Yang Yang

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Assistant Professor of Medicinal Chemistry and Molecular Pharmacology
Phone:
765-494-2926
Specialization: neurological diseases (e.g., autism; epilepsy; pain; dementia); pharmacogenomics; gene therapy; human induced pluripotent stem cells (hiPSCs); genetic mouse models

Education

B.S., B.A. (2005): Life Sciences/Sociology -- Shanghai University
Ph.D. (2011): Physiology/Biology -- Georgia State University
Postdoc. (2011-2014): Yale University School of Medicine
Associate Research Scientist (2014-2017): Yale University School of Medicine

Research

Y-lab studies genetic neurological diseases including autism, epilepsy, pain, and dementia with both mouse models and human-induced pluripotent stem cells (hiPSCs) derived neuron and brain organoid models. Using state-of-the-art technologies (brain slice and in vivo electrophysiology recordings, multi-electrode array recordings, in vivo calcium imaging of freely moving animals, single-cell RNA-sequencing, cleared 3D brain imaging, CRISPR-mediated genome-editing among others), Y-lab aims to understand disease mechanisms underlying these neurological diseases, and to advance pharmacogenomic approaches for disease intervention. 

Lab Members

Xiaoling Chen (Post-Doctoral Research Associate)
Ningren Cui (Research Associate)
Brody Alan Deming (Graduate Student)
Gideon Drafor (Graduate Student)
Maria Isabel Olivero Acosta (Graduate Student)
Zhefu (Jeff) Que (Graduate Student)
Kyle William Wettschurack (Graduate Student)
Jiaxiang Wu (Visiting Scholar)
Lehao Wu (Graduate Student)
Jingliang Zhang (Post-Doctoral Research Associate)
Yuanrui Zhao (Graduate Student)

Interests

Large-scale human genetic studies have identified SCN2A as one of the leading monogenic causes of severe autism and epilepsy. SCN2A encodes the voltage-gated sodium channel Nav1.2, a main mediator of neuronal action potential firing. Funded by NIH and FamilieSCN2A Foundation among other agencies, a major direction in the lab is to understand the disease mechanisms of SCN2A-related autism and epilepsy. We also develop next-generation therapeutic interventions to treat these devastating diseases including small molecules, antisense oligonucleotides, as well as viruses, and CRISPR-based gene therapies.

Teaching

PHRM 847000 Principle of Pharmacogenomics (offered every Spring), course co-coordinator;

PHRM 845000 Integrated Pharmacotherapeutics III (offered every Spring);

Grants

NIH-NINDS R01 NS123154; Yang (PI); 07/15/2021 - 4/30/2026  Neuronal hyperexcitability and seizures in a Scn2a deficient mouse model

NIH-NINDS R01 NS117585; Yang (PI); 04/01/2021 - 03/31/2026 Neuronal and Behavioral Deficits Associated with Scn2a Deficiency in Autism Spectrum Disorder

NIH-NIEHS R01 ES031401; Bowman (MPI), Harrison (MPI), Yang (Co-I); 02/01/2020 - 10/31/2024 Manganese exposure susceptibility as a modifier of excitotoxicity in Alzheimer's Disease

Representative Publications

 

Please check out yangyanglab.org for most up-to-date publications. 

Selected publications

2022

Ma Z, Eaton M, Liu Y, Zhang J, Chen X, Tu X, Shi Y, Que Z, Wettschurack K, Zhang Z, Shi Y, Chen Y, Kimbrough A, Lanman NA, Schust L, Huang Z*, Yang Y*Deficiency of autism-related Scn2a gene in mice disrupts sleep patterns and circadian rhythmsNeurobiology of Disease. 2022 March14; 168:105690.

2021

Que Z&, Olivero-Acosta MI&, Zhang J, Eaton M, Tukker AM, Chen X, Xiao T, Wu J, Xie J, Wettschurack K, Yunis L, Shafer MJ, Schaber JA, Rochet JC, Bowman AB, Yuan C, Huang Z, Hu CD, Trader DJ, Skarnes WC, Yang Y*. Hyperexcitability and pharmacological responsiveness of cortical neurons derived from human iPSCs carrying epilepsy-associated sodium channel Nav1.2-L1342P genetic variantJournal of Neuroscience, an official journal of Society for Neuroscience. 2021 December 8; 41(49): 10194-10208.Featured on the Cover, and previewed in "This Week in The Journal"

Zhang J&, Chen X&, Eaton M, Wu J, Ma Z, Lai S, Park A, Ahmad TS, Que Z, Lee JH, Xiao T, Li Y, Wang Y, Olivero-Acosta MI, Schaber JA, Jayant K, Yuan C, Huang Z, Lanman NA, Skarnes WC, Yang Y*Severe deficiency of the voltage-gated sodium channel Nav1.2 elevates neuronal excitability in adult miceCell Reports. 2021 AUGUST 03, VOLUME 36, ISSUE 5, 109495.   Spotlight preview in Trends in Neurosciences -- The NaVy paradox: reducing sodium currents increases excitability.

Eaton M, Que Z, Zhang J, Beck K, Shi R, McDermott J, Ladisch M*, Yang Y*Multi-electrode array of sensory neurons as an in vitro platform to identify the nociceptive response to pharmaceutical buffer systems of injectable biologics. Pharmaceutical Researchan official journal of the American Association of Pharmaceutical Scientists. 2021 Jul;38(7):1179-86 Featured on the Cover.

Eaton M, Zhang J, Ma Z, Park AC, Lietzke E, Romero CM, Liu Y, Coleman ER, Chen X, Xiao T, Que Z, Lai S, Wu J, Lee JH, Palant S, Nguyen HP, Huang Z, Skarnes WC, Koss WA, Yang Y*Generation and basic characterization of a gene-trap knockout mouse model of Scn2a with a substantial reduction of voltage-gated sodium channel Nav1.2 expressionGenes, Brain and Behavioran official journal of the International Behavioural and Neural Genetics Society. 2021 April; 20(4):e12725 Featured on the Cover.

2020

Verma P&, Eaton M&, Kienle A, Flockerzi D, Yang Y*, Ramkrishna D*. Examining sodium and potassium channel conductances involved in hyperexcitability of chemotherapy-induced peripheral neuropathy: A mathematical and cell culture-based studyFrontiers in Computational Neuroscience2020 Oct 15;14:564980

 

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