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Edward A. O'Neill

Researcher at Merck & Co.

Publications -  81
Citations -  4114

Edward A. O'Neill is an academic researcher from Merck & Co.. The author has contributed to research in topics: Sitagliptin & Placebo. The author has an hindex of 29, co-authored 80 publications receiving 3892 citations. Previous affiliations of Edward A. O'Neill include United States Military Academy.

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FK-506- and CsA-sensitive activation of the interleukin-2 promoter by calcineurin.

TL;DR: It is reported that transfection of a calcineurin catalytic subunit increases the 50% inhibitory concentration of the immunosuppressants FK-506 and CsA, and that a mutant subunit acts in synergy with phorbol ester alone to activate the interleukin-2 promoter in a drug-sensitive manner.
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Calcineurin acts in synergy with PMA to inactivate I kappa B/MAD3, an inhibitor of NF-kappa B.

TL;DR: These data provide the first demonstration in vivo thatactivation of a protein phosphatase can inactivate I kappa B, and suggest one possible explanation for mechanism‐based toxicities associated with FK‐506 and CsA by demonstrating that these drugs can inhibit the calcineurin‐dependent activation of a virtually ubiquitous transcription factor.
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Design and synthesis of potent, selective, and orally bioavailable tetrasubstituted imidazole inhibitors of p38 mitogen-activated protein kinase.

TL;DR: 48, a potent and selective p38 MAP kinase inhibitor which inhibits lipopolysaccharide-stimulated release of TNF-alpha from human blood with an IC50 2.2 nM shows good oral bioavailability in rat and rhesus monkey, and demonstrates significant improvement in measures of disease progression in a rat adjuvant-induced arthritis model.
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The activation state of p38 mitogen-activated protein kinase determines the efficiency of ATP competition for pyridinylimidazole inhibitor binding.

TL;DR: It is demonstrated in vivo that at concentrations consistent with its IC50 as a cytokine inhibitor, SB203580 can inhibit stimulus-induced phosphorylation of p38 at the Thr-Gly-Tyr activation motif.
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Patients with type 2 diabetes mellitus have higher risk for acute pancreatitis compared with those without diabetes

TL;DR: The aetiology of acute pancreatitis is complex, and many risk factors for AP are shared by patients with type 2 diabetes mellitus (T2DM), but few have assessed risk Factors for AP specifically in T2DM patients.