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The National Institute for Biotechnology
in the Negev Ltd.
Ben-Gurion University of the Negev

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Research Field

Research in the Shoshan-Barmatz laboratory focuses on VDAC1, a protein located in the outer mitochondrial membrane that acts as a gatekeeper of mitochondrial functions, including metabolism and energy production. VDAC1 serves as a hub protein, interacting with various other proteins. Its interactome includes proteins associated with DNA and RNA maintenance, and proteins involved in metabolism, apoptosis, signal transduction, and anti-oxidation, and more. This enables the regulation and integration of mitochondrial functions with other cellular activities.

The numerous roles played by VDAC1, as well as its overexpression in disease states, led the Shoshan-Barmatz group to develop several VDAC1-based strategies that lead to dramatic effects on various diseases considered as metabolic diseases, all of which are characterized by VDAC1 overexpression and altered cell metabolism and/or apoptosis. Their studies involve a variety of approaches, such as molecular biology, protein purification, electrophysiology (for monitoring single-channel activity), tissue culture, and the use of animal models for various diseases (e.g., breast, liver, and lung cancers, melanomas, glioblastoma, Alzheimer’s disease, and type 2 diabetes). As such, Prof. Shoshan-Barmatz and her team were able to develop and test VDAC1-based strategies simultaneously attacking several cancer hallmarks, and for use in treating type 2 diabetes, Alzheimer’s disease, and cardiovascular diseases. These VDAC1-based strategies include several VDAC1-interacting small molecules, VDAC1-based peptides, and VDAC1-specific siRNA, all of which have been validated in vitro and in vivo and are protected by dozens of patents.

Prof. Varda Shoshan-Barmatz

Prof. Shoshan-Barmatz studies metabolic diseases associated with mitochondrial dysfunction. Specifically, she focuses on the protein VDAC1 (voltage-dependent anion channel), which serves as a mitochondrial gatekeeper, controlling the metabolic and energetic cross-talk between mitochondria and the rest of the cell; VDAC1 is also a key protein in mitochondria-mediated apoptosis. Due to the central role of VDAC1 in the life and death of the cell and its overexpression in diseases, including cancers, Alzheimer’s disease, cardiovascular diseases, and type 2 diabetes, VDAC1-based strategies have been developed as potential therapeutics for medical intervention in these diseases.

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