ArticleJAK-STAT2012
Determinants of the extent and duration of STAT3 signaling.
Article in JAK-STAT, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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.
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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
17 citing papers in PubMed, 25 citations in OpenAlex.
- Lineage Tracing and Single-Cell RNA Sequencing Reveal a Common Transcriptional State in Breast Cancer Tumor-Initiating Cells Characterized by IFN/STAT1 Activity.Cancer research · 2025Article
- Article
- Overcoming Acquired Drug Resistance to Cancer Therapies through Targeted STAT3 Inhibition.International journal of molecular sciences · 2023Review
- Interleukin 6 trans-signaling is a critical driver of lung allograft fibrosis.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2021Article
- Article
- PTC-209 Anti-Cancer Effects Involved the Inhibition of STAT3 Phosphorylation.Frontiers in pharmacology · 2019Article
- Partial growth hormone insensitivity and dysregulatory immune disease associated with de novo germline activating STAT3 mutations.Molecular and cellular endocrinology · 2018Article
- Glutamine activates STAT3 to control cancer cell proliferation independently of glutamine metabolism.Oncogene · 2017Article
- Vitamin D in hematological disorders and malignancies.European journal of haematology · 2017Review
- Article
- Expression of the miR-302/367 cluster in glioblastoma cells suppresses tumorigenic gene expression patterns and abolishes transformation related phenotypes.International journal of cancer · 2015Article
- Stat5 Exerts Distinct, Vital Functions in the Cytoplasm and Nucleus of Bcr-Abl+ K562 and Jak2(V617F)+ HEL Leukemia Cells.Cancers · 2015Article
- Overexpression of SMYD3 was associated with increased STAT3 activation in gastric cancer.Medical oncology (Northwood, London, England) · 2015Article
- PIAS3, an inhibitor of STAT3, has intensively negative association with the survival of gastric cancer.International journal of clinical and experimental medicine · 2015Article
- HIV-1 gp120 activates the STAT3/interleukin-6 axis in primary human monocyte-derived dendritic cells.Journal of virology · 2014Article
- Resistance of Cancer Cells to Targeted Therapies Through the Activation of Compensating Signaling Loops.Current signal transduction therapy · 2013Article
- Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple molecular mechanisms have been identified that are responsible for the deregulation of the quantitative aspects of JAK-STAT signaling. These mechanisms enhance the extent and the duration of, e.g., STAT3 activation and have profound consequences on the phenotypes of the affected cells. The fine tuning of STAT3 signaling is required to maintain its physiological functions and its deregulation is associated with diverse pathological states. Deregulation can be exerted by the gain of function of components mediating the activation of STAT3 or the loss of function of molecules involved in the deactivation steps of STAT3. Gain of function mutations can involve tyrosine kinases that phosphorylate STAT3, mutations in cytokine and growth factor receptors causing their ligand independent activation, mutations in STAT3 that enhance and prolong its tyrosine phosphorylation and the autocrine or paracrine production and secretion of cytokines, most notably IL-6. Diminished deactivation of phosphorylated STAT3 can be due to the reduced expression of tyrosine phosphatases, inactivating mutations in these enzymes, silencing or functional inactivation of SOCS molecules, post-transcriptional inhibition of PIAS3 expression or deletion mutations in the lymphocyte adaptor protein, LNK. STAT3 variants that exhibit autonomous transactivation potential have been detected in 40% of patients with T-cell large granular lymphocytic leukemia in clonally expanded CD8(+) T cells. These patients also were preferentially affected by neutropenia and rheumatoid disorders and the results suggest that activating STAT3 mutations in T lymphocytes could be a cause of autoimmune diseases.
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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.