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David B. Neau

Researcher at Cornell University

Publications -  13
Citations -  485

David B. Neau is an academic researcher from Cornell University. The author has contributed to research in topics: Peptide & Binding site. The author has an hindex of 11, co-authored 13 publications receiving 412 citations. Previous affiliations of David B. Neau include Purdue University & Argonne National Laboratory.

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Data publication with the structural biology data grid supports live analysis.

Peter A. Meyer, +73 more
TL;DR: A diffraction data publication and dissemination system, Structural Biology Data Grid (SBDG), to preserve primary experimental data sets that support scientific publications and demonstrates that the information archived by SBDG is sufficient to reprocess data to statistics that meet or exceed the quality of the original published structures.
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Identification and analysis of a bottleneck in PCB biodegradation

TL;DR: It is demonstrated that ortho-chlorinated PCB metabolites strongly inhibit DHBD, promote its suicide inactivation and interfere with the degradation of other compounds, which have important implications for bioremediation strategies.
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Structure-Based Development of Small Molecule PFKFB3 Inhibitors: A Framework for Potential Cancer Therapeutic Agents Targeting the Warburg Effect

TL;DR: A small molecular inhibitor, N4A, was identified as an initial lead compound for PFKFB3 inhibitor with therapeutic potential and determined the crystal structure of the PFK FB3•N4A complex to 2.4 Å resolution and attained the more potent YN1.
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Covalent small molecule inhibitors of Ca(2+)-bound S100B.

TL;DR: Five SBiX–S100B complexes were identified and crystallographic structures confirmed their covalent binding to Cys84 near site 2 and thus present straightforward chemical biology strategies for bridging sites 1 and 3.
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C-terminal modification of the insulin B:11-23 peptide creates superagonists in mouse and human type 1 diabetes.

TL;DR: It is shown for both species that mutations at the C-terminal end of this epitope dramatically improve presentation to these T cells, suggesting that pancreas-specific posttranslational modifications of this peptide may play a role in the induction of diabetes and explain how the pathogenic T cells escape deletion in the thymus.