Development of Novel Peptide Inhibitors to BAG-1 - Brunn, Jonathan
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One of the most challenging aspects of treating tumors with chemotherapy is that the tumors can develop a resistance to the chemotherapy and survive while the rest of the healthy, non-cancerous cells perish. Higher doses of chemotherapy deliver fewer positive results and at the expense of greater side effects. The purpose of this book is to identify and exploit a weakness at the molecular level of the anti-apoptotic pathway utilized by cancer cells to turn off the "triggered cell death" mechanism of apoptosis and survive chemotherapy. We specifically target the interaction between the…mehr

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Produktbeschreibung
One of the most challenging aspects of treating tumors with chemotherapy is that the tumors can develop a resistance to the chemotherapy and survive while the rest of the healthy, non-cancerous cells perish. Higher doses of chemotherapy deliver fewer positive results and at the expense of greater side effects. The purpose of this book is to identify and exploit a weakness at the molecular level of the anti-apoptotic pathway utilized by cancer cells to turn off the "triggered cell death" mechanism of apoptosis and survive chemotherapy. We specifically target the interaction between the anti-apoptotic protein Bcl-2 Associated Athanogene (BAG-1) and the 70-kilodalton Heat Shock Protein (HSP-70) that is suspected of driving the chemotherapeutic resistance, and seek to disrupt that interaction via peptidyl-biomimetically engineered peptides that are predicted via an in-house computational software named "Contact" and experimentally verified via Biacore (c) binding assays. The program "Contact" is now available for free download at http://www.engineering.vcu.edu/proteinengineering
Autorenporträt
Merging computational molecular modeling and binding assays to discover the next generation of cancer therapeutics without random combinatorial chemistry, our research uses genetically engineered peptides to mimic the biological processes of cancer at the molecular level and disrupt its molecular signaling pathways to make cancer easier to defeat.