Roles of unphosphorylated STATs in signaling
Open accessAbstract
The seven members of the signal transducer and activator of transcription (STAT) family of transcription factors are activated in response to many different cytokines and growth factors by phosphorylation of specific tyrosine residues. The STAT1 and STAT3 genes are specific targets of activated STATs 1 and 3, respectively, resulting in large increases in the levels of these unphosphorylated STATs (U-STATs) in response to the interferons (STAT1) or ligands that active gp130, such as IL-6 (STAT3). U-STATs drive gene expression by novel mechanisms distinct from those used by phosphorylated STAT (P-STAT) dimers. In this review, we discuss the roles of U-STATs in transcription and regulation of gene expression.
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Nonpeptidic tyrosine kinase-targeted inhibitors have diminished efficacy because the inherent transcriptional activity of unphosphorylated STAT3 can drive MET and MRAS by binding NF-κB.
“However, their efficacy is diminished because the inherent transcriptional activity of unphosphorylated STAT3 could also drive the expression of oncogenes such as MET and MRAS by binding to NF-κB (18–21).”
From Small-molecule PROTAC mediates targeted protein degradation to treat STAT3-dependent epithelial cancer (2022) · cites this paper as [19]
In “The biology of U-STATs” (page unavailable), the paper says increased unphosphorylated STAT3 is likely to drive expression of MET and MRAS. “STAT3-dependent gene expression” describes its interaction with NF-κB, but demonstrates that mechanism for RANTES, not specifically MET or MRAS. The cited passages do not establish that this activity diminishes the efficacy of tyrosine kinase-targeted inhibitors. (LLM, conf=0.86)
Experimental — accuracy not yet measuredTargeted STAT3 degradation can completely inhibit the transcriptional activity of both dimerized and monomeric STAT3.
“Second, the targeted STAT3 degradation can completely inhibit the transcriptional activity of both dimerized and monomeric STAT3 (19, 21, 26).”
From Small-molecule PROTAC mediates targeted protein degradation to treat STAT3-dependent epithelial cancer (2022) · cites this paper as [19]
The STAT3-dependent gene expression section (page not provided) describes transcriptional roles for STAT3 homodimers and unphosphorylated STAT3. It does not address targeted STAT3 degradation or show that degradation completely inhibits either activity. (LLM, conf=0.83)
Experimental — accuracy not yet measuredOne major reason for ineffectiveness of STAT3 dimerization inhibitors is that monomeric STAT3 also has transcriptional activity.
“One major reason for their ineffectiveness is that monomeric STAT3 also has transcriptional activity [175].”
From Proteolysis targeting chimeras (PROTACs) are emerging therapeutics for hematologic malignancies (2020) · cites this paper as [175]
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“Second, the targeted STAT3 degradation can completely inhibit the transcriptional activity of both dimerized and monomeric STAT3 (19, 21, 26).”
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Interferon-γ is a master checkpoint regulator of cytokine-induced differentiation
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Interleukin-11 increases invasiveness of JEG-3 choriocarcinoma cells by modulating STAT3 expression
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- Authors
- Yang, J., & Stark, G. R.
- Affiliations
- Lanzhou University (CN)
- Cleveland Clinic (US)
- Corresponding author
- Yang, Jinbo
- Stark, George R
- Venue
- Cell Research
- Published
- 2008-03-25
- Volume
- 18
- Issue
- 4
- Pages
- 443-451
- ISSN
- 1001-0602 (ISSN-L)
- 1748-7838
- OpenAlex
- W2079870321
- Cited by
- 347
- References
- 87
- Citations by year
- 2026: 3 · 2025: 7 · 2024: 16 · 2023: 16 · 2022: 18 · 2021: 14 · 2020: 19 · 2019: 16 · 2018: 12 · 2017: 16 · 2016: 15 · 2015: 21 · 2014: 36 · 2013: 34 · 2012: 35
- FWCI
- 2.18
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Cell Research (publishedVersion)
- PubMed (publishedVersion)
- Lanzhou University Institutional Repository (submittedVersion, cc-by-nc)
- Topics
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Keywords
- STAT1, STAT3, STAT family, tyrosine phosphorylation, interferon signaling, gp130 signaling, interleukin-6, cytokine signaling, transcriptional regulation, gene expression regulation
- MeSH terms
- Animals, DNA, Gene Expression Regulation, Humans, Phosphorylation, Signal Transduction, Protein Transport, STAT Transcription Factors
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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