ArticleMolecular cell2013
Evidence against a role for β-arrestin1 in STAT1 dephosphorylation and the inhibition of interferon-γ signaling.
Article in Molecular cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed.
- GPCR Biased Signaling in Cancer.Handbook of experimental pharmacology · 2026Review
- Cannabinoid receptor type 1 (CBiScience · 2023Article
- Glycogen metabolism regulates macrophage-mediated acute inflammatory responses.Nature communications · 2020Article
- CCR2 Signaling Selectively Regulates IFN-α: Role of β-Arrestin 2 in IFNAR1 Internalization.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Protein Tyrosine Phosphatases as Potential Regulators of STAT3 Signaling.International journal of molecular sciences · 2018Review
- STAT2 Is a Pervasive Cytokine Regulator due to Its Inhibition of STAT1 in Multiple Signaling Pathways.PLoS biology · 2016Article
- Clusterin, a gene enriched in intestinal stem cells, is required for L1-mediated colon cancer metastasis.Oncotarget · 2015Article
- STAT1-cooperative DNA binding distinguishes type 1 from type 2 interferon signaling.Nature immunology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Signal transducer and activator of transcription 1 (STAT1) is activated by tyrosine phosphorylation upon interferon-γ (IFNγ) stimulation, which results in the expression of genes with antiproliferative and immunomodulatory functions. The inactivation of STAT1 occurs through tyrosine dephosphorylation by the tyrosine phosphatase TC45. It was proposed that recruitment of TC45 required the direct interaction of STAT1 with the scaffold protein β-arrestin1, making β-arrestin1 an essential negative regulator of STAT1 and IFNγ signaling (Mo et al., 2008). We tested the relevance of β-arrestin1 for STAT1 activity. Our results do not confirm β-arrestin1 as a STAT1-interacting protein. The STAT1 phosphorylation/dephosphorylation cycle was found to be unaffected by both the overexpression and the genetic deletion of β-arrestin1. Accordingly, β-arrestin1 did not inhibit STAT1 transcriptional activity or the induction of IFNγ target genes in response to IFNγ. Our data indicate that β-arrestin1 is dispensable for STAT1 dephosphorylation and the termination of IFNγ signaling.
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.