ArticleOncogene2015
Src kinase function controls progenitor cell pools during regeneration and tumor onset in the Drosophila intestine.
Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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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Who cites it
31 citing papers in PubMed, 46 citations in OpenAlex.
- Slap restricts oncogenic Src-family kinase signaling to maintain colonic epithelial homeostasis.eLife · 2026Article
- Damage recognition by intestinal stem cells via Draper promotes adult Drosophila midgut regeneration.The EMBO journal · 2026Article
- Review
- Inter-cell type interactions that control JNK signaling in the Drosophila intestine.Nature communications · 2024Article
- Review
- Crosstalk between chromatin and Shavenbaby defines transcriptional output along the Drosophila intestinal stem cell lineage.iScience · 2024Article
- Article
- Damage-induced regeneration of the intestinal stem cell pool through enteroblast mitosis in the Drosophila midgut.The EMBO journal · 2022Article
- An improved organ explant culture method reveals stem cell lineage dynamics in the adulteLife · 2022Article
- Src acts with WNT/FGFRL signaling to pattern the planarian anteroposterior axis.Development (Cambridge, England) · 2022Article
- Investigating local and systemic intestinal signalling in health and disease with Drosophila.Disease models & mechanisms · 2022Review
- Aging-related upregulation of the homeobox gene caudal represses intestinal stem cell differentiation in Drosophila.PLoS genetics · 2021Article
- Article
- Tissue Adaptation to Environmental Cues by Symmetric and Asymmetric Division Modes of Intestinal Stem Cells.International journal of molecular sciences · 2020Review
- Src Family Tyrosine Kinases in Intestinal Homeostasis, Regeneration and Tumorigenesis.Cancers · 2020Review
- Review
- Long-term live imaging of theeLife · 2018Article
- Expression of lamina proteins Lamin and Kugelkern suppresses stem cell proliferation.Nucleus (Austin, Tex.) · 2018Article
- Ret receptor tyrosine kinase sustains proliferation and tissue maturation in intestinal epithelia.The EMBO journal · 2017Article
- Tissue-resident stem cell activity: a view from the adult Drosophila gastrointestinal tract.Cell communication and signaling : CCS · 2017Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Src non-receptor kinases have been implicated in events late in tumor progression. Here, we study the role of Src kinases in the Drosophila intestinal stem cell (ISC) lineage, during tissue homeostasis and tumor onset. The adult Drosophila intestine contains only two progenitor cell types, division-capable ISCs and their daughters, postmitotic enteroblasts (EBs). We found that Drosophila Src42a and Src64b were required for optimal regenerative ISC division. Conversely, activation of Src42a, Src64b or another non-receptor kinase, Ack, promoted division of quiescent ISCs by coordinately stimulating G1/S and G2/M cell cycle phase progression. Prolonged Src kinase activation caused tissue overgrowth owing to cytokine receptor-independent Stat92E activation. This was not due to increased symmetric division of ISCs, but involved accumulation of weakly specified Notch(+) but division-capable EB-like cells. Src activation triggered expression of a mitogenic module consisting of String/Cdc25 and Cyclin E that was sufficient to elicit division not only of ISCs but also of EBs. A small pool of similarly division-capable transit-amplifying Notch(+) EBs was also identified in the wild type. Expansion of intermediate cell types that do not robustly manifest their transit-amplifying potential in the wild type may also contribute to regenerative growth and tumor development in other tissues in other organisms.
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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.