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hypertrophic and HSF gears

We are currently assessing all presently known disease-causing CryAB mutants for their
capacity to induce protein aggregation and reductive stress in vitro  (Project 1). From such analysis, our investigative team will compile a broad but horizontally based platform, which, by design, will be integrated vertically with physical biochemistry and structural studies (Project 2), mitochrondrial energetics and metabolic studies (Project 3), and redox-dependent transcriptional regulation (Project 4) using R120GCryAB as a prototype in disease models (i.e., flies and mice).

Complementary studies are being pursued on the mechanisms of HSF1 expression and small MW Hsps (e.g., HSPB2) in ischemic cardioprotection, hypertrophy and heart failure.

Graduate students and postdoctoral trainees can select from but are not limited to these ongoing projects in the Benjamin laboratory.  Please Visit our Employment Page for more details.

heat shock desmin related myopathy