ArticleMolecular and cellular biology1997
Mutation in the Jak kinase JH2 domain hyperactivates Drosophila and mammalian Jak-Stat pathways.
Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed, 244 citations in OpenAlex.
- The minor spliceosome component U4atac regulates JAK/STAT signaling to modulate hematopoiesis and immune responses in Drosophila melanogaster.Nature communications · 2026Article
- JAK-STAT signaling in inflammation and stress-related diseases: implications for therapeutic interventions.Molecular biomedicine · 2023Review
- JAK3 Y841 Autophosphorylation Is Critical for STAT5B Activation, Kinase Domain Stability and Dimer Formation.International journal of molecular sciences · 2023Article
- Extracellular matrix protein N-glycosylation mediates immune self-tolerance inProceedings of the National Academy of Sciences of the United States of America · 2021Article
- The S1A protease family membersmicroPublication biology · 2021Article
- Janus Kinases in Leukemia.Cancers · 2021Review
- Oxidised metabolites of the omega-6 fatty acid linoleic acid activate dFOXO.Life science alliance · 2020Article
- Enhancer of Polycomb and the Tip60 complex repress hematological tumor initiation by negatively regulating JAK/STAT pathway activity.Disease models & mechanisms · 2019Article
- Review
- Selective JAKinibs: Prospects in Inflammatory and Autoimmune Diseases.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2019Review
- Drosophila Jak/STAT Signaling: Regulation and Relevance in Human Cancer and Metastasis.International journal of molecular sciences · 2018Review
- The molecular details of cytokine signaling via the JAK/STAT pathway.Protein science : a publication of the Protein Society · 2018Review
- Homeodomain-interacting protein kinase promotes tumorigenesis and metastatic cell behavior.Disease models & mechanisms · 2018Article
- "Do We Know Jack" About JAK? A Closer Look at JAK/STAT Signaling Pathway.Frontiers in oncology · 2018Review
- A Genetic Screen Reveals an Unexpected Role for Yorkie Signaling in JAK/STAT-Dependent Hematopoietic Malignancies inG3 (Bethesda, Md.) · 2017Article
- Cbl-mediated K63-linked ubiquitination of JAK2 enhances JAK2 phosphorylation and signal transduction.Scientific reports · 2017Article
- ADisease models & mechanisms · 2017Article
- Identification of imidazo[1,2-MedChemComm · 2017Article
- The Janus Kinase (JAK) FERM and SH2 Domains: Bringing Specificity to JAK-Receptor Interactions.Frontiers in endocrinology · 2017Review
- Inositol phosphate kinase 2 is required for imaginal disc development in Drosophila.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
13 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 1 institution in 2 countries.
Funding
Abstract
The Jak (Janus) family of nonreceptor tyrosine kinases plays a critical role in cytokine signal transduction pathways. In Drosophila melanogaster, the dominant hop(Tum-l) mutation in the Hop Jak kinase causes leukemia-like and other developmental defects. Previous studies have suggested that the Hop(Tum-l) protein might be a hyperactive kinase. Here, we report on the new dominant mutation hop(T42), which causes abnormalities that are similar to but more extreme than those caused by hop(Tum-l). We determined that Hop(T42) contains a glutamic acid-to-lysine substitution at amino acid residue 695 (E695K). This residue occurs in the JH2 (kinase-like) domain and is conserved among all Jak family members. We determined that Hop(Tum-1) and Hop(T42) both hyperphosphorylated and hyperactivated D-Stat when overexpressed in Drosophila cells. Moreover, we found that the hop(T42) phenotype was partially rescued by a reduction of wild-type D-stat activity. Finally, generation of the corresponding E695K mutation in murine Jak2 resulted in increased autophosphorylation and increased activation of Stat5 in COS cells. These results demonstrate that the mutant Hop proteins do indeed have increased tyrosine kinase activity, that the mutations hyperactivate the Hop-D-Stat pathway, and that Drosophila is a relevant system for the functional dissection of mammalian Jak-Stat pathways. Finally, we propose a model for the role of the Hop-D-Stat pathway in Drosophila hematopoiesis.
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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.