ArticleThe EMBO journal1996
The rapid inactivation of nuclear tyrosine phosphorylated Stat1 depends upon a protein tyrosine phosphatase.
Article in The EMBO journal, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
84 citing papers in PubMed, 317 citations in OpenAlex.
- Nuclear RSK1 mediates interferon-γ-induced proinflammatory activation in human primary macrophages and humanized mice.Science advances · 2026Article
- Lactate Activates the HCAR1/β-Arrestin2/PP2A Signaling Axis to Mediate STAT1/2 Dephosphorylation and Drive Osteosarcoma Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Hemgn Protects Hematopoietic Stem and Progenitor Cells Against Transplantation Stress Through Negatively Regulating IFN-γ Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Crosstalk between nucleocytoplasmic trafficking and the innate immune response to viral infection.The Journal of biological chemistry · 2021Review
- Negative Regulation of the Innate Immune Response through Proteasomal Degradation and Deubiquitination.Viruses · 2021Review
- Phospho-Ser727 triggers a multistep inactivation of STAT3 by rapid dissociation of pY705-SH2 through C-terminal tail modulation.International immunology · 2020Article
- The Methyltransferase-Like Domain of Chikungunya Virus nsP2 Inhibits the Interferon Response by Promoting the Nuclear Export of STAT1.Journal of virology · 2018Article
- Newcastle Disease Virus V Protein Targets Phosphorylated STAT1 to Block IFN-I Signaling.PloS one · 2016Article
- Mutations in the linker domain affect phospho-STAT3 function and suggest targets for interrupting STAT3 activity.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Interferons and viruses: an evolutionary arms race of molecular interactions.Trends in immunology · 2015Review
- Mogrol represents a novel leukemia therapeutic, via ERK and STAT3 inhibition.American journal of cancer research · 2015Article
- DNA binding reduces the dissociation rate of STAT1 dimers and impairs the interdimeric exchange of protomers.BMC biochemistry · 2014Article
- High STAT1 mRNA levels but not its tyrosine phosphorylation are associated with macrophage infiltration and bad prognosis in breast cancer.BMC cancer · 2014Article
- Article
- Protein tyrosine phosphatases as wardens of STAT signaling.JAK-STAT · 2014Review
- Non-genomic STAT5-dependent effects at the endoplasmic reticulum and Golgi apparatus and STAT6-GFP in mitochondria.JAK-STAT · 2013Review
- STATs get their move on.JAK-STAT · 2013Review
- Transient oscillatory dynamics of interferon beta signaling in macrophages.BMC systems biology · 2013Article
- Wedelolactone, a naturally occurring coumestan, enhances interferon-γ signaling through inhibiting STAT1 protein dephosphorylation.The Journal of biological chemistry · 2013Article
- Evidence against a role for β-arrestin1 in STAT1 dephosphorylation and the inhibition of interferon-γ signaling.Molecular cell · 2013Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
After interferon-gamma (IFN-gamma) treatment of cells the appearance of tyrosine phosphorylated Stat1 in the nucleus was maximal within 20-30 min, remained for 2-2.5 h and activated molecules disappeared by 4 h. In the absence of continued signaling from the receptor (imposed by staurosporine treatment) previously activated Stat1 disappeared completely within 60 min, implying continuous generation and removal of active molecules during extended IFN-gamma treatment. Proteasome inhibitors prolonged the time of activation of Stat1 by prolonging signaling from the receptor but not by blocking removal of already activated Stat1 molecules. By analyzing with 35S labeling the distribution of total Stat1 and activated Stat1, we concluded that the Stat1 molecules promptly cycle into the nucleus as tyrosine phosphorylated molecules and later return quantitatively to the cytoplasm as non-phosphorylated molecules. Therefore, the removal of the activated Stat1 molecules from the nucleus appears not to be proteolytic but must depend on a protein tyrosine phosphatase(s).
Indexed as
Identifiers
8947049PMC452449W1702674772What OpenQuestion holds
Registered trials
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.