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Donghee Kim, PhD

Donghee Kim, PhD
Professor and Discipline Chair

Physiology and Biophysics Discipline

Center for Proteomics and Molecular Therapeutics

  • Bachelor of Science (Chemistry and Biochemistry), Massachusetts Institute of Technology, Cambridge MA
  • PhD (Pharmacology and Toxicology), Michigan State University, East Lansing, MI
  • Postdoc/Instructor/Assistant Professor (Cardiovascular Physiology), Harvard Medical School/Brigham and Women’s Hospital, Boston, MA
  • Research Fellow (Pharmacology), Mayo Clinic, Rochester, MN 
  • Associate Professor/Professor (Physiology and Biophysics), Chicago Medical School, North Chicago, IL

Publications

Recent Publications (from 2005)
  • Gazmuri Raul, Cristina Santonocito, Salvatore Aiello, Kim Donghee. Chapter 72: Ventricular arrhythmias. In: Textbook of Critical Care 8th Edition. Edited by Jean-Louis Vincent, Frederick A. Moore, Rinaldo Bellomo, John J. Marini. Elsevier, 2023.
  • Kim D. Hogan JO, White C. TASK inhibition by mild acidosis increases Ca2+ oscillations to mediate pH sensing in rat carotid body chemoreceptor cells. Am J Physiol Lung Cell Mol Physiol 2023 Mar 1;324(3): L259-L270. doi: 10.1152/ajplung.00099.2022.
  • Kim D, Harada K, Inoue M. Expression and function of mitochondrial inhibitor factor-1 and TASK channels in adrenal cells. Biochem Biophys Res Commun. 2023 Jan 11;645:17-23. doi: 10.1016/j.bbrc.2023.01.025.
  • Matsuoka H, Harada K, Sugawara A, Kim D, Inoue M. Expression of p11 and heteromeric TASK channels in mouse adrenal cortical cells and H295R cells. Acta Histochem. 2022 Jul;124(5):151898. doi: 10.1016/j.acthis.2022.151898. (PubMed)
  • Kim D. Hogan JO, White C. Oscillations of intracellular [Ca2+] in rat carotid body glomus cells in normoxia and hypoxia. Am J Physiol (Cell Physiol). 318(2):C430-C438, 2020 (PubMed)
  • Kang D., Wang J., Hogan J.O., Kim D. TASK-1 (K2P3) and TASK-3 (K2P9) in Rabbit Carotid Body Glomus Cells. In: Arterial Chemoreceptors: New directions and Translational Perspectives. Advances in Experimental Medicine and Biology, 1071:35-41, 2018 (PubMed)
  • Wang J, Kim D.  Activation of voltage-dependent K+ channels strongly limits hypoxia-induced elevation of [Ca2+ ]i in rat carotid body glomus cells.  J Physiol.  596: 3119-3136, 2018 (PubMed)
  • Kim D.  Endocytosis: another pathway in receptor-Gq-TASK signalling.  J Physiol. 595:6811-6812, 2017.  (PubMed)
  • Wang J, Hogan JO, Wang R, White C, Kim D.  Role of cystathionine-γ-lyase in hypoxia-induced changes in TASK activity, intracellular [Ca2+] and ventilation in mice.  Respir Physiol Neurobiol. 246:98-106, 2017. (PubMed)
  • Gul R, Park DR, Shawl AI, Im SY, Nam TS, Lee SH, Ko JK, Jang KY, Kim D, Kim UH. Nicotinic Acid Adenine Dinucleotide Phosphate (NAADP) and Cyclic ADP-Ribose (cADPR) Mediate Ca2+ Signaling in Cardiac Hypertrophy Induced by β-Adrenergic Stimulation. PLoS One 11:e0149125, 2016. (PubMed)
  • Wang J, Hogan JO, Kim D. Voltage- and receptor-mediated activation of a non-selective cation channel in rat carotid body glomus cells. Respir Physiol Neurobiol. 237:13-21, 2017. (PubMed)
  • Kim D. Kim IS, Wang J, White C, Carroll JL.  Hydrogen sulfide and hypoxia-induced changes in TASK activity and intracellular Ca2+ concentration in rat carotid body glomus cells.  Respir Physiol Neurobiol 215:30-38, 2015. (PubMed)
  • Kim D, Kang DW.  Role of K2P channels in stimulus-secretion coupling.  Pflügers Archiv - European Journal of Physiology: 467, Page 1001-1011, 2015. (PubMed)
  • Kim D.  Oxygen sensing with ion channels.  Channels (Landes) 8:4, 290-291, 2014 (PubMed)
  • Kang DW, Wang J, Hogan JO, Vennekens R, Freichel M, White C, Donghee Kim. Increase in cytosolic Ca2+ produced by hypoxia and other depolarizing stimuli activates a non-selective cation channel in chemoreceptor cells of rat carotid body.  J. Physiol (Lond) 592(Pt 9):1975-92, 2014. (PubMed)
  • Kim D, Kang DW, Martin EA, Kim IS, Carroll JL. Effects of modulators of AMP-activated protein kinase on TASK-like K+ channels and intracellular Ca2+ concentration in rat carotid body glomus cells. Respir Physiol Neurobiol 195:19-26, 2014 (PubMed)
  • Kang D, Hogan JO, Kim D.  THIK-1 (K2P13.1) is a small-conductance background K+ channel in rat trigeminal ganglion neurons. Pflugers Arch. 466(7):1289-300, 2014. (PubMed)
  • Chen J, Kang D, Xu J, Lake M, Hogan JO, Sun C, Walter K, Yao B, Kim D. Species differences and molecular determinant of TRPA1 cold sensitivity.  Nature Communications 2013;4:2501. doi:10.1038/ ncomms 3501. (PubMed)
  • Kim D.  K(+) channels in O(2) sensing and postnatal development of carotid body glomus cell response to hypoxia. Respir Physiol Neurobiol. 2013 Jan 1;185(1):44-56. (PubMed)
  • Papreck JR, Martin EA, Lazzarini P, Kang D, Kim D. Modulation of K(2P)3.1 (TASK-1), K (2P)9.1 (TASK-3), and TASK-1/3 heteromer by reactive oxygen species. Pflugers Archiv (European Journal of Physiology) Nov;464(5):471-80, 2012. (PubMed)
  • Kim D, Kim IS, Papreck JR, Donnelly DF, Carroll JL. Characterization of the ATP-sensitive K+ channel in the rat carotid body glomus cells, Respir Physiol Neurobiol, 177:245-255, 2011. (PubMed)
  • Kim D, Papreck JR, Kim IS, Donnelly DF, Carroll JL. Changes in oxygen sensitivity of TASK in carotid body glomus cells during early postnatal development, Respir Physiol Neurobiol, 177: 228-235, 2011. (PubMed)
  • Kim D, Cavanaugh EJ, Kim IS, Carroll JL.  Heteromeric TASK-1/3 is the major oxygen-sensitive background K+ channel in rat carotid body glomus cells. J Physiol 587, 2963-2975, 2009. (PubMed)
  • Goldstein SA, Bayliss DA, Kim D, Lesage F, Plant LD, Rajan S. International Union of Pharmacology. LV. Nomenclature and molecular relationships of two-P potassium channels.1: Pharmacol Rev. 2005 Dec;57(4):527-40. (PubMed)
  • Kim, D.  Physiology and pharmacology of two-pore domain K+ channels.  Current Pharmaceutical Design 11: 2717-2736, 2005.
  • Kang DW, Choe CY, Kim D.  Thermosensitivity of the two-pore domain K+ channels TREK-2 and TRAAK.  J. Physiol. 564.1, 103-116, 2005 (PubMed)
  • Chen J, Kim D, Bianchi BR, Cavanaugh EJ, Faltynek CR, Kym PR, Reilly RM.  Pore dilation occurs in TRPA1 but not in TRPM8 channels. Molecular Pain. 2009; 5, 1-6, 2009. (PubMed)
  • Simkin D, Cavanaugh EJ, Kim D. Control of the Single Channel Conductance of K2P10.1 (TREK-2) by the Amino-terminus: Role of Alternative Translation Initiation.  J Physiol 586, 5651-5663, 2008. (PubMed)
  • Cruz-Orengo L, Dhaka A, Heuermann RJ, Yong TJ, Montana MC, Cavanaugh EJ, Kim D, Story GM.  Cutaneous nociception evoked by 15-delta PGJ2 via activation of ion channel TRPA1.  Molecular Pain 4:30 (1-9), 2008. (PubMed)
  • Kim D, Cavanaugh EJ, Simkin D.  Inhibition of transient receptor potential A1 by phosphatidylinositol-4,5-bisphosphate.  Am J Physiol 295:C92-C99, 2008. (PubMed)
  • Cavanaugh EJ, Simkin D, Kim D.  Activation of transient receptor potential A1 channels by mustard oil, tetrahydrocannabinol, and Ca reveals different functional channel states.  Neuroscience 154:1467-1476, 2008 (PubMed)
  • Kim D, Cavanaugh EJ.  Requirement of a cytosolic factor for activation of TRPA1: role of inorganic polyphosphates.  J. Neurosci. 27:6500-6509, 2007. (PubMed)
  • Kang, DW, Choe C, Cavanaugh EJ, Kim D.  Properties of Single TREK-2 (K2P10.1) Channels Expressed in Mammalian cells. J. Physiol. 583.1: 57-69, 2007. (PubMed)
  • Kang DW. Han JH, Kim D.  Mechanism of inhibition of TREK-2 by acetylcholine via Gq.  Am J Physiol 2006 Oct;291(4):C649-56. (PubMed)
  • Kang DW, Kim D.  TREK-1 and TRESK are two major background K+ channels in dorsal root ganglion neurons.  Am J Physiol 2006 Jul;291(1):C138-46.  (PubMed)
  • Goldstein SA, Bayliss DA, Kim D, Lesage F, Plant LD, Rajan S. International Union of Pharmacology. LV. Nomenclature and molecular relationships of two-P potassium channels.1: Pharmacol Rev. 2005 Dec;57(4):527-40. (PubMed)
  • Kim, D.  Physiology and pharmacology of two-pore domain K+ channels.  Current Pharmaceutical Design 11: 2717-2736, 2005. (PubMed)
  • Kang DW, Choe CY, Kim D.  Thermosensitivity of the two-pore domain K+ channels TREK-2 and TRAAK.  J. Physiol. 564.1, 103-116, 2005 (PubMed)

Research Projects

We have two projects that investigate the role of ion channels in the modulation of cell excitability at rest and in response to various stimuli.  (1) The goal of the first project is to understand the mechanisms by which TRP ion channels expressed in chemoreceptor and sensory neurons detect various physicochemical stimuli such as heat, cold, hypoxia, noxious chemicals and Ca.  This is studied using cloned TRP ion channels expressed in cell lines as well as ion channels in dorsal root ganglion and trigeminal neurons.  The TRP ion channel we are currently studying is TRPA1.  (2) The goal of the second project is to understand the mechanisms by which hypoxia and receptor agonists modulate the function of TASK (K2P3/9), TREK (K2P 2/10) and TRP ion channels in chemoreceptor cells.  This is studied using freshly isolated cells from the carotid body, adrenal gland and cerebellar granule neurons that express high levels of these K channels.  The role of mitochondrion as the oxygen sensor that regulates the function of these K2P channels is under investigation.