduction, Laboratory of Gene Function

Research Interests

　Organisms, including humans, are living in the environments that involve many stresses inducing DNA damages. Cells containing damaged DNA quickly respond to arrest the cell cycle, leading to DNA repair, apoptosis, or senescence. Apoptosis usually offers advantages during the life cycle of a multicellular organism. If damages are too severe to repair, cells die by apoptosis and are engulfed by surrounding cells, leading to quick removal of the dead cells to prevent inflammation. In addition, defects in apoptotic processes have been implicated in a variety of diseases. Excessive apoptosis causes atrophy such as neurodegenerative disorders, whereas an insufficient amount of apoptosis results in uncontrolled cell proliferation such as cancer. On the other hand, another form of cellular response to DNA damages is senescence. Senescence was first mentioned as a state of irreversible growth arrest of normal human fibroblasts, and induced by a variety of stimuli including DNA damages. Recently, it was suggested that senescence functions as an effective tumor suppression mechanism by preventing cell proliferation. DNA damages can induce both apoptosis and senescence. However, the molecule mechanisms of cell fate decision between apoptosis and senescence have been under investigation. Our main Research Interest is to clarify how cells are destined for apoptosis or senescence by the same DNA damages.

Research Focus

1. The regulation of apoptosis and cell cycle progression by caspases.

2. Molecular mechanisms of apoptosis and senescence induced by DNA damages.

Recent Publication

• Nagano T., Awai Y., Kuwaba S., Osumi T., Mio K., Iwasaki T., and Kamada S. (2021)
  Riboflavin transporter SLC52A1, a target of p53, suppresses cellular senescence by activating mitochondrial complex II.
  Mol. Biol. Cell. 32:br10.
  
• Nagano T., Iwasaki T., Onishi K., Awai Y., Terachi A., Kuwaba S., Asano S., Katasho R., Nagai K., Nakashima A., Kikkawa U., and Kamada S. (2021)
  LY6D-induced micropinocytosis as a survival mechanism of senescent cells.
  J. Biol. Chem. 296, 1000049.
  
• Nagano T., Yamao S., Terachi A., Yarimizu H., Itoh H., Katasho R., Kawai K., Nakashima A., Iwasaki T., Kikkawa U., and Kamada S. (2019)
  D-amino acid oxidase promotes cellular senescence via the production of reactive oxygen species.
  Life Sci. Alliance 2, e201800045.
  
• Nagano T., Nakashima A., Onishi K., Kawai K., Awai Y., Kinugasa M., Iwasaki T., Kikkawa U., and Kamada S. (2017)
  Proline dehydrogenase promotes senescence through the generation of reactive oxygen species.
  J. Cell Sci.130, 1413-1420.
  
• Nagano T., Nakano M., Nakashima A., Onishi K., Yamao S., Enari M., Kikkawa U., and Kamada S. (2016)
  Identification of cellular senescence-specific genes by comparative transcriptomics.
  Sci. Rep. 6: 31758.

Contact

Office: Biosignal Research Center 4F

Tel&Fax: +81-78-803-5959

Fax: +81-78-803-5951

E-mail: skamada@kobe-u.ac.jp