Associate Professor | Biomedical and Chemical Engineering and Sciences
Program Chair, Biomedical Sciences
Room 316, Gordon L. Nelson Health Sciences Building
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
Postdoctoral Fellowship, Northwestern University, Evanston, IL
Co-organizer - Annual Florida Worm Meeting
BIO 1010 - Biological Discovery I
BIO 3220 - Developmental Biology
BIO 4102 - Advanced Molecular Biology / Eukaryotic Molelcular Biology
BIO 5501 - Cell and Molecular Biology
BIO 5531 - Biology of Aging
BIO 5573 - Scientific Skills
BIO 5576 - Molecular Genetics
Mossiah I, Perez SM, Stanley TR, Foley MK, Kim Guisbert KS, Guisbert E.
Geranylgeranylacetone Ameliorates Beta-Amyloid Toxicity and Extends Lifespan
via the Heat Shock Response in Caenorhabditis elegans. Front
Aging. 2022 Apr 27;3:846977. doi: 10.3389/fragi.2022.846977. PMID: 35821801;
Golden NL, Foley MK, Kim Guisbert KS, Guisbert E. Divergent regulatory roles
of NuRD chromatin remodeling complex subunits GATAD2 and CHD4 in Caenorhabditis
elegans. Genetics. 2022 May 5;221(1):iyac046. doi: 10.1093/genetics/iyac046.
PMID: 35323946; PMCID: PMC9071545.
Stanley TR, Guisbert KSK, Perez SM, Oneka M, Kernin I, Higgins NR, Lobo A,
Subasi MM, Carroll DJ, Turingan RG, Guisbert E. Stress response gene family
expansions correlate with invasive potential in teleost fish. J Exp Biol. 2022
Mar 8;225(Suppl_1):jeb243263. doi: 10.1242/jeb.243263. Epub 2022 Mar 8. PMID:
35258619; PMCID: PMC8987736.
Plagens RN, Mossiah I, Kim Guisbert KS, Guisbert E. Chronic temperature
stress inhibits reproduction and disrupts endocytosis via chaperone titration in
Caenorhabditis elegans. BMC Biol. 2021 Apr 15;19(1):75. doi:
10.1186/s12915-021-01008-1. PMID: 33858388; PMCID: PMC8051109.
Kim Guisbert KS, Mossiah I, Guisbert E. Titration of SF3B1 Activity Reveals
Distinct Effects on the Transcriptome and Cell Physiology. Int J Mol Sci. 2020
Dec 17;21(24):9641. doi: 10.3390/ijms21249641. PMID: 33348896; PMCID:
Golden NL, Plagens RN, Kim Guisbert KS, Guisbert E. Standardized Methods for
Measuring Induction of the Heat Shock Response in Caenorhabditis elegans. J Vis
Exp. 2020 Jul 3;(161). doi: 10.3791/61030. PMID: 32716378.
Qin G, Johnson C, Zhang Y, Zhang H, Yin J, Miller G, Turingan RG, Guisbert E,
Lin Q. Temperature-induced physiological stress and reproductive characteristics
of the migratory seahorse <i>Hippocampus erectus</i> during a thermal stress
simulation. Biol Open. 2018 Jun 25;7(6):bio032888. doi: 10.1242/bio.032888.
PMID: 29764809; PMCID: PMC6031341.
Guruge C, Rfaish SY, Byrd C, Yang S, Starrett AK, Guisbert E, Nesnas N. Caged
Proline in Photoinitiated Organocatalysis. J Org Chem. 2019 May
3;84(9):5236-5244. doi: 10.1021/acs.joc.9b00220. Epub 2019 Apr 3. PMID:
30908906; PMCID: PMC6510250.
Kim Guisbert KS, Guisbert E. SF3B1 is a stress-sensitive splicing factor that
regulates both HSF1 concentration and activity. PLoS One. 2017 Apr
26;12(4):e0176382. doi: 10.1371/journal.pone.0176382. PMID: 28445500; PMCID:
Ma J, Grant CE, Plagens RN, Barrett LN, Kim Guisbert KS, Guisbert E.
Cellular Proteomes Drive Tissue-Specific Regulation of the Heat Shock Response.
G3 (Bethesda). 2017 Mar 10;7(3):1011-1018. doi: 10.1534/g3.116.038232. PMID:
28143946; PMCID: PMC5345702.
Recognition & Awards
SGA Faculty of the Year, 2021
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.