ArticleProceedings of the National Academy of Sciences of the United States of America1995
STAT3 activation by cytokines utilizing gp130 and related transducers involves a secondary modification requiring an H7-sensitive kinase.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 206 citations in OpenAlex.
- Proximal protein landscapes of the type I interferon signaling cascade reveal negative regulation by PJA2.Nature communications · 2024Article
- Inactivity of Stat3 in sensory and non-sensory cells of the mature cochlea.Frontiers in molecular neuroscience · 2024Article
- Deciphering intercellular signaling complexes by interaction-guided chemical proteomics.Nature communications · 2023Article
- The complementary roles of STAT3 and STAT1 in cancer biology: insights into tumor pathogenesis and therapeutic strategies.Frontiers in immunology · 2023Review
- STAT3 suppresses the AMPKα/ULK1-dependent induction of autophagy in glioblastoma cells.Journal of cellular and molecular medicine · 2022Article
- The Roles of Post-Translational Modifications in STAT3 Biological Activities and Functions.Biomedicines · 2021Review
- Targeting Janus Kinases and Signal Transducer and Activator of Transcription 3 to Treat Inflammation, Fibrosis, and Cancer: Rationale, Progress, and Caution.Pharmacological reviews · 2020Review
- The critical role that STAT3 plays in glioma-initiating cells: STAT3 addiction in glioma.Oncotarget · 2018Article
- STAT3 signaling in immunity.Cytokine & growth factor reviews · 2016Review
- STAT3 Represses Nitric Oxide Synthesis in Human Macrophages upon Mycobacterium tuberculosis Infection.Scientific reports · 2016Article
- Neuroendocrine Regulation of Metabolism.Journal of neuroendocrinology · 2016Review
- Human Cytomegalovirus Immediate-Early 1 Protein Rewires Upstream STAT3 to Downstream STAT1 Signaling Switching an IL6-Type to an IFNγ-Like Response.PLoS pathogens · 2016Article
- STAT3 association with microtubules and its activation are independent of HDAC6 activity.DNA and cell biology · 2015Article
- EGFR signaling and autophagy dependence for growth, survival, and therapy resistance.Cell cycle (Georgetown, Tex.) · 2014Review
- IL-6-STAT3 signaling and premature senescence.JAK-STAT · 2013Review
- Inhibition of a novel specific neuroglial integrin signaling pathway increases STAT3-mediated CNTF expression.Cell communication and signaling : CCS · 2013Article
- Leptin signaling and circuits in puberty and fertility.Cellular and molecular life sciences : CMLS · 2013Review
- Inhibition of the Jak-STAT pathway prevents CNTF-mediated survival of axotomized oxytocinergic magnocellular neurons in organotypic cultures of the rat supraoptic nucleus.Experimental neurology · 2013Article
- Ciliary neurotrophic factor receptor regulation of adult forebrain neurogenesis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Intranuclear crosstalk between extracellular regulated kinase1/2 and signal transducer and activator of transcription 3 regulates JEG-3 choriocarcinoma cell invasion and proliferation.TheScientificWorldJournal · 2013Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ciliary neurotrophic factor, oncostatin M, leukemia-inhibitory factor, and interleukin 6 are related cytokines that initiate signaling by homodimerizing the signal-transducing receptor component gp130 or by heterodimerizing gp130 with a gp130-related receptor component. Receptor dimerization in turn activates receptor-associated kinases of the Jak/Tyk family, resulting in the rapid tyrosine phosphorylation of several intracellular proteins, including those of two members of the signal transducers and activators of transcription (STAT) family--STAT1 and STAT3. Here we show that all cytokines that utilize gp130 sequentially induce two distinct forms of STAT3 in all responding cells examined, with the two forms apparently differing because of a time-dependent secondary serine/threonine phosphorylation involving an H7-sensitive kinase. While both STAT3 forms bind DNA and translocate to the nucleus, the striking time-dependent progression from one form to the other implies other important functional differences between the two forms. Granulocyte colony-stimulating factor, which utilizes a receptor highly related to gp130, also induces these two forms of STAT3. In contrast to a number of other cytokines and growth factors, all cytokines using gp130 and related signal transducers consistently and preferentially induce the two forms of STAT3 as compared with STAT1; this characteristic STAT activation pattern is seen regardless of which Jak/Tyk kinases are used in a particular response, consistent with the notion that the receptor components themselves are the primary determinants of which STATs are activated.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.