ArticleThe American journal of pathology2013
Death-associated protein kinase controls STAT3 activity in intestinal epithelial cells.
Article in The American journal of pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 14 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.
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.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Death-associated protein kinase 1: a double-edged sword in health and disease.Frontiers in immunology · 2025Review
- Loss of death-associated protein kinase 1 in human bone marrow mesenchymal stem cells decreases immunosuppression of CD4+ T cells.The Journal of international medical research · 2020Article
- Activation of death-associated protein kinase 1 promotes neutrophil apoptosis to accelerate inflammatory resolution in acute respiratory distress syndrome.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- STAT3/NF-κB-Regulated Lentiviral TK/GCV Suicide Gene Therapy for Cisplatin-Resistant Triple-Negative Breast Cancer.Theranostics · 2017Article
- DAPK interacts with Patronin and the microtubule cytoskeleton in epidermal development and wound repair.eLife · 2016Article
- DANGER is involved in high glucose-induced radioresistance through inhibiting DAPK-mediated anoikis in non-small cell lung cancer.Oncotarget · 2016Article
- DAPK loss in colon cancer tumor buds: implications for migration capacity of disseminating tumor cells.Oncotarget · 2015Article
- Differential nucleobase protection against 5-fluorouracil toxicity for squamous and columnar cells: implication for tissue function and oncogenesis.Investigational new drugs · 2015Article
- LATS2 inhibits the activity of NF-κ B signaling by disrupting the interaction between TAK1 and IKKβ.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- miRNA-26b Overexpression in Ulcerative Colitis-associated Carcinogenesis.Inflammatory bowel diseases · 2015Article
- Death-associated protein kinase: A molecule with functional antagonistic duality and a potential role in inflammatory bowel disease (Review).International journal of oncology · 2015Review
- IL-6/STAT3/SOCS3 signaling pathway playing a regulatory role in ulcerative colitis carcinogenesis.International journal of clinical and experimental medicine · 2015Article
- Insights into the functions of the death associated protein kinases from C. elegans and other invertebrates.Apoptosis : an international journal on programmed cell death · 2014Review
- Repeated H2 O2 exposure drives cell cycle progression in an in vitro model of ulcerative colitis.Journal of cellular and molecular medicine · 2013Article
Corrections and comments
- Correction · 2015-10-03Concerns/Issues about Image · Updated to Retraction ·
- Retraction · 2016-12-16Investigation by Company/Institution · Investigation by Journal/Publisher · Manipulation of Images · Misconduct - Official Investigation(s) and/or Finding(s) · Misconduct by Author · Upgrade/Update of Prior Notice(s) · · Regine Schneider-Stock has insitutional finding of misconduct;
- RetractedRetractions.2017
Authors and funding
21 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The TNF-IL-6-STAT3 pathway plays a crucial role in promoting ulcerative colitis-associated carcinoma (UCC). To date, the negative regulation of STAT3 is poorly understood. Interestingly, intestinal epithelial cells of UCC in comparison to ulcerative colitis show high expression levels of anti-inflammatory death-associated protein kinase (DAPK) and low levels of pSTAT3. Accordingly, epithelial DAPK expression was enhanced in STAT3(IEC-KO) mice. To unravel a possible regulatory mechanism, we used an in vitro TNF-treated intestinal epithelial cell model. We identified a new function of DAPK in suppressing TNF-induced STAT3 activation as DAPK siRNA knockdown and treatment with a DAPK inhibitor potentiated STAT3 activation, IL-6 mRNA expression, and secretion. DAPK attenuated STAT3 activity directly by physical interaction shown in three-dimensional structural modeling. This model suggests that DAPK-induced conformational changes in the STAT3 dimer masked its nuclear localization signal. Alternatively, pharmacological inactivation of STAT3 led to an increase in DAPK mRNA and protein levels. Chromatin immunoprecipitation showed that STAT3 restricted DAPK expression by promoter binding, thereby reinforcing its own activation by inducing IL-6. This novel negative regulation principle might balance TNF-induced inflammation and seems to play an important role in the inflammation-associated transformation process as confirmed in an AOM+DSS colon carcinogenesis mouse model. DAPK as a negative regulator of STAT3 emerges as therapeutic option in the treatment of ulcerative colitis and UCC.
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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.