Molecular biology of transaldolase—We have shown that changes in the level of transaldolase expression alter activity of the oxidative phase of the pentose phosphate pathway, NADPH production, and consequently, regeneration of intracellular glutathione and the maintenance of mitochondrial transmembrane potential. Transaldolase activity influences susceptibility to cell death signals, including Fas- and HIV-induced pathways. TAL serves as a critical determinant of tissue and cell type-specific functioning of the PPP and sensitivity to apoptotic signals.
NIH; RO1 DK49221, funding period: 2/1/2000–1/31/2006.
Involvement of the HRES-1 Human Endogenous Retrovirus in SLE—The long-term objective of this project is to understand the role of the HRES-1 locus at 1q42 in pathogenesis of SLE.
NIH; ROI AI48079; funding period 6/1/2000–5/31/2007
Mitochondrial dysfunction in SLE—Mitochondrial dysfunction in T lymphocytes of SLE has been identified in the PI’s laboratory in 2002. This work was based on the discovery of mitochondrial hyperpolarization (MHP) as an early checkpoint of apoptosis controlled by transaldolase. The project is focused on characterizing the molecular basis of mitochondrial dysfunction and its relationship to T cell activation and cell death pathway selection in SLE.
NIH; R21 AI061066-01, funding period, 9/1/2004–08/31/2007
Research Projects Currently Ongoing
Pathogenesis of transaldolase deficiency—Children’s Miracle Network, 1/1/2006–12/31/2006
Pathogenesis of transaldolase deficiency has become a major focus of research for the PI. Presently, this project is funded by a grant of $20,000 from Children’s Miracle Network.