ArticleMolecular and cellular biology2000
ets-2 is a target for an akt (Protein kinase B)/jun N-terminal kinase signaling pathway in macrophages of motheaten-viable mutant mice.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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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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Who cites it
34 citing papers in PubMed, 72 citations in OpenAlex.
- E3 Ubiquitin ligases Cbl-b and c-Cbl maintain the homeostasis of macrophages by regulating the M-CSF/M-CSFR signaling axis.Cell death & disease · 2025Article
- A DUSP6 inhibitor suppresses inflammatory cardiac remodeling and improves heart function after myocardial infarction.Disease models & mechanisms · 2023Article
- Cooperative Binding of ETS2 and NFAT Links Erk1/2 and Calcineurin Signaling in the Pathogenesis of Cardiac Hypertrophy.Circulation · 2021Article
- Biophysical Techniques for Target Validation and Drug Discovery in Transcription-Targeted Therapy.International journal of molecular sciences · 2020Review
- ETS2 promotes epithelial-to-mesenchymal transition in renal fibrosis by targeting JUNB transcription.Laboratory investigation; a journal of technical methods and pathology · 2020Article
- XEDAR inhibits the proliferation and induces apoptosis of gastric cancer cells by regulating JNK signaling pathway.Bioscience reports · 2019Article
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- EGF suppresses the expression of miR-124a in pancreatic β cell lines via ETS2 activation through the MEK and PI3K signaling pathways.International journal of biological sciences · 2019Article
- Blocking immunoinhibitory receptor LILRB2 reprograms tumor-associated myeloid cells and promotes antitumor immunity.The Journal of clinical investigation · 2018Article
- Ets2 knockdown inhibits tumorigenesis in esophageal squamous cell carcinoma in vivo and in vitro.Oncotarget · 2016Article
- EGFR inhibition evokes innate drug resistance in lung cancer cells by preventing Akt activity and thus inactivating Ets-1 function.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- CKIP-1 regulates macrophage proliferation by inhibiting TRAF6-mediated Akt activation.Cell research · 2014Article
- Function of the transforming growth factor-β1/c-Jun N-terminal kinase signaling pathway in the action of thalidomide on a rat model of pulmonary fibrosis.Experimental and therapeutic medicine · 2014Article
- IL-4 directly signals tissue-resident macrophages to proliferate beyond homeostatic levels controlled by CSF-1.The Journal of experimental medicine · 2013Article
- Differential expression of CD148 on leukocyte subsets in inflammatory arthritis.Arthritis research & therapy · 2013Article
- The function of the conserved regulatory element within the second intron of the mammalian Csf1r locus.PloS one · 2013Article
- Inactivation of Rb in stromal fibroblasts promotes epithelial cell invasion.The EMBO journal · 2012Article
- Role for Ets-2(Thr-72) transcription factor in stage-specific thymocyte development and survival.The Journal of biological chemistry · 2012Article
- Transcription factor ets-2 plays an important role in the pathogenesis of pulmonary fibrosis.American journal of respiratory cell and molecular biology · 2011Article
- Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
The transcription factor ets-2 was phosphorylated at residue threonine 72 in a colony-stimulating factor 1 (CSF-1)- and mitogen-activated protein kinase-independent manner in macrophages isolated from motheaten-viable (me-v) mice. The CSF-1 and ets-2 target genes coding for Bcl-x, urokinase plasminogen activator, and scavenger receptor were also expressed at high levels independent of CSF-1 addition to me-v cells. Akt (protein kinase B) was constitutively active in me-v macrophages, and an Akt immunoprecipitate catalyzed phosphorylation of ets-2 at threonine 72. The p54 isoform of c-jun N-terminal kinase-stress-activated kinase (JNK- SAPK) coimmunoprecipitated with Akt from me-v macrophages, and treatment of me-v cells with the specific phosphatidylinositol 3-kinase inhibitor LY294002 decreased cell survival, Akt and JNK kinase activities, ets-2 phosphorylation, and Bcl-x mRNA expression. Therefore, ets-2 is a target for phosphatidylinositol 3-kinase-Akt-JNK action, and the JNK p54 isoform is an ets-2 kinase in macrophages. Constitutive ets-2 activity may contribute to the pathology of me-v mice by increasing expression of genes like the Bcl-x gene that promote macrophage survival.
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Registered trials
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