ArticleThe Journal of cell biology2004
Nucleocytoplasmic shuttling by nucleoporins Nup153 and Nup214 and CRM1-dependent nuclear export control the subcellular distribution of latent Stat1.
Article in The Journal of cell biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
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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
82 citing papers in PubMed, 171 citations in OpenAlex.
- An Nrf2-Nup214 positive feedback loop sustains the antioxidant response and promotes microbial infection in ticks.bioRxiv : the preprint server for biology · 2026Article
- M-Motif, a potential non-conventional NLS in YAP/TAZ and other cellular and viral proteins that inhibits classic protein import.iScience · 2025Article
- Review
- Fam102a translocates Runx2 and Rbpjl to facilitate Osterix expression and bone formation.Nature communications · 2025Article
- A novel loss-of-function variant inFrontiers in cellular and infection microbiology · 2025Article
- Designing monomeric IFNγ: The significance of domain-swapped dimer structure in IFNγ immune responses.The Journal of biological chemistry · 2024Article
- Unravelling the interaction between Influenza virus and the nuclear pore complex: insights into viral replication and host immune response.Virusdisease · 2024Review
- Exploring Cellular Gateways: Unraveling the Secrets of Disordered Proteins within Live Nuclear Pores.Research square · 2024Article
- Structural anisotropy results in mechano-directional transport of proteins across nuclear pores.Nature physics · 2024Article
- Review
- Nuclear Import and Export of YAP and TAZ.Cancers · 2023Review
- Review
- Secretoglobin 3A2 protects lung from developing cigarette smoke-induced pulmonary emphysema.The international journal of biochemistry & cell biology · 2023Article
- An inhibitory effect on the nuclear accumulation of phospho-STAT1 by its unphosphorylated form.Cell communication and signaling : CCS · 2022Article
- STAT proteins: a kaleidoscope of canonical and non-canonical functions in immunity and cancer.Journal of hematology & oncology · 2021Review
- Measuring and Interpreting Nuclear Transport in Neurodegenerative Disease-The Example of C9orf72 ALS.International journal of molecular sciences · 2021Review
- ETV7 limits antiviral gene expression and control of influenza viruses.Science signaling · 2021Article
- Crosstalk between nucleocytoplasmic trafficking and the innate immune response to viral infection.The Journal of biological chemistry · 2021Review
- Review
- Unphosphorylated STAT3 in heterochromatin formation and tumor suppression in lung cancer.BMC cancer · 2020Article
22 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interferon stimulation of cells leads to the tyrosine phosphorylation of latent Stat1 and subsequent transient accumulation in the nucleus that requires canonical transport factors. However, the mechanisms that control the predominantly cytoplasmic localization in unstimulated cells have not been resolved. We uncovered that constitutive energy- and transport factor-independent nucleocytoplasmic shuttling is a property of unphosphorylated Stat1, Stat3, and Stat5. The NH(2)- and COOH-terminal Stat domains are generally dispensable, whereas alkylation of a single cysteine residue blocked cytokine-independent nuclear translocation and thus implicated the linker domain into the cycling of Stat1. It is revealed that constitutive nucleocytoplasmic shuttling of Stat1 is mediated by direct interactions with the FG repeat regions of nucleoporin 153 and nucleoporin 214 of the nuclear pore. Concurrent active nuclear export by CRM1 created a nucleocytoplasmic Stat1 concentration gradient that is significantly reduced by the blocking of energy-requiring translocation mechanisms or the specific inactivation of CRM1. Thus, we propose that two independent translocation pathways cooperate to determine the steady-state distribution of Stat1.
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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.