ArticleOncogene2004
Drosophila Src-family kinases function with Csk to regulate cell proliferation and apoptosis.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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.
The trial behind it
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
41 citing papers in PubMed, 62 citations in OpenAlex.
- An exploratory analysis of the effects of human FYN and its Drosophila ortholog in Drosophila tissues.Scientific reports · 2026Article
- A novel model based on protein post-translational modifications comprising the immune landscape and prediction of colorectal cancer prognosis.Journal of gastrointestinal oncology · 2024Article
- Necrosensor: a genetically encoded fluorescent sensor for visualizing necrosis in Drosophila.Biology open · 2024Article
- Activated Src kinase promotes cell cannibalism in Drosophila.The Journal of cell biology · 2023Article
- An allosteric switch between the activation loop and a c-terminal palindromic phospho-motif controls c-Src function.Nature communications · 2023Article
- A Van Gogh/Vangl tyrosine phosphorylation switch regulates its interaction with core Planar Cell Polarity factors Prickle and Dishevelled.PLoS genetics · 2023Article
- Engineered kinases as a tool for phosphorylation of selected targets in vivo.The Journal of cell biology · 2022Article
- Cullin-5 mutants reveal collective sensing of the nucleocytoplasmic ratio in Drosophila embryogenesis.Current biology : CB · 2022Article
- Apoptosis regulation by the tyrosine-protein kinase CSK.Frontiers in cell and developmental biology · 2022Review
- Hippo signaling suppresses tumor cell metastasis via a Yki-Src42A positive feedback loop.Cell death & disease · 2021Article
- Methionine restriction breaks obligatory coupling of cell proliferation and death by an oncogene Src ineLife · 2021Article
- Mbt/PAK4 together with SRC modulates N-Cadherin adherens junctions in the developingBiology open · 2019Article
- A Gene Expression Screen inG3 (Bethesda, Md.) · 2019Article
- Article
- C-terminal Src kinase (Csk) regulates the tricellular junction protein Gliotactin independent of Src.Molecular biology of the cell · 2018Article
- Hippo, TGF-β, and Src-MAPK pathways regulate transcription of the upd3 cytokine in Drosophila enterocytes upon bacterial infection.PLoS genetics · 2017Article
- Mapping Heart Development in Flies: Src42A Acts Non-Autonomously to Promote Heart Tube Formation in Drosophila.Veterinary sciences · 2017Article
- The interplay between obesity and cancer: a fly view.Disease models & mechanisms · 2016Review
- Adherens Junction and E-Cadherin complex regulation by epithelial polarity.Cellular and molecular life sciences : CMLS · 2016Review
- C-terminal Src Kinase Gates Homeostatic Synaptic Plasticity and Regulates Fasciclin II Expression at the Drosophila Neuromuscular Junction.PLoS genetics · 2016Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Elevated Src protein levels and activity are associated with the development and progression of a variety of cancers. The consequences of deregulated Src activity have been studied extensively in cell culture; however, the effects of this deregulation in vivo, as well as the mechanisms of Src-induced tumorigenesis, remain poorly understood. In this study, the effect of expressing wild-type and constitutively active Drosophila Src-family kinases (SFKs) in the developing eye was examined. Overexpression of either wild-type Drosophila SFK (Src64 and Src42) is sufficient to induce ectopic proliferation in G1/G0-arrested, uncommitted cells in eye imaginal discs. In addition, both kinases trigger apoptosis in vivo, in a dosage-dependent manner. Constitutively active mutants are hypermorphic as they trigger proliferation and death more potently than their wild-type counterparts. Moreover, SFK-induced proliferation and apoptosis are largely independent events, as blocking ectopic proliferation does not block cell death. Further, DCsk (the Drosophila homolog of the C-terminal Src kinase) phosphorylates and interacts genetically with the wild-type SFKs, but not with the constitutively active mutants in which a conserved C-terminal tyrosine was mutated to phenylalanine, providing the first in vivo evidence that Csk regulates SFKs during development through phosphorylation of their C-terminal tyrosine.
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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.