Kari Hoyt

Kari Hoyt

Kari Hoyt, PhD

Unit / Department / Division
Pharmaceutics and Pharmacology
Outcomes and Translational Sciences Affiliated Faculty
412 Riffe Building
Email Address
Phone Number

Professional Interests

Professional Interests

My lab focuses its research efforts on the cellular mechanisms that trigger and contribute to neuronal death and dysfunction. We use a combination of in vivo (transgenic and toxin mouse models) and in vitro (primary brain cultures, including neurons, glia, and neural progenitor/stem cells) experimental approaches to investigate the over-arching idea that dysregulation of kinase pathways and subsequent transcriptional activation/inhibition contribute to neuronal death and dysfunction, and that small molecule approaches to modulating these signaling pathways are viable therapeutic approaches to enhancing neuronal function and survival in a number of neurological/psychiatric disease states. Calcium deregulation, oxidative stress and mitochondrial dysfunction are among the causes often implicated in neuronal death, and are also under study in the lab. Overall, we seek to understand both the molecular events contributing to neurodegeneration as well as the mechanisms by which neurons protect themselves from such damage. Our goal is to develop therapeutic strategies, based on modulation of these signaling pathways, for the prevention/treatment of neurodegenerative and neuropsychiatric diseases.


  • PhD, Pharmacology, University of Pittsburgh School of Medicine


  • Dean's Innovative Research Award, 2019

Journal Articles

  • Aten S, Page CE, Kalidindi A, Wheaton K, Niraula A, Godbout JP, Hoyt KR, Obrietan K. miR-132/212 is induced by stress and its dysregulation triggers anxiety-related behavior. Neuropharmacology. 2018 Oct 18;144:256-270.
  • Wheaton KL, Hansen KF, Aten S, Sullivan KA, Yoon H, Hoyt KR, Obrietan K. The Phosphorylation of CREB at Serine 133 Is a Key Event for Circadian Clock Timing and Entrainment in the Suprachiasmatic Nucleus. J Biol Rhythms. 2018 Oct;33(5):497-514.
  • Aten S, Hansen KF, Snider K, Wheaton K, Kalidindi A, Garcia A, Alzate-Correa D, Hoyt KR, Obrietan K. miR-132 couples the circadian clock to daily rhythms of neuronal plasticity and cognition. Learn Mem. 2018 May;25(5):214-229.
  • Wheaton K, Aten S, Queiroz LS, Sullivan K, Oberdick J, Hoyt KR, Obrietan K. Circadian expression and functional characterization of PEA-15 within the mouse suprachiasmatic nucleus. Eur J Neurosci. 2018 Apr;47(7):845-857.
  • Choi YS, Horning P, Aten S, Karelina K, Alzate-Correa D, Arthur JSC, Hoyt KR, Obrietan K. Mitogen- and Stress-Activated Protein Kinase 1 Regulates Status Epilepticus-Evoked Cell Death in the Hippocampus. 2017 Sep-Oct;9(5):1759091417726607.
  • Choi YS, Lee B, Hansen KF, Aten S, Horning P, Wheaton KL, Impey S, Hoyt KR, Obrietan K. Status epilepticus stimulates NDEL1 expression via the CREB/CRE pathway in the adult mouse brain. Neuroscience. 2016 09 07;331:1-12.
  • Snider KH, Dziema H, Aten S, Loeser J, Norona FE, Hoyt K, Obrietan K. Modulation of learning and memory by the targeted deletion of the circadian clock gene Bmal1 in forebrain circuits. Behav Brain Res. 2016 07 15;308:222-35.
  • Kumar S, Pan CC, Shah N, Wheeler SE, Hoyt KR, Hempel N, Mythreye K, Lee NY. Activation of Mitofusin2 by Smad2-RIN1 Complex during Mitochondrial Fusion. Mol Cell. 2016 05 19;62(4):520-31.
  • Aten S, Hansen KF, Hoyt KR, Obrietan K. The miR-132/212 locus: a complex regulator of neuronal plasticity, gene expression and cognition. RNA Dis. 2016;3(2).
  • Sakamoto K, Norona FE, Alzate-Correa D, Scarberry D, Hoyt KR, Obrietan K. Clock and light regulation of the CREB coactivator CRTC1 in the suprachiasmatic circadian clock. J Neurosci. 2013 May 22;33(21):9021-7.