ArticleMolecular and cellular biology2014
STAT1β is not dominant negative and is capable of contributing to gamma interferon-dependent innate immunity.
Article in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 42 citations in OpenAlex.
- Signal Transduction and Transcription Activator 1 in Pan-Cancer: Prognostic and Immunological Value.Clinical and experimental medicine · 2026Article
- IFNγ shapes macrophage inflammatory responses by STAT1 isoform-specific epigenetic and transcriptional mechanisms.BMC genomics · 2026Article
- STAT1β modulates the tumor immune microenvironment to improve prognosis in ovarian cancer: a comprehensive study of transcriptional and protein expression differences.Journal of ovarian research · 2025Article
- STAT Signature Dish: Serving Immunity with a Side of Dietary Control.Biomolecules · 2025Review
- Review
- Article
- Transcriptional control of interferon-stimulated genes.The Journal of biological chemistry · 2024Review
- Astrocyte-induced Cdk5 expedites breast cancer brain metastasis by suppressing MHC-I expression to evade immune recognition.Nature cell biology · 2024Article
- JAK-STAT signaling maintains homeostasis in T cells and macrophages.Nature immunology · 2024Article
- Article
- The implications of alternative pre-mRNA splicing in cell signal transduction.Experimental & molecular medicine · 2023Review
- Regulation of macrophage IFNγ-stimulated gene expression by the transcriptional coregulator CITED1.Journal of cell science · 2023Article
- Mouse Trophoblast Cells Can Provide IFN-Based Antiviral Protection to Embryonic Stem Cells via Paracrine Signaling.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- STAT1 and Its Crucial Role in the Control of Viral Infections.International journal of molecular sciences · 2022Review
- CITED2 inhibits STAT1-IRF1 signaling and atherogenesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Review
- Nuclear ADP-ribosylation drives IFNγ-dependent STAT1α enhancer formation in macrophages.Nature communications · 2021Article
- Untwining Anti-Tumor and Immunosuppressive Effects of JAK Inhibitors-A Strategy for Hematological Malignancies?Cancers · 2021Review
- High Dose IFN-Frontiers in immunology · 2021Article
- The Dual Role of STAT1 in Ovarian Cancer: Insight Into Molecular Mechanisms and Application Potentials.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor STAT1 is essential for interferon (IFN)-mediated immunity in humans and mice. STAT1 function is tightly regulated, and both loss- and gain-of-function mutations result in severe immune diseases. The two alternatively spliced isoforms, STAT1α and STAT1β, differ with regard to a C-terminal transactivation domain, which is absent in STAT1β. STAT1β is considered to be transcriptionally inactive and to be a competitive inhibitor of STAT1α. To investigate the functions of the STAT1 isoforms in vivo, we generated mice deficient for either STAT1α or STAT1β. As expected, the functions of STAT1α and STAT1β in IFN-α/β- and IFN-λ-dependent antiviral activity are largely redundant. In contrast to the current dogma, however, we found that STAT1β is transcriptionally active in response to IFN-γ. In the absence of STAT1α, STAT1β shows more prolonged IFN-γ-induced phosphorylation and promoter binding. Both isoforms mediate protective, IFN-γ-dependent immunity against the bacterium Listeria monocytogenes, although with remarkably different efficiencies. Our data shed new light on the potential contributions of the individual STAT1 isoforms to STAT1-dependent immune responses. Knowledge of STAT1β's function will help fine-tune diagnostic approaches and help design more specific strategies to interfere with STAT1 activity.
Indexed as
Identifiers
What 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.