L
Lawrence M. Pfeffer
Researcher at University of Tennessee Health Science Center
Publications - 210
Citations - 11899
Lawrence M. Pfeffer is an academic researcher from University of Tennessee Health Science Center. The author has contributed to research in topics: Interferon & Signal transduction. The author has an hindex of 55, co-authored 202 publications receiving 11010 citations. Previous affiliations of Lawrence M. Pfeffer include University of Tennessee & King Hussein Cancer Center.
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Journal ArticleDOI
NF-κB activation by tumour necrosis factor requires the Akt serine–threonine kinase
Osman N. Ozes,Lindsey D. Mayo,Jason A. Gustin,Susan R. Pfeffer,Lawrence M. Pfeffer,David B. Donner +5 more
TL;DR: It is shown that the Akt serine–threonine kinase is involved in the activation of NF-κB by tumour necrosis factor (TNF), and that Akt is part of a signalling pathway that is necessary for inducing key immune and inflammatory responses.
Journal Article
Biological Properties of Recombinant α-Interferons: 40th Anniversary of the Discovery of Interferons
Lawrence M. Pfeffer,Charles A. Dinarello,Ronald B. Herberman,Bryan R.G. Williams,Ernest C. Borden,Ronald Bordens,Mark R. Walter,Tattanahalli L. Nagabhushan,Paul P. Trotta,Sidney Pestka +9 more
TL;DR: Recent developments in the understanding of the antiviral and immunoregulatory properties of IFN-alpha, the nature of the multisubunit IFn-alpha receptor, and the molecular mechanisms of signal transduction are reviewed.
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STAT3 as an adapter to couple phosphatidylinositol 3-kinase to the IFNAR1 chain of the type I interferon receptor.
TL;DR: STAT3, a transcription factor for acute phase response genes, was found to act as an adapter molecule in signal transduction from the type I interferon receptor.
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The Role of miR-21 in Cancer.
TL;DR: In this paper, the role of miR-21 and its target genes in different cancers, and provide insight into how this oncogenic miRNA regulates cancer cell proliferation, migration, and apoptosis by suppressing the expression of tumor suppressors.
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Interferon α/β Promotes Cell Survival by Activating Nuclear Factor κB through Phosphatidylinositol 3-Kinase and Akt
TL;DR: STAT3, PI-3K, and Akt are components of an IFN signaling pathway that promotes cell survival through NF-κB activation, and Ly294002, a dominant-negative PI- 3K construct, and kinase-dead Akt block IFN-promoted cell survival, enhancing apoptotic cell death.