JAK-STAT Signaling: From Interferons to Cytokines*

By C. Schindler, D. Levy, T. Decker. Journal of Biological Chemistry, 2007

1,281 citations recorded by the source corpus.

Published, JBC Papers in Press, May 14, 2007, DOI 10.1074/jbc.R700016200 Christian Schindler, David E. Levy, and Thomas Decker From the Departments of Microbiology and Medicine, Columbia University, New York, New York 10032, Departments of Pathology and Microbiology, New York University School of Medicine, New York, New York 10016, and Max F. Perutz Laboratories, Department of Microbiology and Immunobiology, University of Vienna, Dr. Bohr-Gasse 9, A1030 Vienna, Austria

Subfields: Immunology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/3d06a1b3e7b61b7ef43433e00a601ad7eb112245

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Citations in the corpus

• Interferons at age 50: past, current and future impact on biomedicine (2007, background): “Subsequently seven STAT and four JAK family members were identified; these transcription factors and tyrosine kinases have been shown to be essential for responses not only to IFNs but also to other cytokines and growth factors as wel”
• Lysine acetylation: codified crosstalk with other posttranslational modifications (2008, background): “Lysine Acetylation in Interferon Signaling As an important part of the initial antiviral defense, interferon (IFN) is rapidly induced to bind and activate its receptors, which in turn trigger phosphorylation, dimerization, and nuclear translocation of STAT proteins (Schindler et al., 2007).”
• Hyper-progressors after Immunotherapy: Analysis of Genomic Alterations Associated with Accelerated Growth Rate (2017, background): “However, immune checkpoint inhibitors can lead to elevated interferon (IFN)-g (22), which in turn activates JAK-STAT signaling (23) resulting in an increase in interferon regulatory factor (IRF)-8 expression (24).”