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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Michael A. O'Reilly

Dept. of Pediatrics

Box 850

The Univ. of Rochester

School of Medicine and Dentistry

[email]@*.rochester.edu

Name/email consistency: high

 
 
 
 
 
 
 

Affiliations

  • Dept. of Pediatrics, Box 850, The Univ. of Rochester, School of Medicine and Dentistry. 2003 - 2013
  • Department of Pediatrics, School of Medicine and Dentistry, Children's Hospital at Strong, University of Rochester, USA. 2000 - 2005
  • Division of Neonatology, Department of Pediatrics, and Department of Radiation Oncology, School of Medicine and Dentistry, USA. 2000

References

  1. Neonatal hyperoxia alters the host response to influenza A virus infection in adult mice through multiple pathways. Buczynski, B.W., Yee, M., Martin, K.C., Lawrence, B.P., O'Reilly, M.A. Am. J. Physiol. Lung Cell Mol. Physiol. (2013) [Pubmed]
  2. Angiotensin II: tapping the cell cycle machinery to kill endothelial cells. O'Reilly, M.A. Am. J. Physiol. Lung Cell Mol. Physiol. (2012) [Pubmed]
  3. Lung development and the host response to influenza A virus are altered by different doses of neonatal oxygen in mice. Buczynski, B.W., Yee, M., Paige Lawrence, B., O'Reilly, M.A. Am. J. Physiol. Lung Cell Mol. Physiol. (2012) [Pubmed]
  4. Neonatal hyperoxia enhances the inflammatory response in adult mice infected with influenza A virus. O'Reilly, M.A., Marr, S.H., Yee, M., McGrath-Morrow, S.A., Lawrence, B.P. Am. J. Respir. Crit. Care Med. (2008) [Pubmed]
  5. Type II epithelial cells are critical target for hyperoxia-mediated impairment of postnatal lung development. Yee, M., Vitiello, P.F., Roper, J.M., Staversky, R.J., Wright, T.W., McGrath-Morrow, S.A., Maniscalco, W.M., Finkelstein, J.N., O'Reilly, M.A. Am. J. Physiol. Lung Cell Mol. Physiol. (2006) [Pubmed]
  6. Redox activation of p21Cip1/WAF1/Sdi1: a multifunctional regulator of cell survival and death. O'Reilly, M.A. Antioxid. Redox Signal. (2005) [Pubmed]
  7. p21(Cip1/WAF1/Sdi1) does not affect expression of base excision DNA repair enzymes during chronic oxidative stress. O'reilly, M.A., Vitiello, P.F., Gehen, S.C., Staversky, R.J. Antioxid. Redox Signal. (2005) [Pubmed]
  8. The Cdk and PCNA domains on p21Cip1 both function to inhibit G1/S progression during hyperoxia. Helt, C.E., Staversky, R.J., Lee, Y.J., Bambara, R.A., Keng, P.C., O'Reilly, M.A. Am. J. Physiol. Lung Cell Mol. Physiol. (2004) [Pubmed]
  9. Activation of the G2 cell cycle checkpoint enhances survival of epithelial cells exposed to hyperoxia. O'Reilly, M.A., Staversky, R.J., Finkelstein, J.N., Keng, P.C. Am. J. Physiol. Lung Cell Mol. Physiol. (2003) [Pubmed]
  10. Induced p21Cip1 in premature baboons with CLD: implications for alveolar hypoplasia. O'Reilly, M.A., Watkins, R.H., Staversky, R.J., Maniscalco, W.M. Am. J. Physiol. Lung Cell Mol. Physiol. (2003) [Pubmed]
  11. The cyclin-dependent kinase inhibitor p21 protects the lung from oxidative stress. O'Reilly, M.A., Staversky, R.J., Watkins, R.H., Reed, C.K., de Mesy Jensen, K.L., Finkelstein, J.N., Keng, P.C. Am. J. Respir. Cell Mol. Biol. (2001) [Pubmed]
  12. DNA damage and cell cycle checkpoints in hyperoxic lung injury: braking to facilitate repair. O'Reilly, M.A. Am. J. Physiol. Lung Cell Mol. Physiol. (2001) [Pubmed]
  13. p53-independent induction of GADD45 and GADD153 in mouse lungs exposed to hyperoxia. O'Reilly, M.A., Staversky, R.J., Watkins, R.H., Maniscalco, W.M., Keng, P.C. Am. J. Physiol. Lung Cell Mol. Physiol. (2000) [Pubmed]
  14. Bcl-2 family gene expression during severe hyperoxia induced lung injury. O'Reilly, M.A., Staversky, R.J., Huyck, H.L., Watkins, R.H., LoMonaco, M.B., D'Angio, C.T., Baggs, R.B., Maniscalco, W.M., Pryhuber, G.S. Lab. Invest. (2000) [Pubmed]
 
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