I am a biologist that uses molecular approaches to understand basic cellular processes with a focus on the heat shock response. Our primary model system is the small roundworm, C. elegans, but we also utilize cultured human cell lines to validate and extend our findings.
B.S., University of Michigan, highest honors, 1997
Ph.D., University of California, San Francisco 2006
Co-organizer - Annual Florida Worm Meeting
BIO 1010 - Biological Discovery I
BIO 3220 - Developmental Biology
BIO 5501 - Cell and Molecular Biology
BIO 5531 - Biology of Aging
BIO 5573 - Scientific Skills
BIO 5576 - Molecular Genetics
Pedrosa Nunes K, Guisbert E, Szasz T, Webb C. The Innate Immune System Via Toll-Like Receptors (TLRs) in Type 1 Diabetes – Mechanistic Insights. Major Topics in Type 1 Diabetes. 2015. Intech. p 1-20.
Guisbert E*, Czyz DM*, Richter K*, McMullen PD, Morimoto RI. Identification of a Tissue-selective Heat Shock Response Regulatory Network. PLOS Genetics. 2013 Apr;9(4):e1003466.
Guisbert E, Morimoto RI. Regulation and Function of the Heat Shock Response. Protein Quality Control in Neurodegenerative Diseases. 2013. Springer. p 1-18.
Morimoto R, Prahlad V, Ben-Zvi A, Gidalevitz T, Westerheide S, Anckar J, Sistonen L, Guisbert E, Czyz D, Voisine C, Silva C, Beam M. Restoring Proteostasis via Chaperone Networks in Ageing and Neurodegenerative Disease. FASEB J. 2009 Apr, 23;91.1.
Guisbert E, Yura T, Rhodius VA, Gross CA. Convergence of molecular, modeling and systems approaches for an understanding of the Escherichia coli heat shock response. Microbiol Mol Biol Rev. 2008 Sep:72(3):545-54.
Yura T*, Guisbert E*, Poritz M, Lu CZ, Campbell E, Gross CA. Analysis of sigma32 mutants defective in chaperone-mediated feedback control reveals unexpected complexity of the heat shock response. Proc Natl Acad Sci USA. 2007 Nov, 6;104(45):17638-43.
Guisbert E*, Rhodius V*, Ahuja N, Witkin E, Gross CA. Hfq modulates the sigmaE-mediated envelope stress response and the sigma32-mediated cytoplasmic stress response in E. coli. J. Bacteriol. 2007 Mar;189(5):1963-73.
Guisbert E, Herman C, Lu CZ, Gross CA. A chaperone network controls the heat shock response in E. coli. Genes Dev. 2004 Nov 15;18(22):2812-21.
Howard CT, Guisbert EA, and Merriman RL. In vivo antitumor activity of CI-994 (N-acetyl-dinaline, GOE 5549) alone and in combination with adriamycin against mammary adenocarcinoma 16C. Proc. Am Assoc. Cancer Res., 1998.
Howard CT, Elliot WL, Guisbert EA, Bergeron RJ, Porter CW, and Merriman RL. Tissue distribution of the polyamine analog N1,N 11-Diethylnorspermine (CI-1006,DENSPM) in nude mice. Proc. Am. Assoc. Cancer Res., 38:95, 1997.
Merriman R, Corbett T, Guisbert E, Howard C, Leopold W, Sebolt-Leopold J, Young B, and Sun Y. Evaluation of the mutational status of Ras genes in mouse tumor models used in anticancer drug discovery. Proc. Am. Assoc. Cancer Res., 38:350, 1997.
Recognition & Awards
Best in showcase poster for Cellular and Molecular Biology at the 2016 Northrop Grumman Showcase
Second place undergraduate poster at the 2016 Florida Worm Meeting
ACS Postdoctoral Fellowship 2009-2011
Keystone Travel Scholarship Award 2009
NIH Training Grant NIH-TG-AG000260-10S1 2007-2008
NSF Predoctoral Fellowship 1998-2001
Phi Beta Kappa Honor Society 1997
My primary research focus is the heat shock response. The heat shock response is a universal stress response that is also critical for normal growth and associated with a number of human diseases. The heat shock response activates a protective transcriptional program during sudden temperature increases, but it primarily senses protein misfolding and activates molecular chaperones that assist protein refolding.
The central role of protein folding in the cell explains the requirement for the heat shock response during normal growth, aging and development. Furthermore, the heat shock response is intimately associated with a wide variety of human diseases. For example, many cancers demonstrate strong induction of the heat shock response in the absence of increased temperature. In contrast, activation of the heat shock response appears to be beneficial in many models of neurodegenerative diseases.
We have completed a genome-wide screen to identify new regulators of the heat shock response. Many of these genes were previously associated with neurodegenerative diseases and cancer. Now, our primary focus is to characterize these new regulatory pathways and explore their roles in disease. Our research has revealed that regulation of the heat shock response is customized for each tissue and we are also exploring the molecular basis of this discovery.