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Bradley M Keegan

Researcher at University of Notre Dame

Publications -  10
Citations -  116

Bradley M Keegan is an academic researcher from University of Notre Dame. The author has contributed to research in topics: Chemistry & Hsp90. The author has an hindex of 5, co-authored 7 publications receiving 62 citations. Previous affiliations of Bradley M Keegan include Wake Forest University.

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Cannabinoid Receptor Interacting Protein 1a Competition with β-Arrestin for CB1 Receptor Binding Sites

TL;DR: It is determined that agonist-mediated reduction of the density of cell surface endogenously expressed CB1Rs was clathrin and dynamin dependent and could be modeled as agonists-induced aggregation of transiently expressed GFP-CB1R.
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The role and therapeutic potential of Hsp90, Hsp70, and smaller heat shock proteins in peripheral and central neuropathies.

TL;DR: Modulation of Hsp90 by small molecules represents an attractive therapeutic approach against both peripheral and central neuropathies and can be counterbalanced by activation of the HSR.
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Discovery of Novel Hsp90 C-Terminal Inhibitors Using 3D-Pharmacophores Derived from Molecular Dynamics Simulations.

TL;DR: A unique approach that enables the derivation and analysis of interactions between ligands and proteins from molecular dynamics trajectories was used to derive pharmacophore models for virtual screening (VS) and identify suitable binding sites for SB design.
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Assay design and development strategies for finding Hsp90 inhibitors and their role in human diseases.

TL;DR: The tools and assays summarized in this review should be used to develop Hsp90-targeting drugs with high specificity, potency, and drug-like properties that may prove immensely useful in the clinic.
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Chronic baclofen desensitizes GABA(B)-mediated G-protein activation and stimulates phosphorylation of kinases in mesocorticolimbic rat brain.

TL;DR: It is postulate that those neuroadaptive effects of GABAB stimulation mediated by G-proteins and their sequelae correlate with tolerance to several of baclofen's effects, whereas sustained signaling via kinase cascades points to cross-talk between GABAB receptors and alternative mechanisms that are resistant to desensitization.