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Kurt R. Auger

Researcher at GlaxoSmithKline

Publications -  59
Citations -  10952

Kurt R. Auger is an academic researcher from GlaxoSmithKline. The author has contributed to research in topics: Phosphatidylinositol & Protein subunit. The author has an hindex of 35, co-authored 58 publications receiving 10580 citations. Previous affiliations of Kurt R. Auger include Harvard University & Tufts University.

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Oncogenes and signal transduction

TL;DR: The protein-tyrosine kinase oncogenes will be the primary focus of the review as discussed by the authors, however, biochemical connections between the protein tyrosine Kinases and oncoproteins of the Ras,Raf,Fos,Jun, and Rel families as well as the protein kinase C family are also discussed.
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Inhibition of BET recruitment to chromatin as an effective treatment for MLL-fusion leukaemia

TL;DR: It is shown that a novel small molecule inhibitor of the BET family, GSK1210151A (I-BET151), has profound efficacy against human and murine MLL-fusion leukaemic cell lines, through the induction of early cell cycle arrest and apoptosis, establishing the displacement of BET proteins from chromatin as a promising epigenetic therapy for these aggressive leukaemias.
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PDGF-dependent tyrosine phosphorylation stimulates production of novel polyphosphoinositides in intact cells.

TL;DR: Both the temporal production of these novel phospholipids after PDGF stimulation and the observation of the enzymatic activities that produce them in alpha-P-tyr immunoprecipitates suggest that these phospholIPids are excellent candidates for mediators of the PDGF mitogenic response.
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Purification and characterization of phosphoinositide 3-kinase from rat liver.

TL;DR: The purified phosphoinositide 3-kinase preparation contained an 85-kDa protein and a protein doublet of approximately 110 kDa, which was the same protein previously shown to associate with polyoma virus middle T antigen and the platelet-derived growth factor receptor.
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Endotoxin and tumor necrosis factor induce interleukin-1 gene expression in adult human vascular endothelial cells.

TL;DR: It is reported here that bacterial endotoxin and recombinant human tumor necrosis factor cause accumulation of IL-1 beta mRNA in adult human vascular endothelial cells, which might play an early role in the pathogenesis of vasculitis, allograft rejection, and arteriosclerosis.