ArticleCellular signalling2009
Cytokine-induced activation of mixed lineage kinase 3 requires TRAF2 and TRAF6.
Article in Cellular signalling, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 43 citations in OpenAlex.
- Article
- Infectious Diseases.Advances in neurobiology · 2024Review
- Review
- Transmembrane TNF and Its Receptors TNFR1 and TNFR2 in Mycobacterial Infections.International journal of molecular sciences · 2021Review
- The regulatory function of mixed lineage kinase 3 in tumor and host immunity.Pharmacology & therapeutics · 2021Review
- TNF receptor-associated factor 6 interacts with ALS-linked misfolded superoxide dismutase 1 and promotes aggregation.The Journal of biological chemistry · 2020Article
- G Protein-Coupled Receptor Systems and Their Role in Cellular Senescence.Computational and structural biotechnology journal · 2019Review
- Osmotic and heat stress-dependent regulation of MLK4β and MLK3 by the CHIP E3 ligase in ovarian cancer cells.Cellular signalling · 2017Article
- TNFα-induced DLK activation contributes to apoptosis in the beta-cell line HIT.Naunyn-Schmiedeberg's archives of pharmacology · 2017Article
- Article
- MLK3 Signaling in Cancer Invasion.Cancers · 2016Review
- Loss of TRB3 alters dynamics of MLK3-JNK signaling and inhibits cytokine-activated pancreatic beta cell death.The Journal of biological chemistry · 2014Article
- Prolactin prevents hepatocellular carcinoma by restricting innate immune activation of c-Myc in mice.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- The E3 ligase CHIP mediates ubiquitination and degradation of mixed-lineage kinase 3.Molecular and cellular biology · 2014Article
- Domain specificity of MAP3K family members, MLK and Tak1, for JNK signaling in Drosophila.Genetics · 2014Article
- TNF and MAP kinase signalling pathways.Seminars in immunology · 2014Review
- Lysine 63-linked ubiquitination modulates mixed lineage kinase-3 interaction with JIP1 scaffold protein in cytokine-induced pancreatic β cell death.The Journal of biological chemistry · 2013Article
- HIV-1 Nef interacts with HCV Core, recruits TRAF2, TRAF5 and TRAF6, and stimulates HIV-1 replication in macrophages.Journal of innate immunity · 2013Article
- Mixed lineage kinase 3 is required for matrix metalloproteinase expression and invasion in ovarian cancer cells.Experimental cell research · 2012Article
- Tumor necrosis factor receptor-associated factor family protein 2 is a key mediator of the epidermal growth factor-induced ribosomal S6 kinase 2/cAMP-responsive element-binding protein/Fos protein signaling pathway.The Journal of biological chemistry · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Mixed lineage kinase 3 (MLK3) is a mitogen-activated protein kinase kinase kinase (MAP3K) that activates multiple mitogen-activated protein kinase (MAPK) pathways in response to growth factors, stresses and the pro-inflammatory cytokine, tumor necrosis factor (TNF). MLK3 is required for optimal activation of stress activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) signaling by TNF, however, the mechanism by which MLK3 is recruited and activated by the TNF receptor remains poorly understood. Here we report that both TNF and interleukin-1 beta (IL-1 beta) stimulation rapidly activate MLK3 kinase activity. We observed that TNF stimulates an interaction between MLK3 and TNF receptor associated factor (TRAF) 2 and IL-1 beta stimulates an interaction between MLK3 and TRAF6. RNA interference (RNAi) of traf2 or traf6 dramatically impairs MLK3 activation by TNF indicating that TRAF2 and TRAF6 are critically required for MLK3 activation. We show that TNF also stimulates ubiquitination of MLK3 and MLK3 can be conjugated with lysine 48 (K48)- and lysine 63 (K63)-linked polyubiquitin chains. Our results suggest that K48-linked ubiquitination directs MLK3 for proteosomal degradation while K63-linked ubiquitination is important for MLK3 kinase activity. These results reveal a novel mechanism for MLK3 activation by the pro-inflammatory cytokines TNF and IL-1 beta.
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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.