ArticleThe Biochemical journal1997
Stat1 associates with c-kit and is activated in response to stem cell factor.
Article in The Biochemical journal, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
28 citing papers in PubMed, 111 citations in OpenAlex.
- Phase II open label trial of imatinib in polycythemia rubra vera.International journal of hematology · 2008Trial
- STAT1 and herpesviruses: Making lemonade from lemons.Virology · 2025Review
- Tyrosine kinases: multifaceted receptors at the intersection of several neurodegenerative disease-associated processes.Frontiers in dementia · 2024Review
- Oncogenic KIT Modulates Type I IFN-Mediated Antitumor Immunity in GIST.Cancer immunology research · 2021Article
- Review
- SRC-like adaptor protein 2 (SLAP2) is a negative regulator of KIT-D816V-mediated oncogenic transformation.Scientific reports · 2018Article
- The stem cell factor (SCF)/c-KIT signalling in testis and prostate cancer.Journal of cell communication and signaling · 2017Article
- Normal peripheral prostate stromal cells stimulate prostate cancer development: roles of c-kit signal.American journal of translational research · 2015Article
- KIT-D816V oncogenic activity is controlled by the juxtamembrane docking site Y568-Y570.Oncogene · 2014Article
- Primordial germ cells and gastrointestinal stromal tumors respond distinctly to a cKit overactivating allele.Human molecular genetics · 2013Article
- c-Kit is required for growth and survival of the cells of origin of Brca1-mutation-associated breast cancer.Oncogene · 2012Article
- Mechanisms of STAT protein activation by oncogenic KIT mutants in neoplastic mast cells.The Journal of biological chemistry · 2011Article
- Potential involvement of the stem cell factor receptor c-kit in alopecia areata and androgenetic alopecia: histopathological, immunohistochemical, and semiquantitative investigations.Acta histochemica et cytochemica · 2010Article
- Article
- Mechanisms of oncogenic KIT signal transduction in primary gastrointestinal stromal tumors (GISTs).Oncogene · 2004Article
- Receptor tyrosine kinase signaling and primordial germ cell development.Cell cycle (Georgetown, Tex.) · 2004Article
- Coactivation of STAT and Ras is required for germ cell proliferation and invasive migration in Drosophila.Developmental cell · 2003Article
- Analysing c-kit internalization using a functional c-kit-EGFP chimera containing the fluorochrome within the extracellular domain.Oncogene · 2002Article
- Constitutive activation of FLT3 stimulates multiple intracellular signal transducers and results in transformation.Leukemia · 2000Article
- Essential role of signal transducer and activator of transcription (Stat)5a but not Stat5b for Flt3-dependent signaling.The Journal of experimental medicine · 2000Article
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interaction of stem cell factor (SCF), a haematopoietic growth factor, with the receptor tyrosine kinase c-kit leads to autophosphorylation of c-kit as well as tyrosine phosphorylation of various substrates. Little is known about the role of the JAK/STAT pathway in signal transduction via receptor tyrosine kinases, although this pathway has been well characterized in cytokine receptor signal transduction. We recently found that the Janus kinase Jak2 associates with c-kit and that SCF induces rapid and transient phosphorylation of Jak2. Here we present evidence that SCF activates the transcription factor Stat1. Phosphorylated c-kit co-immunoprecipitates with Stat1 within 1 min of SCF stimulation of the human cell line MO7e. Co-precipitation experiments using glutathione S-transferase fusion proteins indicate that association with c-kit is mediated by the Stat1 SH2 domain. Stat1 is rapidly tyrosine-phosphorylated in response to SCF in MO7e cells, the murine cell line FDCP-1 and normal progenitor cells. SCF-induced phosphorylation of Jak2 and Stat1 was also observed in murine 3T3 fibroblasts stably transfected with full-length human c-kit receptor. Furthermore c-kit directly phosphorylates Stat1 fusion proteins in in vitro kinase assays. Electrophoretic mobility-shift assays with nuclear extracts from SCF-stimulated cell lines and normal progenitor cells indicate that activated Stat1 binds the m67 oligonucleotide, a high-affinity SIE promoter sequence. These results demonstrate that Stat1 is activated in response to SCF, and suggest that Stat1 is a component of the SCF signal-transduction pathway.
Indexed as
Identifiers
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.