ArticleProceedings of the National Academy of Sciences of the United States of America1997
Receptor-associated constitutive protein tyrosine phosphatase activity controls the kinase function of JAK1.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 69 citations in OpenAlex.
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- A Potent and Selective Small-Molecule Degrader of STAT3 Achieves Complete Tumor Regression In Vivo.Cancer cell · 2019Article
- The Growth Hormone Receptor: Mechanism of Receptor Activation, Cell Signaling, and Physiological Aspects.Frontiers in endocrinology · 2018Review
- Neuroimmunology of the Interleukins 13 and 4.Brain sciences · 2016Article
- The γ-secretase cleavage product of polycystin-1 regulates TCF and CHOP-mediated transcriptional activation through a p300-dependent mechanism.Developmental cell · 2012Article
- Deficiency of activated STAT1 in head and neck cancer cells mediates TAP1-dependent escape from cytotoxic T lymphocytes.Cancer immunology, immunotherapy : CII · 2011Article
- Sustained signaling by canonical helper T cell cytokines throughout the reactive lymph node.Nature immunology · 2010Article
- JAK redux: a second look at the regulation and role of JAKs in the heart.American journal of physiology. Heart and circulatory physiology · 2009Review
- Stat3 activation is required for the growth of U87 cell-derived tumours in mice.European journal of cancer (Oxford, England : 1990) · 2009Article
- Redox regulation of interleukin-4 signaling.Immunity · 2008Article
- Sorafenib inhibits activation of human peripheral blood T cells by targeting LCK phosphorylation.Leukemia · 2008Article
- Conditioned medium from enterohemorrhagic Escherichia coli-infected T84 cells inhibits signal transducer and activator of transcription 1 activation by gamma interferon.Infection and immunity · 2006Article
- PI3K-AKT pathway negatively controls EGFR-dependent DNA-binding activity of Stat3 in glioblastoma multiforme cells.Oncogene · 2005Article
- Inhibition of constitutively active Stat3 suppresses proliferation and induces apoptosis in glioblastoma multiforme cells.Oncogene · 2002Article
- Regulation of STAT1 nuclear export by Jak1.Molecular and cellular biology · 2000Article
- Complex roles of Stat1 in regulating gene expression.Oncogene · 2000Review
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Exposure of cells to protein tyrosine phosphatase (PTP) inhibitors causes an increase in the phosphotyrosine content of many cellular proteins. However, the level at which the primary signaling event is affected is still unclear. We show that Jaks are activated by tyrosine phosphorylation in cells that are briefly exposed to the PTP inhibitor pervanadate (PV), resulting in tyrosine phosphorylation and functional activation of Stat6 (in addition to other Stats). Mutant cell lines that lack Jak1 activity fail to support PV-mediated [or interleukin 4 (IL-4)-dependent] activation of Stat6 but can be rescued by complementation with functional Jak1. The docking sites for both Jak1 and Stat6 reside in the cytoplasmic domain of the IL-4 receptor alpha-chain (IL-4Ralpha). The glioblastoma-derived cell lines T98G, GRE, and M007, which do not express the IL-4Ralpha chain, fail to support Stat6 activation in response to either IL-4 or PV. Complementation of T98G cells with the IL-4Ralpha restores both PV-mediated and IL-4-dependent Stat6 activation. Murine L929 cells, which do not express the gamma common chain of the IL-4 receptor, support PV-mediated but not IL-4-dependent Stat6 activation. Thus, Stat6 activation by PV is an IL-4Ralpha-mediated, Jak1-dependent event that is independent of receptor dimerization. We propose that receptor-associated constitutive PTP activity functions to down-regulate persistent, receptor-linked kinase activity. Inhibition or deletion of PTP activity results in constitutive activation of cytokine signaling pathways.
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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.