In my lab, we use cellular and animal models to study the basic mechanisms underlying age-related neurodegeneration and cancer. Though it might not seem like it, these two areas of research are related.
One bridge that connects them at the molecular level is what we call “stress-response factors.” These are a group of transcription factors defined by their function. Their job is to regulate gene expression to cope with stressors, such as high temperatures, infections, and whatever environmental disturbances come our way.
These stress-response factors are well-maintained and have an essential pro-survival role. My lab aims to use the roundworm C. elegans as a model to study how these could be used to mediate health decline in aging and provide potential treatment avenues for age-related diseases, specifically neurodegenerative disorders like the Alzheimer’s, Huntington’s, and Parkinson’s diseases. While strengthening the stress-response pathways and increasing survival is good in that context, there is a flipside to that coin: cancer.
Stress-response factors can be activated and re-purposed in a bad way under certain pathological conditions. One example is malignant transformation in cancer, in which dampening the pro-survival function of stress-response is beneficial. Our lab tries to find the switch for stress-response factors that leads to either health enhancement in aging or supporting malignancy, so that we can kill cancer cells without affecting the normal ones. That is why I study both sides of the coin when it comes to understanding these transcription factors.
B.S., Peking University, Beijing, China, 2005
Ph.D., Pennsylvania State University, 2012
Honors and Awards
2002-03 Guang-Hua Scholarship, Peking University, Beijing, China
2003-04 Dean’s award for Academic Distinction, Peking University
2006 Braddock Graduate Fellowship, Pennsylvania State University
2014 Postdoctoral Fellowship, National Ataxia Foundation
2014-16 Postdoctoral Award, Chicago Biomedical Consortium
2014-16 Postdoctoral Fellowship, BrightFocus Foundation for Alzheimer’s Disease
2016-2017 Ruth L. Kirschstein National Research Service Award
2020-2025 NIH Maximizing Investigators' Research Award (MIRA) for ESI
Joined OMRF Scientific Staff in 2017
Edwards SL, Erdenebat P, Morphis AC, Kumar L, Wang L, Chamera T, Georgescu C, Wren JD, Li J. Insulin/IGF-1 signaling and heat stress differentially regulate HSF1 activities in germline development. Cell Rep 36:109623, 2021 August, PMID: 34469721, PMCID: PMC8442575
Li J, Chauve L, Phelps G, Brielmann RM, Morimoto RI. E2F coregulates an essential HSF developmental program that is distinct from the heat-shock response. Genes Dev 30:2062-2075, 2016 Sep, PMID: 27688402, PMCID: PMC5066613
Li J, Gilmour DS. Distinct mechanisms of transcriptional pausing orchestrated by GAGA factor and M1BP, a novel transcription factor. EMBO J. 2013 Jul 3;32(13):1829-41. PMID: 23708796 PMCID: PMC3981175
Li J, Liu Y, Rhee HS, Ghosh SK, Bai L, Pugh BF, Gilmour DS. Kinetic competition between elongation rate and binding of NELF controls promoter-proximal pausing. Mol Cell. 2013 Jun 6;50(5):711-22. PMID: 23746353 PMCID: PMC3695833
Fay A, Misulovin Z, Li J, Schaaf CA, Gause M, Gilmour DS, Dorsett D. Cohesin selectively binds and regulates genes with paused RNA polymerase. Curr Biol. 2011 Oct 11;21(19):1624-34. PMID: 21962715 PMCID: PMC3193539
Lee C, Li X, Hechmer A, Eisen M, Biggin MD, Venters BJ, Jiang C, Li J, Pugh BF, Gilmour DS. NELF and GAGA factor are linked to promoter-proximal pausing at many genes in Drosophila. Mol Cell Biol. 2008 May;28(10):3290-300. PMID: 18332113 PMCID: PMC2423147
Huang J, Gan Q, Han L, Li J, Zhang H, Sun Y, Zhang Z, Tong T. SIRT1 overexpression antagonizes cellular senescence with activated ERK/S6k1 signaling in human diploid fibroblasts. PLoS One. 2008 Mar 5;3(3):e1710. PMID: 18320031 PMCID: PMC2249701