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Michael D. Waterfield

Researcher at Ludwig Institute for Cancer Research

Publications -  152
Citations -  30785

Michael D. Waterfield is an academic researcher from Ludwig Institute for Cancer Research. The author has contributed to research in topics: Kinase & Proto-oncogene tyrosine-protein kinase Src. The author has an hindex of 76, co-authored 151 publications receiving 30122 citations. Previous affiliations of Michael D. Waterfield include University of Fribourg & University College London.

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Solution structure of the C-terminal SH2 domain of the p85 alpha regulatory subunit of phosphoinositide 3-kinase.

TL;DR: The solution structure of the uncomplexed C-terminal SH2 (C-SH2) domain of the p85 alpha subunit of PI 3-kinase has been determined by means of multinuclear, double and triple-resonance NMR experiments and restrained molecular-dynamics simulatedannealing calculations.
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Cluster analysis of an extensive human breast cancer cell line protein expression map database.

TL;DR: The ChiClust tool was used here to order the breast cell lines into groups according to biological characteristics including morphology in vitro and tumour forming ability in vivo, and ChiMap was then used to highlight eight major protein feature‐changes detected between breast cancer cell lines that either do or do not proliferate in nude mice.
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Normal Activation of P70 S6 Kinase by Insulin in Cells Overexpressing Dominant Negative 85-kDa Subunit of Phosphoinositide 3-Kinase

TL;DR: The results raise the possibility that a wortmannin-sensitive pathway independent of heteromeric PI 3-kinase is involved in the activation of p70 S6 kinase by insulin.
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Differential Proteome Analysis of Replicative Senescence in Rat Embryo Fibroblasts

TL;DR: A two-dimensional differential proteome analysis of replicative senescence in serially passaged rat embryo fibroblasts revealed 49 spots whose expression was altered more than 2-fold, including gelsolin, a candidate tumor suppressor for breast cancer, and α-glucosidase II, a member of the family of glucosidases that includes klotho; a defect in klOTHo expression in mice results in a syndrome that resembles human aging.
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Major Role of Epidermal Growth Factor Receptor and Src Kinases in Promoting Oxidative Stress-dependent Loss of Adhesion and Apoptosis in Epithelial Cells

TL;DR: The data demonstrate that EGFR and Src together play a central role in oxidative stress-induced phosphorylation, which in turn results in loss of adhesion, morphological changes, and cell damage in epithelial cells, which provides a general model for redox signaling in other cell systems.