ArticleOncogene2002
IL-6 mediated activation of STAT3 bypasses Janus kinases in terminally differentiated B lineage cells.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 23 citations in OpenAlex.
- ZEB1 promotes pathogenic Th1 and Th17 cell differentiation in multiple sclerosis.Cell reports · 2021Article
- Oncogenic D816V-KIT signaling in mast cells causes persistent IL-6 production.Haematologica · 2020Article
- Antibody Array Revealed PRL-3 Affects Protein Phosphorylation and Cytokine Secretion.PloS one · 2017Article
- Endogenous transmembrane protein UT2 inhibits pSTAT3 and suppresses hematological malignancy.The Journal of clinical investigation · 2016Article
- Lung Adenocarcinomas and Lung Cancer Cell Lines Show Association of MMP-1 Expression With STAT3 Activation.Translational oncology · 2015Article
- The Hyper-IgE Syndromes: Lessons in Nature, From Bench to Bedside.The World Allergy Organization journal · 2012Article
- Effects of AG490 on lens epithelial cell death induced by H(2)O(2).Japanese journal of ophthalmology · 2010Article
- STAT3 is a substrate of SYK tyrosine kinase in B-lineage leukemia/lymphoma cells exposed to oxidative stress.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- A quantitative high-throughput screen for modulators of IL-6 signaling: a model for interrogating biological networks using chemical libraries.Molecular bioSystems · 2009Article
- Interleukin-6 in aging and chronic disease: a magnificent pathway.The journals of gerontology. Series A, Biological sciences and medical sciences · 2006Review
- Activation of Stat3 by receptor tyrosine kinases and cytokines regulates survival in human non-small cell carcinoma cells.Oncogene · 2003Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cytokine signaling generally occurs through receptors lacking tyrosine kinase activity. Aggregation of receptors leads to activation of receptor associated Janus kinases (Jaks) which in turn phosphorylate members of a family of transcription factors (STATs) that translocate to the nucleus and regulate gene expression. In the case of Interleukin-6 (IL-6), the consensus for signaling in B lineage cells has been that Jak1, Jak2 and Tyk2 are all phosphorylated upon ligand binding and participate in activation of downstream elements, in particular STAT3. In other cell types, Jak1 has been demonstrated to be absolutely required for IL-6 mediated activation of STAT3. In the present studies, we have identified a series of end stage B cell (plasma cell) lines that fail to express Jak1, but phosphorylate STAT3 in response to IL-6. No evidence was found for a requirement of other Jak family members in the activation of STAT3. STAT3 tyrosine phosphorylation was inhibited in a dose dependent manner by the MEK inhibitor U0126, but not by inhibitors of PI-3K or Src kinases. Moreover, STAT3 phosphorylation was similarly inhibited in lines expressing Jak1 wherein Jak1 was phosphorylated upon IL-6 stimulation and Jak1 phosphorylation was not inhibited by U0126. These results indicate that the MAPK pathway plays a critical role in IL-6 mediated tyrosine phosphorylation of STAT3 and suggests that Jak kinases may not be required in this cascade. Thus, it may be important to re-evaluate the role of Jak kinases in other cytokine signaling pathways as well.
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