Jay Brenman, PhD

Professor

Research Description

All cells and organisms must monitor and maintain their energy levels for survival. One particular protein kinase, AMP-activated protein kinase (AMPK) plays a central role in energy balance. AMPK consists of a protein complex encoded by three subunits, a serine-threonine kinase catalytic subunit (α) and two regulatory subunits (ß, γ). When AMPK signaling is disrupted cells undergo cell death and organisms can not survive limited starvation.

AMPK has many potential biomedically-relevant functions. AMPK is proposed to be a therapeutic target for Type 2 diabetes and Metabolic syndrome (obesity, insulin resistance, cardiovascular disease). In addition, since cancer cells have larger energetic requirements than non-dividing cells, targeting AMPK might be an attractive approach for attacking cancer.

We identified mutations in the AMPK kinase domain (AMPKα) during a genetic screen looking for “neurodegeneration mutants” in Drosophila. Inactivation of AMPK leads to neurodegeneration-like phenotypes in neurons and abnormal metabolism in other cells. Our lab uses combinations of genetics, biochemistry/proteomics and cell culture models to try to further identify new molecules involved in AMPK signaling. We are particularly interested in how AMPK signaling and molecules it regulates are relevant to:

  • Neurodegeneration
  • Metabolism (Type 2 Diabetes/Cardiac Disease)
  • Cancer

I am the Director of Graduate Studies for the Neuroscience PhD Curriculum and the Cell Biology and Physiology Curriculum.

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Affiliations