Directory

Nien-Pei Tsai's directory photo.

Nien-Pei Tsai

Associate Professor

Primary Affiliation

Neurotechnology for Memory and Cognition

Affiliations

Status Affiliate Faculty

Home Department of Molecular and Integrative Physiology

Phone 244-5620

Email nptsai@illinois.edu

Address

  • Biography

    Nien-Pei Tsai is an associate professor in the Department of Molecular and Integrative Physiology. His primary affiliation is Neurotechnology for Memory and Cognition.

    Education

    • B.S., National Taiwan University, Taipei, Taiwan, 2002

    • M.Sc., National Yang-Ming University, Taipei, Taiwan, 2004

    • Ph.D., University of Minnesota, Minneapolis, MN, 2009

  • Honors

    • 2020: James and Maxine Heath Excellence in Teaching Award

    • 2019: Arnold O. Beckman Research Award

    • 2016 - 2022: Teachers Ranked as Excellent

    • 2015, 2018: NARSAD Young Investigator Award

    • 2014: Simons Foundation Autism Initiative-Explorer Award

    • 2011: National Research Service Award (NRSA) from NIH

    • 2011: Meritorious Award at Postdoctoral Symposium at UTSW

    • 2010: Dr. Marvin and Hadassah Bacaner Research Award, University of Minnesota

    • 2008: Veneziale-Steer Research Award, University of Minnesota

    • 2008: Milne Brandenberg Graduate Research Award, University of Minnesota

  • Research

    Research areas:

    • Gene Regulation

    • Neuroscience

    Research interests:

    • Neurobiology

    • Synaptic transmission

    • Learning and memory

    • Neurological and behavioral disorders

    An imbalance in neuronal and synaptic excitability is a common abnormality observed in patients with various psychiatric and neurological disorders, including autism spectrum disorders, epilepsy and Alzheimer's disease. The dysregulation of excitability is thought to exacerbate disease symptoms. Identifying and understanding the mechanisms underlying the dysregulation of excitability could reveal novel therapeutic targets for these diseases. To achieve this goal, we utilize various approaches including molecular and cell biology, biochemistry, electrophysiology, and mouse genetics to understand the regulation of excitability homeostasis at synaptic, neuronal, network and system levels, and how the deficits of those affect behavior in diseases. 

    Current focuses of the lab include:

    1. Studying activity-dependent translational control in fragile X syndrome

    2. Exploring novel transcriptional and post-transcriptional regulators in neurodevelopment 

    3. Determining the role of cellular stress response in neuronal plasticity

    4. Characterizing the molecular mechanisms contributing to comorbid seizures in Alzheimer's disease

  • 2022

    • Baculis, B. C., Kesavan, H., Weiss, A. C., Kim, E. H., Tracy, G. C., Ouyang, W., Tsai, N. P., & Chung, H. J. (2022). Homeostatic regulation of extracellular signal-regulated kinase 1/2 activity and axonal Kv7.3 expression by prolonged blockade of hippocampal neuronal activity. Frontiers in Cellular Neuroscience, 16, [838419]. https://doi.org/10.3389/fncel.2022.838419
    • Liu, X., Kumar, V., Tsai, N. P., & Auerbach, B. D. (2022). Hyperexcitability and Homeostasis in Fragile X Syndrome. Frontiers in Molecular Neuroscience, 14, [805929]. https://doi.org/10.3389/fnmol.2021.805929
    • Lizarazo S, Yook Y, and Tsai NP (2022) Amyloid beta induces Fmr1-dependent translational suppression and hyposynchrony of neural activity via phosphorylation of eIF2a and eEF2. J Cell Physiol 237:2929-2942
    • Lizarazo, S., Yook, Y., & Tsai, N. P. (2022). Amyloid beta induces Fmr1-dependent translational suppression and hyposynchrony of neural activity via phosphorylation of eIF2a and eEF2. Journal of Cellular Physiology, 237(7), 2929-2942. https://doi.org/10.1002/jcp.30754
    • Lizarazo, S., Yook, Y., & Tsai, N. P. (2022). Amyloid beta induces Fmr1-dependent translational suppression and hyposynchrony of neural activity via phosphorylation of eIF2a and eEF2. Journal of Cellular Physiology, 237(7), 2929-2942. https://doi.org/10.1002/jcp.30754
    • Lodes DE, Zhu J, and Tsai NP (2022) E3 Ubiquitin Ligase Nedd4-2 Exerts Neuroprotective Effects During Endoplasmic Reticulum Stress. J Neurochem 160:613-624
    • Lodes, D. E., Zhu, J., & Tsai, N. P. (2022). E3 ubiquitin ligase Nedd4-2 exerts neuroprotective effects during endoplasmic reticulum stress. Journal of Neurochemistry, 160(6), 613-624. https://doi.org/10.1111/jnc.15567

    2021

    • Eagleman, D. E., Zhu, J., Liu, D. C., Seimetz, J., Kalsotra, A., & Tsai, N. P. (2021). Unbiased Proteomic Screening Identifies a Novel Role for the E3 Ubiquitin Ligase Nedd4-2 in Translational Suppression During ER Stress. Journal of Neurochemistry, 157(6), 1809-1820. https://doi.org/10.1111/jnc.15219
    • Lee KY, Zhu J, Cutia CA, Christian-Hinman CA, Rhodes JS and Tsai NP (2021) Infantile spasms–linked Nedd4-2 mediates hippocampal plasticity and learning via cofilin signaling. EMBO Rep 22:e52645
    • Liu DC, Lee KY, Lizarazo S, Cook JK and Tsai NP (2021) ER stress-induced modulation of neural activity and seizure susceptibility is impaired in a fragile X syndrome mouse model. Neurobiol Dis 158, 105450

    2020

    • Eagleman DE, Zhu J, Liu DC, Seimetz J, Kalsotra A and Tsai NP (2020) Unbiased Proteomic Screening Identifies a Novel Role for the E3 Ubiquitin Ligase Nedd4-2 in Translational Suppression during ER Stress. J Neurochem 157:1809-1820
    • Liu DC, Soriano S, Yook Y, Lizarazo S, Eagleman DE and Tsai NP (2020) Chronic activation of Gp1 mGluRs leads to distinct refinement of neural network activity through non-canonical p53 and Akt signaling. eNeuro 7, 0438-19.2020

    2019

    • Liu DC, Eagleman DE and Tsai NP (2019) Novel Roles of ER Stress in Repressing Neural Activity and Seizures through Mdm2- and p53-dependent Protein Translation. PLOS Genet. 15(9):e1008364
    • Zhu J, Lee KY, Jong TY and Tsai NP (2019) C2-lacking isoform of Nedd4-2 regulates excitatory synaptic strength through GluA1 ubiquitination-independent mechanisms. J Neurochem 151: 289-300

    2018

    • Jewett KA, Lee KY, Eagleman DE, Soriano S and Tsai NP (2018) Dysregulation and restoration of homeostatic network plasticity in fragile X syndrome mice. Neuropharmacology 138:182-192
    • Lee KY, Jewett KA, Chung HJ and Tsai NP (2018) Loss of fragile X protein FMRP impairs homeostatic synaptic downscaling through tumor suppressor p53 and ubiquitin E3 ligase Nedd4-2. Hum Mol Genet. 27:2805–2816

    2017

    • Liu DC, Seimetz J, Lee KY, Kalsotra A, Chung HJ, Lu H and Tsai NP (2017) Mdm2 mediates FMRP- and Gp1 mGluR-dependent protein translation and neural network activity. Hum Mol Genet. 26:3895–3908
    • Zhu J, Lee KY, Jewett KA, Man HY, Chung HJ and Tsai NP (2017) Epilepsy-associated gene Nedd4-2 mediates neuronal activity and seizure susceptibility through AMPA receptors. PLOS Genet. 13:e1006634

    2015

    • Jewett KA, Zhu J, and Tsai NP (2015) The tumor suppressor p53 guides GluA1 homeostasis through Nedd4-2 during chronic elevation of neuronal activity. J Neurochem 135:226-233