ArticleThe Journal of biological chemistry2012
c-Jun and Ets2 proteins regulate expression of spleen tyrosine kinase in T cells.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Spleen tyrosine kinase (Syk) regulates systemic lupus erythematosus (SLE) T cell signaling.PloS one · 2013Trial
- The geroprotectors trametinib and rapamycin combine additively to extend mouse healthspan and lifespan.Nature aging · 2025Article
- Exploring the molecular mechanism of Tripterygium Wilfordii Hook F in treating systemic lupus erythematosus via network pharmacology and molecular docking.Clinical rheumatology · 2025Article
- Nerve Growth Factor and Autoimmune Diseases.Current issues in molecular biology · 2023Review
- Cutaneous Lupus Erythematosus: An Update on Pathogenesis and Future Therapeutic Directions.American journal of clinical dermatology · 2023Review
- Ets-2 deletion in myeloid cells attenuates IL-1α-mediated inflammatory disease caused by a Ptpn6 point mutation.Cellular & molecular immunology · 2021Article
- ETS2 promotes epithelial-to-mesenchymal transition in renal fibrosis by targeting JUNB transcription.Laboratory investigation; a journal of technical methods and pathology · 2020Article
- BLK pathway-associated rs13277113 GA genotype is more frequent in SLE patients and associated with low gene expression and increased flares.Clinical rheumatology · 2017Article
- Disturbed T Cell Signaling and Altered Th17 and Regulatory T Cell Subsets in the Pathogenesis of Systemic Lupus Erythematosus.Frontiers in immunology · 2015Review
- The pathology of T cells in systemic lupus erythematosus.Journal of immunology research · 2014Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Effector T cells and T cells from patients with systemic lupus erythematosus (SLE) express increased levels of the spleen tyrosine kinase (Syk). Syk binds to the T cell receptor (TCR)-CD3 complex and transduces the TCR-mediated signal in the cell more efficiently than the canonical CD3ζ chain. The reasons for the increased expression of Syk are unclear. In the present study, we found that Syk is regulated by the transcription factor c-Jun in cooperation with Ets2. c-Jun and Ets2 bound to the SYK promoter in close proximity and increased the promoter activity in a specific manner. Disruption of c-Jun and Ets2 expression by siRNA resulted in decreased expression of Syk. Overexpression of c-Jun but not Ets2 resulted in increase in Syk protein. c-Jun and Ets2 co-immunoprecipitated and had an additive effect on Syk expression. c-Jun-driven SYK promoter activation showed a similar pattern in B cells; however, as expected, basal promoter activity was much higher in B cells as compared with T cells. Overexpression of c-Jun led to increase in intracytoplasmic calcium flux following TCR stimulation. Moreover, we found that SLE T cells had increased levels of c-Jun at baseline and phosphorylated c-Jun upon activation. Finally, disruption of c-Jun and Ets2 in SLE T cells resulted in a decrease in calcium flux upon TCR stimulation. In conclusion, c-Jun in cooperation with Ets2 increases the expression of Syk and contributes to Syk-mediated heightened calcium responses in SLE T cells.
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Registered trials
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