Jun Nakamura

 

Research Associate Professor 
Environmental Sciences & Engineering

Jun Nakamura’s Biosketch 
Curriculum Vitae 
REACH NC (Collexis) Research Profile

Office

354 Rosenau Hall 
135 Dauer Drive 
Campus Box 7431 
27599-7431 
USA 
T: 919-966-6140 
ynakamur@email.unc.edu


Education

1984  Osaka Prefecture University  MS, Veterinary Science

1984  Osaka Prefecture University  DVM, Veterinary Medicine

1999  University of North Carolina at Chapel Hill  PhD, Environmental Sciences and Engineering


Research Interests

  • Aging
  • Cancer
  • Environment (general)
  • Technology

 Research Activities

Dr. Nakamura’s interests focus on investigating mechanisms of DNA damage response to endogenous and exogenous reactive agents. The reverse genetic approach provides a powerful method for the study of gene function and regulation. DT40 cells originated from a chicken B-lymphocyte line and their knockout mutants are observed to show a strong phenotypic resemblance to murine mutants. Using a series of isogenic DT40 knockout mutants with high-throughput format, we determined that cells deficient in the FANC/BRCA pathway and homologous recombination are hypersensitive to formaldehyde at concentrations found in human plasma. Until that time, formaldehyde had been determined to cause DNA-protein crosslinks but little was known about how such lesions are repaired. Our results suggest that the use of syngeneic mutant cell lines, which is a very modern technology, is capable of deciphering the physical causes of DNA damage that are missed by more classical technologies. Indeed, the use of syngeneic lines to the analytic ability of toxicology is worthy of interest to more than simply the DNA repair field. Dr. Nakamura is also interested in synthetic lethality caused by poly(ADPribose)polymerase inhibitors and their translational research.


Key Publications

Ridpath, J.R., Takeda, S., Swenberg, J.A., Nakamura, J. (2010) 
Convenient, multi-well plate-based DNA damage response analysis using DT40 mutants is applicable to a high-throughput genotoxicity assay with characterization of modes of action.
Environ Mol Mutagen, p.In Press.

Asagoshi, K., Tano, K., Chastain, II, P., Adachi, N., Sonoda, E., Kikuchi, K., Koyama, H., Nagata, K., Kaufman, D., Takeda, S., Wilson, S.H., Watanabe, M., Swenberg, J.A., Nakamura, J. (2010) 
FEN1 Functions in Long Patch Base Excision Repair Under Conditions of Oxidative Stress in Vertebrate Cells
Mol Can Res: vol.21, p.204-15.

Pachkowski, B.F., Tano, K., Afonin, V., Elder, R.H., Takeda, S., Watanabe, M., Swenberg, J.A., Nakamura, J. (2009) 
Cells deficient in PARP-1 show an accelerated accumulation of DNA single strand breaks, but not AP sites, over the PARP-1-proficient cells exposed to MMS
Mutat Res: vol.671, p.93-9.

Masunaga, S., Tano, K., Watanabe, M., Kashino, G., Suzuki, M., Kinashi, Y., Ono, K., Nakamura, J. (2009) 
Evaluation of the potential of hexamethylenetetramine as a combined agent with gamma-radiation and cisplatin treatment in vivo, compared with tirapazamine.
Brit J Radiol.: vol.82, p.392-400.

Ridpath, J.R., Nakamura, A., Tano, K., Luke, A.M., Sonoda, E., Arakawa, H., Buerstedde, J.-M., Gillespie, D.A.F., Sale, J.E., Yamazoe, M., Bishop, D.K., Takata, M., Takeda, S., Watanabe, M., Swenberg, J.A., Nakamura, J. (2007) 
Cells deficient in the FANC/BRCA pathway are hypersensitive to plasma levels of formaldehyde.
Cancer Research: vol.67, p.11117-11122.