ArticleMolecular and cellular biology2004
c-Kit-mediated overlapping and unique functional and biochemical outcomes via diverse signaling pathways.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 60 citations in OpenAlex.
- N6-methyl-2'-deoxyadenosine promotes self-renewal of BFU-E progenitor in erythropoiesis.iScience · 2023Article
- c-Kit Receptor Maintains Sensory Axon Innervation of the Skin through Src Family Kinases.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Sterile α-motif domain requirement for cellular signaling and survival.The Journal of biological chemistry · 2020Article
- N822K- or V560G-mutated KIT activation preferentially occurs in lipid rafts of the Golgi apparatus in leukemia cells.Cell communication and signaling : CCS · 2019Article
- Receptor tyrosine kinase (c-Kit) inhibitors: a potential therapeutic target in cancer cells.Drug design, development and therapy · 2016Review
- Src signaling pathways in prostate cancer.Cancer metastasis reviews · 2014Review
- Detecting protein-protein interactions based on kinase-mediated growth induction of mammalian cells.Scientific reports · 2014Article
- Structural and functional properties of platelet-derived growth factor and stem cell factor receptors.Cold Spring Harbor perspectives in biology · 2013Review
- Primordial germ cells and gastrointestinal stromal tumors respond distinctly to a cKit overactivating allele.Human molecular genetics · 2013Article
- Role of intracellular tyrosines in activating KIT-induced myeloproliferative disease.Leukemia · 2012Article
- A CSF-1 receptor phosphotyrosine 559 signaling pathway regulates receptor ubiquitination and tyrosine phosphorylation.The Journal of biological chemistry · 2011Article
- A KIT juxtamembrane PY567 -directed pathway provides nonredundant signals for erythroid progenitor cell development and stress erythropoiesis.Experimental hematology · 2009Article
- Protein-tyrosine phosphatase alpha regulates stem cell factor-dependent c-Kit activation and migration of mast cells.The Journal of biological chemistry · 2008Article
- KIT associated intracellular tyrosines play an essential role in EpoR co-signaling.Cellular signalling · 2008Article
- Gleevec increases levels of the amyloid precursor protein intracellular domain and of the amyloid-beta degrading enzyme neprilysin.Molecular biology of the cell · 2007Article
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- Activating mutations and/or expression levels of tyrosine kinase receptors GRB7, RAS, and BRAF in testicular germ cell tumors.Neoplasia (New York, N.Y.) · 2005Article
- Repression of c-kit and its downstream substrates by GATA-1 inhibits cell proliferation during erythroid maturation.Molecular and cellular biology · 2005Article
- A clinical and biological overview of gastrointestinal stromal tumors.Medical oncology (Northwood, London, England) · 2005Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A critical issue in understanding receptor tyrosine kinase signaling is the individual contribution of diverse signaling pathways in regulating cellular growth, survival, and migration. We generated a functionally and biochemically inert c-Kit receptor that lacked the binding sites for seven early signaling pathways. Restoring the Src family kinase (SFK) binding sites in the mutated c-Kit receptor restored cellular survival and migration but only partially rescued proliferation and was associated with the rescue of the Ras/mitogen-activated protein kinase, Rac/JNK kinase, and phosphatidylinositol 3-kinase (PI-3 kinase)/Akt pathways. In contrast, restoring the PI-3 kinase binding site in the mutated receptor did not affect cellular proliferation but resulted in a modest correction in cell survival and migration, despite a complete rescue in the activation of the PI-3 kinase/Akt pathway. Surprisingly, restoring the binding sites for Grb2, Grb7, or phospholipase C-gamma had no effect on cellular growth or survival, migration, or activation of any of the downstream signaling pathways. These results argue that SFKs play a unique role in the control of multiple cellular functions and in the activation of distinct biochemical pathways via c-Kit.
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What Socratic 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 Socratic graph.