Arnold Scott Kristof, MD

Research Focus: 

Lung infections and injury are an important cause of death and illness all over the world in spite of the advent of modern antibiotics and anti-inflammatory medications. Research focuses on the underlying molecular mechanisms that control whether lung cells live or die when inflamed. Specifically, the relationship between the pro-survival protein ‘mammalian target of rapamycin’ (mTOR), and the cell death and inflammation protein ‘signal transducer and activator of transcription-1’ (STAT1). Using genetic, genomic, and proteomic techniques to define how, when, and where the proteins interact to control cell survival, the research reveals mechanisms that control the susceptibility to and severity of lung injury, as well as the processes by which inflammation affects the growth and survival of tumours in the lung.

Epithelial cell, apoptosis, transcription, protein kinase, transcription factor, innate immunity, host defense, cancer, acute lung injury
Royal Victoria Hospital
A.S. Kristof. mTOR Signaling in Lymphangioleiomyomatosis. Lymph. Res. Biol. 8(1): 33-42; 2010
J.A. Fielhaber, Y.S. Han, J. Tan, S. Xing, C.M. Biggs, K.B. Joung, and A.S. Kristof. Inactivation of Mammalian Target of Rapamycin Increases STAT1 Nuclear Content and Transcriptional Activity in Alpha4 and Protein Phosphatase 2A-dependent Fashion. J. Biol. Chem. 284(36): 24341-24353; 2009
A.S. Kristof, J. Fielhaber, A. Triantafillopoulos, S. Nemoto, J. Moss. Phosphatidylinositol 3-Kinase-dependent Suppression of the Human Inducible Nitric Oxide Synthase Promoter is Mediated by FKHRL1. J. Biol. Chem. 281(33): 23958-23968; 2006
Kristof AS, Marks-Konczalik J, Billings E, Moss J. Stimulation of STAT1-dependent Gene Transcription by Lipopolysaccharide and Interferon- is Regulated by Mammalian Target of Rapamycin. Journal of Biological Chemistry; 278: 33637-33644; 2003