ArticleOncogene2003
A genetic screen for modifiers of the lats tumor suppressor gene identifies C-terminal Src kinase as a regulator of cell proliferation in Drosophila.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 49 citations in OpenAlex.
- Unveiling the Tumor Suppressors: Insights from Drosophila.Advances in experimental medicine and biology · 2025Review
- Activated Src kinase promotes cell cannibalism in Drosophila.The Journal of cell biology · 2023Article
- Toll-7 promotes tumour growth and invasion in Drosophila.Cell proliferation · 2022Article
- Utilizing the Hippo pathway as a therapeutic target for combating endocrine-resistant breast cancer.Cancer cell international · 2021Review
- Hippo-Yap/Taz signaling: Complex network interactions and impact in epithelial cell behavior.Wiley interdisciplinary reviews. Developmental biology · 2020Review
- A Gene Expression Screen inG3 (Bethesda, Md.) · 2019Article
- Article
- Cell Extrusion: A Stress-Responsive Force for Good or Evil in Epithelial Homeostasis.Developmental cell · 2018Review
- C-terminal Src kinase (Csk) regulates the tricellular junction protein Gliotactin independent of Src.Molecular biology of the cell · 2018Article
- C-terminal Src kinase-mediated EPIYA phosphorylation of Pragmin creates a feed-forward C-terminal Src kinase activation loop that promotes cell motility.Cancer science · 2016Article
- C-terminal Src Kinase Gates Homeostatic Synaptic Plasticity and Regulates Fasciclin II Expression at the Drosophila Neuromuscular Junction.PLoS genetics · 2016Article
- The Hippo pathway promotes cell survival in response to chemical stress.Cell death and differentiation · 2015Article
- The Notch-mediated hyperplasia circuitry in Drosophila reveals a Src-JNK signaling axis.eLife · 2015Article
- Src kinase function controls progenitor cell pools during regeneration and tumor onset in the Drosophila intestine.Oncogene · 2015Article
- Article
- Transcriptional profiling of Drosophila S2 cells in early response to Drosophila C virus.Virology journal · 2013Article
- Regulation of the SRC family kinases by Csk.International journal of biological sciences · 2012Review
- Oncogenic signaling by tyrosine kinases of the SRC family in advanced colorectal cancer.American journal of cancer research · 2012Article
- Cell competition and its implications for development and cancer.Journal of genetics and genomics = Yi chuan xue bao · 2011Review
- Identifying cellular pathways modulated by Drosophila palmitoyl-protein thioesterase 1 function.Neurobiology of disease · 2010Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Disrupting mechanisms that control cell proliferation, cell size and apoptosis can cause changes in animal and tissue size and contribute to diseases such as cancer. The LATS family of serine/threonine kinases control tissue size by regulating cell proliferation and function as tumor suppressor genes in both Drosophila and mammals. In order to understand the role of lats in size regulation, we performed a genetic modifier screen in Drosophila to identify components of the lats signaling pathway. Mutations in the Drosophila homolog of C-terminal Src kinase (dcsk) were identified as dominant modifiers of both lats gain-of-function and loss-of-function phenotypes. Homozygous dcsk mutants have enlarged tissue phenotypes similar to lats and FACS and immunohistochemistry analysis of these tissues revealed that dcsk also regulates cell proliferation during development. Animals having mutations in both dcsk and lats display cell overproliferation phenotypes more severe than either mutant alone, demonstrating these genes function together in vivo to regulate cell numbers. Furthermore, homozygous dcsk phenotypes can be partially suppressed by overexpression of lats, indicating that lats is a downstream mediator of dcsk function in vivo. Finally, we show that dCSK phosphorylates LATS in vitro at a conserved C-terminal tyrosine residue, which is critical for normal LATS function in vivo. Taken together, these results demonstrate a role for dCSK in regulating cell numbers during development by inhibiting cell proliferation and suggest that lats is one of the mediators of the dcsk phenotype.
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What OpenQuestion holds
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.