• Ph.D. Case Western Reserve University, OH, 2005, Molecular Biology & Microbiology
  • M.S. Case Western Reserve University, OH, 1999, Biochemistry
  • B.S. Seoul Women's University, Korea, 1995, Chemistry

Research Interests

Obesity is a rapidly growing global health issue that is often associated with metabolic disorders including type 2 diabetes. Brown adipose tissue (BAT) is a unique organ that is specialized for energy expenditure. When activated, BAT takes up large amounts of lipids and glucose from the blood and dissipates nutrient-derived chemical energy as heat via UCP1-mediated thermogenesis. Because of these properties, BAT has recently emerged as a potential therapeutic target for treating human obesity and diabetes. Dr. Chang has a major interest in understanding the molecular mechanisms underlying BAT metabolism and thermogenesis. Her work has focused on the transcriptional regulation of BAT thermogenesis by NT-PGC-1alpha, a splice variant of PGC-1alpha transcriptional coactivator. Shared and unique functions of PGC-1alpha and NT-PGC-1alpha in the activation of BAT thermogenesis have been elucidated. Her current work focuses on the molecular mechanisms controlling cold-induced glucose uptake and utilization in BAT.

Department: Gene Regulation and Metabolism Lab

Selected Publications

  1. Gettys TW, Chang JS. (2019). An optimized immunoblotting protocol for accurate detection of endogenous PGC-1alpha isoforms in various rodent tissues. Methods in Molecular Biology. 1966:7-16.
  2. Kim J, Park MS, Ha K, Park C, Lee J, Mynatt RL, Chang JS. (2018). NT-PGC-1a deficiency decreases mitochondrial fatty acid oxidation in brown adipose tissue and alters substrate utilization in vivo. Journal of Lipid Research. 59(9):1660-1670.
  3. Chang JS*, Ghosh S, Newman S, Salbaum JM. (2018). A map of the PGC-1a- and NT-PGC-1a-regulated transcriptional network in brown adipose tissue. Scientific Reports. 8:7876. *Senior author
  4. Jeong JH, Chang JS, Jo Y. (2018). Intracellular glycolysis in brown adipose tissue is essential for optogenetically induced nonshivering thermogenesis in mice. Scientific Reports. 8:6672.
  5. Chang JS*, Ha K. (2018). A truncated PPAR gamma 2 localizes to mitochondria and regulates mitochondrial respiration in brown adipocytes. PLoS One. 13(3):e0195007. *Senior author
  6. Chang JS*, Ha K. (2017). An Unexpected Role for the Transcriptional Coactivator Isoform NT-PGC-1a in the Regulation of Mitochondrial Respiration in Brown Adipocytes. J Biol Chem,292(24):9958-9966. *Senior author
  7. Chang JS*, Jun H, Park M. (2016). Transcriptional coactivator NT-PGC-1a promotes gluconeogenic gene expression and enhances hepatic gluconeogenesis. Physiological Reports, 4(20), 2016, e13013. *Senior author
  8. Kim J, Fernand VE, Henagan TM, Shin J, Huypens P, Newman S, Chang JS. (2016). Regulation of brown and white adipocyte transcriptome by the transcriptional coactivator NT-PGC-1a. PLoS One. 11(7):e0159990.
  9. Park JH, Kang HJ, Lee YK, Kang H, Kim J, Chung JH, Chang JS, McPherron AC, Lee SB. (2015). Inactivation of EWS reduces PGC-1a protein stability and mitochondrial homeostasis. PNAS. 112(19):6074-6079.
  10. Henagan TM, Cefalu WT, Ribnicky DM, Noland RC, Dunville K, Campbell WW, Stewart LK, Forney LA, Gettys TW, Chang JS, Morrison CD. (2015). In vivo effects of dietary quercetin and quercetin-rich red onion extract on skeletal muscle mitochondria, metabolism, and insulin sensitivity. Genes & Nutrition. 10(1):451.
  11. Jun HJ, Joshi Y, Patil Y, Noland RC, Chang JS. (2014). NT-PGC-1a activation attenuates high-fat diet-induced obesity by enhancing brown fat thermogenesis and adipose tissue oxidative metabolism. Diabetes, 63(11):3615-3625.
  12. Wen X, Wu J, Chang JS, Wang J, Zhang Y, Gettys TW, Zhang Y (2014). Effect of exercise intensity on isoform-specific expressions of NT-PGC-1a mRNA in mouse skeletal muscle. BioMed Research International, 2014:402175.
  13. Jun HJ, Gettys TW, Chang JS. (2012). Transcriptional activity of PGC-1a and NT-PGC-1a is differentially regulated by Twist-1 in brown fat metabolism. PPAR Res, 2012:320454.
  14. Chang JS, Gettys TW. (2013). Analyzing phosphorylation-dependent regulation of subcellular localization and transcriptional activity of transcriptional coactivator NT-PGC-1alpha. Methods Mol Biol, 952:163-173.
  15. Chang JS, Fernand V, Zhang Y, Shin J, Jun HJ, Joshi Y, Gettys TW. (2012). NT-PGC-1a is sufficient to link ß3-adrenergic receptor activation to the transcriptional and physiological components of adaptive thermogenesis. J Biol Chem, 287(12):9100-9111.
  16. Chi, R.T., Torres, O.T., Segarra, V.A., Lansley, T., Chang, J.S., Newpher, T.M., Lemmon, S.K. (2012). Role of Scd5, a protein phosphatase-1 targeting protein, in phosphoregulation of Sla1 during endocytosis. Journal of Cell Science. 125:4728-4739.
  17. Chang JS, Huypens P, Zhang Y, Black C, Kralli A, Gettys TW. (2010). Regulation of NT-PGC-1a subcellular localization and function of PKA-dependent modulation of nuclear export by CRM1. J Biol Chem, 285(23), 18039-18050.
  18. Zhang Y, Huypens P, Adamson AW, Chang JS, Henagan TM, Boudreau A, Lenard NR, Burk D, Klein J, Perwitz N, Shin J, Fasshauer M, Kralli A, Gettys TW. (2009). Alternative mRNA splicing produces a novel biologically active short isoform of PGC-1 alpha. J Biol Chem, 284(47), 32813-32826.
  19. Eiring AM, Neviani P, Santhanam R, Oaks JJ, Chang JS, Notari M, Perrotti D. (2008). Identification of novel post-transcriptional targets of the BCR/ABL oncoprotein by ribonomics: requirement of E2F3 for BCR/ABL leukemogenesis. Blood. 111(2):816-828.
  20. Koschmieder S, D´Alo F, Radomska H, Schöneich C, Chang JS, Konopleva M, Perrotti D, Serve H, and Tenen DG. (2007). CDDO induces granulocytic differentiation of myeloid leukemic blasts through translational up-regulation of p42 CCAAT enhancer binding protein alpha. Blood. 110(10):3695-3705.
  21. Chang JS, Santhanam R, Trotta R, Neviani P, Eiring AM, Briercheck E, Ronchetti M, Roy DC, Calabretta B, Caligiuri MA, and Perrotti D. (2007). High levels of the BCR/ABL oncoprotein are required for the MAPK-hnRNP E2-dependent suppression of C/EBPa-driven Myeloid Differentiation. Blood. 110(3):994-1003.
  22. Notari M, Neviani P, Santhanam R, Blaser BW, Chang JS, Galietta A, Willis AE, Roy DC, Caligiuri MA, Marcucci G, Perrotti D. (2006). A MAPK/hnRNP K pathway controls BCR/ABL oncogenic potential by regulating c-myc mRNA translation. Blood. 107(6): 2507-2516.
  23. Chang JS, Henry KR, Geli M, Lemmon SK. (2006). Cortical recruitment and nuclearcytoplasmic shuttling of Scd5p, a protein phosphatase-1 targeting protein involved in actin organization and endocytosis. Molecular Biology of the Cell. 17: 251–262.
  24. Neviani P, Santhanam R, Trotta R, Notari N, Blaser BW, Liu S, Mao H, Chang JS, Galietta A, Caligiuri MA, Marcucci G, Perrotti D. (2005). The tumor suppressor PP2A is functionally inactivated in blast crisis CML through the inhibitory activity of the BCR/ABL-regulated SET protein. Cancer Cell. 8(5): 355–368.
  25. Henry KR., D’Hondt K, Chang JS, Nix DA, Cope MJTV, Chan CSM, Drubin DG, Lemmon SK. (2003). The actin regulating kinase Prk1p negatively regulates Scd5p, a suppressor of clathrin deficiency, in actin organization and endocytosis. Current Biology. 13(17): 1564–1569.
  26. Chang JS, Henry KR, Wolf BL, Geli M, Lemmon SK. (2002). Protein phosphatase-1 binding to Scd5p is important for regulation of actin organization and endocytosis in yeast. Journal of Biological Chemistry. 277(50): 48002–48008.
  27. Henry KR, D’Hondt K, Chang JS, Newpher T, Huang K, Hudson RT, Riezman H, Lemmon SK. (2002). Scd5p and clathrin function are important for cortical actin organization, endocytosis, and localization of Sla2p in yeast. Molecular Biology of the Cell. 13(8): 2607–2625.
  28. Chang JS, McPheeters DS. (2001). Identification of a U2/U6 helix Ia mutant that influences 3' splice site selection during nuclear pre-mRNA splicing. RNA. 6: 1120–1130.