Luiz C. Godoy, Ph.D.
Massachusetts Institute of Technology
Department of Biological Engineering
77 Massachusetts Avenue
Cambridge, MA 02139
Dr. Godoy earned his bachelor's degree in Biological Sciences from the Federal University of São Carlos, Brazil, in 1997. In 2003, he obtained his PhD in Microbiology and Immunology at the Federal University of São Paulo. Since then, Dr. Godoy has held postdoctoral appointments in the University of São Paulo Medical School (2003-2005) and the University of Massachusetts Medical School (2005-2008). He joined Dr. Wogan's research group as a postdoctoral associate in March 2008.
Research Interests and Goals
Dr. Godoy has a strong background in immunology, having worked extensively on a mouse model of a systemic mycosis during his PhD training. During his postdoctoral experience, he has studied the involvement of nitric oxide in cell signaling in several contexts. At the University of Sao Paulo, he characterized the S-nitrosation-mediated regulatory property of nitric oxide in signaling initiated by the molecule CD40, with important implications for the fate of inflammation in pathological conditions such as sepsis. The peroxynitrite-dependent effects of nitric oxide were the object of his research at the University of Massachusetts, leading to the finding of a mechanism of resistance to oxidative stress in which the nuclear translocation of cytochrome c plays an important role. Currently, Dr. Godoy is investigating regulatory properties of nitric oxide in mechanisms controlling growth and resistance to chemotherapeutic agents in human melanoma cells.
Search PubMed for articles
Godoy LC et al. Endogenously produced nitric oxide mitigates sensitivity of melanoma cells to cisplatin. Proc Natl Acad Sci USA, 109(50): 20373-8, 2012.
Chowdhury R et al. Nitric oxide produced endogenously is responsible for hypoxia-induced HIF-1α stabilization in colon carcinoma cells. Chem Res Toxicol, 25(10): 2194-202, 2012.
Godoy, LC, et al. Loss of CD40 endogenous S-nitrosylation during inflammatory response in endotoxemic mice and patients with sepsis. Shock, 33(6): 626-633, 2010.
De Lorenzo BH, et al. Macrophage suppression following phagocytosis of apoptotic neutrophils is mediated by the S100A9 calcium-binding protein. Immunobiology, 215(5): 341-347, 2010.
Godoy LC, et al. Disruption of the M80-Fe ligation stimulates the translocation of cytochrome c to the cytoplasm and nucleus in nonapoptotic cells. Proc Natl Acad Sci USA, 106(8): 2653-2658, 2009.
Li CQ, et al. Nitric oxide activation of Keap1/Nrf2 signaling in human colon carcinoma cells. Proc Natl Acad Sci USA, 106(34): 14547-14551, 2009.
Popi, AF, et al. B-1 cells facilitate Paracoccidioides brasiliensis infection in mice via IL-10 secretion. Microbes and Infection, Jun;10(7): 817-824, 2008.
Brito, RRN, et al. Role of distinct immune components in the radiation-induced abrogation of systemic lupus erythematosus development in mice. Lupus (Basingstoke), 16: 947-954, 2007.
Godoy, LC, et al. Immunity and hypersensitivity to gp43 in susceptible and resistant mice infected with Paracoccidioides brasiliensis. Medical Mycology, Oct;41(5): 427-436, 2003.