ArticleProceedings of the National Academy of Sciences of the United States of America2004
Targeted mutations of the juxtamembrane tyrosines in the Kit receptor tyrosine kinase selectively affect multiple cell lineages.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. 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
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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
28 citing papers in PubMed, 62 citations in OpenAlex.
- Targeting receptor tyrosine kinases: from molecular mechanisms to clinical therapeutics.Signal transduction and targeted therapy · 2026Review
- Review
- Pulling back the curtain: The hidden functions of receptor tyrosine kinases in development.Current topics in developmental biology · 2022Article
- Stem Cell Factor-Inducible MITF-M Expression in Therapeutics for Acquired Skin Hyperpigmentation.Theranostics · 2020Article
- MAPK and PI3K signaling: At the crossroads of neural crest development.Developmental biology · 2018Review
- Mechanisms of erythrocyte development and regeneration: implications for regenerative medicine and beyond.Development (Cambridge, England) · 2018Review
- Direct engagement of the PI3K pathway by mutant KIT dominates oncogenic signaling in gastrointestinal stromal tumor.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Receptor tyrosine kinase (c-Kit) inhibitors: a potential therapeutic target in cancer cells.Drug design, development and therapy · 2016Review
- C-Kit Promotes Growth and Migration of Human Cardiac Progenitor Cells via the PI3K-AKT and MEK-ERK Pathways.PloS one · 2015Article
- Receptor tyrosine kinase signaling: regulating neural crest development one phosphate at a time.Current topics in developmental biology · 2015Review
- KIT-D816V oncogenic activity is controlled by the juxtamembrane docking site Y568-Y570.Oncogene · 2014Article
- KIT signaling governs differential sensitivity of mature and primitive CML progenitors to tyrosine kinase inhibitors.Cancer research · 2013Article
- 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
- The C-kit receptor-mediated signal transduction and tumor-related diseases.International journal of biological sciences · 2013Review
- SH2 domain-containing phosphatase 2 is a critical regulator of connective tissue mast cell survival and homeostasis in mice.Molecular and cellular biology · 2012Article
- Article
- The structural insights of stem cell factor receptor (c-Kit) interaction with tyrosine phosphatase-2 (Shp-2): an in silico analysis.BMC research notes · 2010Article
- Kit ligand cytoplasmic domain is essential for basolateral sorting in vivo and has roles in spermatogenesis and hematopoiesis.Developmental biology · 2010Article
- Green fluorescent protein transgene driven by Kit regulatory sequences is expressed in hematopoietic stem cells.Haematologica · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Loss-of-function mutations in the murine dominant white spotting/c-kit locus affect a diverse array of biological processes and cell lineages and cause a range of phenotypes, including severe anemia, defective pigmentation, sterility, mast cell deficits, a lack of interstitial cells of Cajal, spatial learning memory deficits, and defects in peripheral nerve regeneration. Here we show that tyrosine residues 567 and 569 in the juxtamembrane (Jx) domain of the murine Kit receptor tyrosine kinase are crucial for the function of Kit in melanogenesis and mast cell development, but are dispensable for the normal development of erythroid, interstitial cells of Cajal and germ cells. Furthermore, adult mice lacking both tyrosines exhibit splenomegaly, dysregulation of B-cell and megakaryocyte development, and enlarged stomachs. Analysis of signal transduction events induced by the mutant receptors after ligand stimulation indicates that Jx tyrosine mutations diminish receptor autophosphorylation and selectively attenuate activation of extracellular signal-regulated kinase/mitogen-activated protein kinases. Together, these observations demonstrate that the Jx domain of Kit plays a cell-type specific regulatory role in vivo and illustrate how engineered mutations in Kit can be used to understand the complex biological and molecular events that result from activating a receptor tyrosine kinase.
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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.