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Research Interests

Cancer Biology and Therapeutics

Cardiovascular Science

  • David Auerbach, PhD
    Assistant Professor
    Research Interests:

    Cellular, animal, and clinical approaches to investigate the susceptibility and mechanisms for electrical disturbances in both the brain (seizures) and heart (arrhythmias.)

    CURE Epilepsy Foundation: The Cameron Boyce Foundation and CURE Epilepsy Partner to Fund New SUDEP Research (1/2022)

    ABC News (Washington, DC): Victor and Libby Boyce raise epilepsy awareness in honor of late son Cameron (1/2022)

    Upstate News: Upstate Professor Auerbach receives International CURE Epilepsy award (11/2021)

    Upstate Health Link on Air and Upstate News: Scientist hopes study of electrical disturbances in the heart and brain could lead to new therapies (7/2020)

    Pediheart Podcast # 5: Antiseizure and AntiDepressants in LQTS (2/23/18)

    Eureka Alert: The heart-brain connection: The link between LQTS and seizures (7/29/16)

  • Arkadii Perzov, PhD
    Professor
    Research Interests:

    Biophysical mechanisms of cardiac arrhythmias; fluorescence imaging.

  • Justin Ryan, PhD
    Assistant Professor
  • Nathan Tucker, PhD
    Associate Professor
  • Norifumi Urao, MD/PhD
    Assistant Professor
    Research Interests:

    Mechanism of wound healing and tissue repair/bone marrow stem cell reactivity to stress and injury/oxidative stress and epigenetic gene regulation

  • Richard Veenstra, PhD
    Professor
    Research Interests:

    Regulation of connexin-specific-gap-junctions; gap junction channel biophysics.

  • Xinrui Wang, PhD
    Assistant Professor
    Research Interests:

    Every 34 seconds, someone in the United States experience a heart attack, or what is medically termed a myocardial infarction. A heart attack occurs when a heart blood vessel becomes clogged thereby starving the heart of oxygen and energy. If the clot is not removed quickly, the muscle cells (cardiomyocytes) die, and the tissue becomes permanently damaged. The cardiac dysfunction caused by myocardial infarction would be ameliorated by myocardial regeneration and contractile function maintenance.

    Lysine acetylation, catalyzed by acetyltransferases, is a reversible protein modification regulating cellular processes that enables cells to react specifically and rapidly to internal and external perturbations. A regulatory role of lysine acetylation has been revealed in cardiovascular diseases. However, the potential of targeting acetyltransferases for managing myocardial infarction is not yet fully studied.

    Our research focuses on the lysine (K) acetyltransferase Kat5, commonly known as Tip60 (Tat-interactive protein 60kD). Using a mouse model in which the Kat5 gene can be conditionally disrupted in cardiomyocytes, our recent findings show that depletion of Tip60 after myocardial infarction promotes cardiomyocyte regeneration, reduces scarring, and preserves contractile function. These beneficial effects of genetic Tip60 knockout were mimicked by a small molecule Tp60 inhibitor. However, the notable enhancement in systolic function does not solely stem from reduced scarring in Tip60 depleted or inhibited hearts.

    The transcriptomic analysis indicates the involvement of Tip60 in cardiomyocyte excitability, contractility, and mitochondrial function. The defects in these pathways collectively lead to cardiac dysfunction after myocardial infarction. Accordingly, the ongoing projects in our lab aim to (1) investigate the role of Tip60 in physiological and pathological calcium signaling and mitochondrial function, and (2) address whether the cellular electrical and mechanical changes induced by genetic depletion or drug inhibition of Tip60 account for the organ-scale functional recovery after myocardial infarction.

    Studying the role of Tip60 in electrical, biomechanical, and metabolic pathways will reveal novel molecular linkage between lysine acetylation and myocardial contraction, providing insights for the development of strategies to re-muscularize the injured myocardium. Proving that inhibition of Tip60 after myocardial infarction promotes myocardial regeneration and maintains excitation-contraction-metabolism coupling would identify this versatile protein as a unique therapeutic target for treating ischemic heart disease.

Cell Signaling

  • Xinrui Wang, PhD
    Assistant Professor
    Research Interests:

    Every 34 seconds, someone in the United States experience a heart attack, or what is medically termed a myocardial infarction. A heart attack occurs when a heart blood vessel becomes clogged thereby starving the heart of oxygen and energy. If the clot is not removed quickly, the muscle cells (cardiomyocytes) die, and the tissue becomes permanently damaged. The cardiac dysfunction caused by myocardial infarction would be ameliorated by myocardial regeneration and contractile function maintenance.

    Lysine acetylation, catalyzed by acetyltransferases, is a reversible protein modification regulating cellular processes that enables cells to react specifically and rapidly to internal and external perturbations. A regulatory role of lysine acetylation has been revealed in cardiovascular diseases. However, the potential of targeting acetyltransferases for managing myocardial infarction is not yet fully studied.

    Our research focuses on the lysine (K) acetyltransferase Kat5, commonly known as Tip60 (Tat-interactive protein 60kD). Using a mouse model in which the Kat5 gene can be conditionally disrupted in cardiomyocytes, our recent findings show that depletion of Tip60 after myocardial infarction promotes cardiomyocyte regeneration, reduces scarring, and preserves contractile function. These beneficial effects of genetic Tip60 knockout were mimicked by a small molecule Tp60 inhibitor. However, the notable enhancement in systolic function does not solely stem from reduced scarring in Tip60 depleted or inhibited hearts.

    The transcriptomic analysis indicates the involvement of Tip60 in cardiomyocyte excitability, contractility, and mitochondrial function. The defects in these pathways collectively lead to cardiac dysfunction after myocardial infarction. Accordingly, the ongoing projects in our lab aim to (1) investigate the role of Tip60 in physiological and pathological calcium signaling and mitochondrial function, and (2) address whether the cellular electrical and mechanical changes induced by genetic depletion or drug inhibition of Tip60 account for the organ-scale functional recovery after myocardial infarction.

    Studying the role of Tip60 in electrical, biomechanical, and metabolic pathways will reveal novel molecular linkage between lysine acetylation and myocardial contraction, providing insights for the development of strategies to re-muscularize the injured myocardium. Proving that inhibition of Tip60 after myocardial infarction promotes myocardial regeneration and maintains excitation-contraction-metabolism coupling would identify this versatile protein as a unique therapeutic target for treating ischemic heart disease.

  • Richard JH Wojcikiewicz, PhD
    Professor and Chair
    Research Interests:

    Intracellular signaling via InsP3 receptors and their regulation by the ubiquitin/proteasome pathway and Bcl-2 family proteins.

Computational Biology/Machine Learning

Drug Discovery and Development

  • Yamin Li, PhD
    Assistant Professor
    Research Interests:

    Development of lipid nanoparticles for the delivery of small molecule drugs, proteins, and DNA/RNA for gene therapy, cancer immunotherapy, mRNA vaccines, etc.

  • Hong Lu, PhD
    Assistant Professor
    Research Interests:

    • Nuclear receptors in regulation of hepatic gene expression and liver diseases
    • Progression of alcoholic/non-alcoholic fatty liver to steatohepatitis, liver cirrhosis, and liver cancer
    • Development of liver-targeting prodrugs and liver-specific  delivery of genes/proteins
    • Liver-lung-dual-specific mRNA delivery for the treatment of ARDS and sepsis

  • Juntao Luo, PhD
    Professor
    Research Interests:

    Nanomedicine, drug delivery, cancer imaging and cancer treatment; gene delivery and gene therapy, protein/peptide delivery. biomaterials in tissue engineering; combinatorial chemistry and drug discovery; High throughput screening; microarrays. 

Epilepsy

Macrophages and Wound Healing

  • Norifumi Urao, MD/PhD
    Assistant Professor
    Research Interests:

    Mechanism of wound healing and tissue repair/bone marrow stem cell reactivity to stress and injury/oxidative stress and epigenetic gene regulation

Sepsis and Immune Modulation

  • Juntao Luo, PhD
    Professor
    Research Interests:

    Nanomedicine, drug delivery, cancer imaging and cancer treatment; gene delivery and gene therapy, protein/peptide delivery. biomaterials in tissue engineering; combinatorial chemistry and drug discovery; High throughput screening; microarrays. 

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