Of alphas and betas: distinct and overlapping functions of STAT3 isoforms
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STAT3 is a pleiotropic factor activated by many different signals including cytokines, growth factors and oncogenes. It is involved in a striking number of functions and can activate distinct repertoires of genes in different contexts. Like other STAT factors, STAT3 exists in two isoforms generated by alternative splicing, the full length STAT3alpha and the truncated STAT3beta, generally thought to act as a dominant negative factor. However, STAT3beta is not transcriptionally inactive and is able to both activate and repress genes depending on cellular environment. These unique properties of the STAT3beta isoform may contribute to the extraordinary functional complexity of STAT3 physiological and pathological actions, revealed by conditional mutagenesis studies and not yet fully understood. With this in mind, we try here to summarize what is known about the structure and function of the alpha and beta STAT3 isoforms, both in vitro and in vivo. In addition, we report unpublished data describing the phenotype of mice where the STAT3alpha isoform was specifically ablated.
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Striking changes in the levels of STAT3α and STAT3β have been noted during myeloid differentiation.
“Given the striking changes in the levels of STAT3α and STAT3β noted during myeloid differentiation [12–14]”
From Selective STAT3-α or -β expression reveals spliceform-specific phosphorylation kinetics, nuclear retention and distinct gene expression outcomes (2012) · cites this paper as [13]
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Ser727-dependent transcriptional activation by association of p300 with STAT3 upon IL-6 stimulation
Schuringa, J.-J., Schepers, H., Vellenga, E., & Kruijer, W. (2001) · FEBS Letters · doi:10.1016/s0014-5793(01)02354-7 · Cited by 124 · see citing works
Yeh, M., Gharavi, N. M., Choi, J., Hsieh, X., Reed, E., Mouillesseaux, K. P., Cole, A. L., Reddy, S. T., & Berliner, J. A. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m312198200 · Cited by 116 · see citing works
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STAT3 in hepatocellular carcinoma: new perspectives
Svinka, J., Mikulits, W., & Eferl, R. (2014) · Hepatic Oncology · doi:10.2217/hep.13.7 · Cited by 63 · see citing works
Ng, I. H. W., Ng, D. C. H., Jans, D. A., & Bogoyevitch, M. A. (2012) · Biochemical Journal · doi:10.1042/bj20120941 · Cited by 63 · see citing works
- Authors
- Dewilde, S.
- Affiliations
- University of Turin (IT)
- Corresponding author
- Dewilde, Sarah
- Venue
- Frontiers in Bioscience
- Publisher
- IMR Press
- Published
- 2008
- Volume
- Volume
- Issue
- 13
- Pages
- 6501
- ISSN
- 1093-4715 (ISSN-L)
- 1093-9946
- DOI
- 10.2741/3170
- OpenAlex
- W1964416733
- Cited by
- 53
- References
- 2
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 4 · 2023: 5 · 2021: 4 · 2020: 1 · 2019: 5 · 2018: 4 · 2017: 1 · 2016: 1 · 2015: 2 · 2014: 5 · 2013: 3 · 2012: 4
- FWCI
- 0.37
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Frontiers in bioscience (publishedVersion)
- PubMed (publishedVersion)
- Institutional Research Information System University of Turin (University of Turin) (submittedVersion)
- Funders
- Ministero dell’Istruzione, dell’Università e della Ricerca
- Topics
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Keywords
- STAT3, STAT3β, alternative splicing, dominant negative regulation, gene activation and repression, transcriptional regulation, conditional mutagenesis, cytokine signaling, oncogene signaling
- MeSH terms
- Animals, Astrocytes, Glial Fibrillary Acidic Protein, Humans, Nerve Tissue Proteins, Neurons, Recombinant Proteins, Cytokines, Alternative Splicing, Mice, Knockout, Protein Isoforms, STAT3 Transcription Factor, Mice
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