John Kyriakis, Ph.D.

Professor
Laboratory of Stress Signal Transduction and Gene Regulation

Tufts Medical Center

800 Washington Street, Box 8486

Boston, MA 02111

617-636-5190

John Kyriakis

Dr. Kyriakis received his A.B. from Cornell University and his Ph.D. from Boston University. He did postdoctoral work in the Diabetes Research Unit at Massachusetts General Hospital. He then continued at the Massachusetts General Hospital Diabetes Research Unit/Harvard Medical School for ten years as an independent faculty member. He has made several contributions to our understanding of the mechanisms by which growth and stress stimuli trigger changes in cell function. He is currently an Investigator with the MCRI, and Professor of Medicine at Tufts University School of Medicine. He is director of the MCRI Laboratory of Stress Signal Transduction and Gene Regulation. He is an Associate Editor of The Journal of Biological Chemistry, and serves on the Editorial Board of The American Journal of Physiology (Cell Physiology).

Publications

Zhong J, Gavrilescu LC, Molnár A, Murray L, Garafalo S, Kehrl JH, Simon AR, Van Etten RA, Kyriakis JM. GCK is essential to systemic inflammation and pattern recognition receptor signaling to JNK and p38. Proceedings of the National Academy of Sciences, USA 2009; 106:4372-4377 PubMed Abstract

Kyriakis JM. Thinking outside the box about Ras. Journal of Biological Chemistry 2008; 284(17):10993-10994 PubMed Abstract

Nogueira E, Fidalgo M, Molnar A, Kyriakis J, Force T, Zalvide J, Pombo CM. SOK1 translocates from the Golgi to the nucleus upon chemical anoxia and induces apoptotic cell death. Journal of Biological Chemistry 2008;283(23):16248-16258. PubMed Abstract

Zhong J, Kyriakis JM. Dissection of a signaling pathway by which pathogen-associated molecular patterns (PAMPs) recruit the JNK and p38 MAPKs and trigger cytokine release. Journal of Biological Chemistry 2007;282(33):24246-24254. PubMed Abstract

Pombo CM, Force T, Kyriakis J, Nogueira E, Fidalgo M, Zalvide J. The GCK II and III subfamilies of the STE20 group kinases. Frontiers in Bioscience 2007;12:850-859. PubMed Abstract

Kyriakis JM. The integration of signaling by multiprotein complexes containing Raf kinases. Biochemica et Biophysica Acta 2007;1773(8):1238-1247. PubMed Abstract

Goruppi S, Patten RD, Force T, Kyriakis JM. Helix-loop-helix protein p8, a transcriptional regulator required for cardiomyocyte hypertrophy and cardiac fibroblast matrix metalloprotease induction. Molecular and Cellular Biology 2006;27(3):993-1006. PubMed Abstract

Xu D, Patten RD, Force T, Kyriakis JM. Gene 33/RALT is induced by hypoxia in cardiomyocytes, where it promotes cell death by suppressing phosphatidylinositol 3-kinase and extracellular signal-regulated kinase survival signaling. Molecular and Cellular Biology 2006;26(13):5043-5054. PubMed Abstract

Chadee DN, Xu D, Hung G, Andalibi A, Lim DJ, Luo Z, Gutmann DH, Kyriakis JM. Mixed-lineage kinase 3 regulates B-Raf through maintenance of the B-Raf/Raf-1 complex and inhibition by the NF2 tumor suppressor protein. Proceedings of the National Academy of Sciences, USA 2006;103(12):4463-4468. PubMed Abstract

Xu D, Makkinje A, Kyriakis JM. Gene 33 is an endogenous inhibitor of Epidermal Growth Factor (EGF) receptor signaling and mediates dexamethasone-induced suppression of EGF function. Journal of Biological Chemistry 2005;280(4):2924-2933. PubMed Abstract