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Ivor Benjamin

Professor of Biochemistry and of Medicine

B.A. Hunter College

M.D. Johns Hopkins University

Research

References

ivor.benjamin@hsc.utah.edu

Ivor Benjamin's Lab Page

Ivor Benjamin's PubMed Literature Search

Research

Research opportunities for graduate, medical, and MD/PhD students and postdoctoral trainees are available in the Benjamin Laboratory. Among diverse yet complementary projects, my laboratory focuses on the genetics of heritable cardiomyopathies, transcriptional regulation of stress response pathways (e.g., HSF1), molecular mechanisms of left ventricular remodeling, and the role of molecular chaperones (i.e., heat shock proteins) in protein aggregation diseases.

Recent work from the Benjamin laboratory has generated a dominant mutant allele in the mouse, which faithfully recapitulates cardiac sudden death and heart failure seen in humans. Surprisingly, our genetic and biochemical studies in the mouse led to the discovery that the mutant CRYAB caused reductive stress, as opposed to the well-studied phenomenon of oxidative stress. ‘Reductive stress’ is defined as the excessive production of reducing equivalents in the form of NADPH or reduced glutathione (GSH). Specifically, our mouse studies have identified G6PD, the rate-limiting enzyme of the pentose phosphate pathway, was necessary and sufficient for CryABR120G cardiomyopathy (Figure 1). These findings are not only an important advance for studying a small animal model of a human disease but have introduced a new biological mechanism for heritable disorders. In principle, a small molecular inhibitor of G6PD could be used as a therapeutic intervention for similar protein aggregation disorders (Figure 1).

From Utah’s unique history in genealogy, the discipline of human genetics has propelled the University of Utah into international acclaim with notable firsts in numerous fields, especially cardiovascular genetics. Our campus now sports its first Nobel Laureate, Dr. Mario Capecchi, who was awarded the 2007 Prize for Physiology and Medicine for his pioneering work on gene targeting in knockout mice. We encourage you to explore the many projects being undertaken in diverse model systems (i.e., yeast, flies, mice) by our investigative team and collaborators who are fervently committed to pursuing groundbreaking research in heart and vascular diseases. We are confident your time spent with us will provide you the coveted platform to achieve your future aspirations in cardiovascular medicine, industry and the emerging fields of clinical and translation sciences.

Dysregulation of G6PD activity triggers reductive stress and disease pathogenesis of R120GCryAB. Cell 2007

References