G
George Stark Stark
Researcher at Cleveland Clinic Lerner Research Institute
Publications - 58
Citations - 14446
George Stark Stark is an academic researcher from Cleveland Clinic Lerner Research Institute. The author has contributed to research in topics: Signal transduction & STAT1. The author has an hindex of 41, co-authored 58 publications receiving 13449 citations. Previous affiliations of George Stark Stark include Case Western Reserve University & Cleveland Clinic.
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Journal ArticleDOI
Jak-STAT pathways and transcriptional activation in response to IFNs and other extracellular signaling proteins
TL;DR: A previously unrecognized direct signal transduction pathway to the nucleus has been uncovered: IFN-receptor interaction at the cell surface leads to the activation of kinases of the Jak family that phosphorylate substrate proteins called STATs (signal transducers and activators of transcription).
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Interferons at age 50: past, current and future impact on biomedicine.
Ernest C. Borden,Ganes C. Sen,Gilles Uzé,Robert H. Silverman,Richard M. Ransohoff,Graham R. Foster,George Stark Stark +6 more
TL;DR: The goal is to offer a molecular and clinical perspective that will enable IFNs or their TLR agonist inducers to reach their full clinical potential.
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SIGIRR, a negative regulator of Toll-like receptor-interleukin 1 receptor signaling.
David N Wald,Jinzhong Qin,Zhendong Zhao,Youcun Qian,Mayumi Naramura,Liping Tian,Jennifer E. Towne,John E. Sims,George Stark Stark,Xiaoxia Li +9 more
TL;DR: Inflammation is enhanced in SIGIRR-deficient mice, as shown by their enhanced chemokine induction after IL-1 injection and reduced threshold for lethal endotoxin challenge and biochemical analysis indicated that SIGirR binds to the TLR–IL-1R signaling components in a ligand-dependent way.
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Stat1-dependent and -independent pathways in IFN-γ-dependent signaling
TL;DR: The paradigm that emerged from studies during the past decade established a central role for Jak-Stat signaling pathways in promoting the diverse cellular responses induced by interferon gamma, but recent studies have shown that the IFN-gamma receptor activates additional signaling pathways and can regulate gene expression by Stat1-independent pathways.
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Defective TNF-α-Induced Apoptosis in STAT1-Null Cells Due to Low Constitutive Levels of Caspases
Aseem Kumar,Mairead Commane,Thomas W. Flickinger,Curt M. Horvath,Curt M. Horvath,George Stark Stark,George Stark Stark +6 more
TL;DR: Variant STAT1 proteins carrying point mutations that inactivate domains required for STAT dimer formation nevertheless restored protease expression and sensitivity to apoptosis, indicating that the functions of STAT1 required for these activities are different from those that mediate induced gene expression.