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Scott M. Ulrich

Researcher at Ithaca College

Publications -  18
Citations -  2140

Scott M. Ulrich is an academic researcher from Ithaca College. The author has contributed to research in topics: HDAC8 & Acetylation. The author has an hindex of 9, co-authored 17 publications receiving 1730 citations. Previous affiliations of Scott M. Ulrich include University of California.

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Suppression of Oxidative Stress by β-Hydroxybutyrate, an Endogenous Histone Deacetylase Inhibitor

TL;DR: It is reported that the ketone body d-β-hydroxybutyrate (βOHB) is an endogenous and specific inhibitor of class I histone deacetylases (HDACs), and treatment of mice with βOHB conferred substantial protection against oxidative stress.
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Histone Deacetylase 8 in Neuroblastoma Tumorigenesis

TL;DR: The data point toward an important role of HDAC8 in neuroblastoma pathogenesis and identify this HDAC family member as a specific drug target for the differentiation therapy of neuroblastomas.
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Design and evaluation of 'Linkerless' hydroxamic acids as selective HDAC8 inhibitors

TL;DR: New HDAC inhibitors designed to exploit a unique sub-pocket in the HDAC8 active site that is unusually malleable and can accommodate inhibitor structures that are distinct from the canonical 'zinc binding group-linker-cap group' structures of SAHA, TSA, and similarHDAC inhibitors.
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A Quorum-Sensing Antagonist Targets Both Membrane-Bound and Cytoplasmic Receptors and Controls Bacterial Pathogenicity

TL;DR: The most potent antagonist protects Caenorhabditis elegans from quorum-sensing-mediated killing by Chromobacterium violaceum, validating the notion that targeting quorum sensing has potential for antimicrobial drug development.
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Mechanism by which a recently discovered allosteric inhibitor blocks glutamine metabolism in transformed cells.

TL;DR: It is shown that 968 has the highest affinity for monomeric GAC and that the dose-dependent binding of 968 to GAC monomers directly matches its dose- dependent inhibition of enzyme activity and cellular transformation, which offer exciting new strategies for interfering with the metabolic reprogramming critical for malignant transformation.