ArticlePloS one2013
PKCθ/β and CYLD are antagonistic partners in the NFκB and NFAT transactivation pathways in primary mouse CD3+ T lymphocytes.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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
13 citing papers in PubMed, 17 citations in OpenAlex.
- Article
- Notch and NF-κB: Coach and Players of Regulatory T-Cell Response in Cancer.Frontiers in immunology · 2018Review
- Genetic alterations in adult T-cell leukemia/lymphoma.Cancer science · 2017Review
- Pharmacological Inhibition of PKCθ Counteracts Muscle Disease in a Mouse Model of Duchenne Muscular Dystrophy.EBioMedicine · 2017Article
- The Deubiquitinating Enzyme Cylindromatosis Dampens CD8Frontiers in immunology · 2017Article
- PKD3 deficiency causes alterations in microtubule dynamics during the cell cycle.Cell cycle (Georgetown, Tex.) · 2016Article
- Spatio-Temporal Regulation of PKC Isoforms Imparts Signaling Specificity.Frontiers in immunology · 2016Review
- CYLD-mediated signaling and diseases.Current drug targets · 2015Review
- Protein kinase C in cellular transformation: a valid target for therapy?Biochemical Society transactions · 2014Review
- Tumor suppressor cylindromatosis (CYLD) controls HIV transcription in an NF-κB-dependent manner.Journal of virology · 2014Article
- Ubiquitous points of control over regulatory T cells.Journal of molecular medicine (Berlin, Germany) · 2014Review
- NOTCH1 Can Initiate NF-κB Activation via Cytosolic Interactions with Components of the T Cell Signalosome.Frontiers in immunology · 2014Article
- Changes in the MALT1-A20-NF-κB expression pattern may be related to T cell dysfunction in AML.Cancer cell international · 2013Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
In T cells PKCθ mediates the activation of critical signals downstream of TCR/CD28 stimulation. We investigated the molecular mechanisms by which PKCθ regulates NFκB transactivation by examining PKCθ/β single and double knockout mice and observed a redundant involvement of PKCθ and PKCβ in this signaling pathway. Mechanistically, we define a PKCθ-CYLD protein complex and an interaction between the positive PKCθ/β and the negative CYLD signaling pathways that both converge at the level of TAK1/IKK/I-κBα/NFκB and NFAT transactivation. In Jurkat leukemic T cells, CYLD is endoproteolytically processed in the initial minutes of stimulation by the paracaspase MALT1 in a PKC-dependent fashion, which is required for robust IL-2 transcription. However, in primary T cells, CYLD processing occurs with different kinetics and an altered dependence on PKC. The formation of a direct PKCθ/CYLD complex appears to regulate the short-term spatial distribution of CYLD, subsequently affecting NFκB and NFAT repressional activity of CYLD prior to its MALT1-dependent inactivation. Taken together, our study establishes CYLD as a new and critical PKCθ interactor in T cells and reveals that antagonistic PKCθ/β-CYLD crosstalk is crucial for the adjustment of immune thresholds in primary mouse CD3(+) T cells.
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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.