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Philip Cohen

Researcher at University of Dundee

Publications -  625
Citations -  115349

Philip Cohen is an academic researcher from University of Dundee. The author has contributed to research in topics: Protein kinase A & Phosphorylation. The author has an hindex of 154, co-authored 555 publications receiving 110856 citations. Previous affiliations of Philip Cohen include University of Washington & Medical Research Council.

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Inhibition of glycogen synthase kinase-3 by insulin mediated by protein kinase B.

TL;DR: It is shown that agents which prevent the activation of both MAPKAP kinase-1 and p70S6k by insulin in vivo do not block the phosphorylation and inhibition of GSK3, and it is demonstrated that PKB is the product of the proto-oncogene protein kinase B (PKB, also known as Akt/RAC).
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Specificity and mechanism of action of some commonly used protein kinase inhibitors

TL;DR: The results demonstrate that the specificities of protein kinase inhibitors cannot be assessed simply by studying their effect on kinases that are closely related in primary structure, and proposes guidelines for the use of protein Kinase inhibitors in cell-based assays.
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PD 098059 Is a Specific Inhibitor of the Activation of Mitogen-activated Protein Kinase Kinase in Vitro and in Vivo

TL;DR: The results indicate that the activation of Raf is suppressed and that its inactivation is accelerated by a downstream component(s) of the MAP kinase pathway.
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The ground state of embryonic stem cell self-renewal

TL;DR: It is shown that extrinsic stimuli are dispensable for the derivation, propagation and pluripotency of ES cells and reveal that ES cells have an innate programme for self-replication that does not require extrinsics instruction.
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Characterization of a 3-phosphoinositide-dependent protein kinase which phosphorylates and activates protein kinase Bα

TL;DR: In this paper, a protein kinase that phosphorylates PKB α at Thr308 and increases its activity over 30-fold was found to play a key role in mediating the activation of PKB by insulin and growth factors.