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Department of Physiology and Functional Genomics

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Home   Faculty Yun Kyoung Kang, Ph.D.

Yun Kyoung Kang, Ph.D.

Yun Kyoung Kang, Ph.D.

Yun Kyoung Kang, Ph.D.

Research Assistant Professor

(352) 273-7879
Office: M531
Email:  kangyk@ufl.edu

Research Description:

My long-term research goal is to enhance our understanding of the fundamental aspects of aging which is inevitable for all living organisms. As an intrinsic degenerative process, aging increases vulnerability to various diseases, which significantly decreases quality of life and ultimately leads to mortality.

One reason of the age-induced pathogenesis is due to the age-induced gradual deterioration of the immune system, namely immunosenescence. Given that phenotypic diversity results from the communication between individual’s genotype and his/her environment, it is very logical to speculate that individual variations in his/her aging process and immunosenescence are influenced by both genotype and environmental factors, particularly nutrient intake which is the most direct and pervasive environmental factor.

Ever since all eukaryotes began to rely on mitochondria for their energy metabolism to utilize nutrients, mitochondrial homeostasis is a key player in organismal survival. Unlike single cell organism, all metazoan organisms separate specific metabolic pathways in different tissues and their mitochondria. This multi-tissue compartmentation demands coordination of each ‘tissue-specific’ mitochondria for the optimal metabolic performance and systemic homeostasis. Thus, I would like to investigate the molecular and cellular mechanisms by which nutrient metabolisms control our immune system to defend aging-associated pathological conditions with focuses on inter-tissue communication between liver/gut to brain or muscle to brain/neuron via circulatory metabolome and proteome.

As suboptimal metabolic performance plays a crucial role in pathogeneses of various diseases by influencing one’s immunity, I believe that tailoring optimal metabolic regimen-diet and exercise to maximize the one’s immunity to defend age-induced pathogeneses would be the best personalized preventive and therapeutic strategy to extend healthy life span.

I am studying the roles of estrogen, estrogen receptor (ER)s and their RNA binding coregulators in age-induced pathogeneses including neurodegeneration, cancer and metabolic syndrome. The well-documented longer life span of females in comparison to males and its association with sex differences in steroid hormones, metabolic rate and immune functions brought my attention to the roles of sex steroids in metabolism and immunity. My immediate focus is to characterize the roles for RBM39/CAPER-mediated mitochondrial dynamics in TRIM21-mediated systemic immunity by identifying downstream genetic and metabolic factors and their roles in liver/muscle-to-brain communications. Ongoing projects include studies on (1) the roles of peripheral mitochondrial dynamics in peripheral proteostasis and neurodegeneration via circulatory proteome and (2) the roles of glucose-induced mitochondrial dynamics in TRIM21-mediated systemic immunity via circulatory metabolome during metastasis. These studies utilize molecular and cellular biology, biochemistry, genetics (with both C. elegans and mouse), next generation sequencing, proteomics, metabolomics and super resolution imaging techniques.

Complete list of Published work in My Bibliography:

http://www.ncbi.nlm.nih.gov/sites/myncbi/1ZcUhKnFjxkA-/bibliograpahy/40066076/public/?sort=date&direction=ascending

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