CKIT

Alison C. MacLeod, Lillian R. Klug, Michael Heinrich

    Research output: Chapter in Book/Report/Conference proceedingChapter

    Abstract

    KIT is a type III receptor tyrosine kinase encoded by a gene locus on the long arm of chromosome 4. It is closely related to Fms-like tyrosine kinase 3 (FLT3), platelet-derived growth factor receptor alpha and beta (PDGFRa, PDGFRß), and colony-stimulating factor 1 receptor (CSF1R). Depending on its degree of glycosylation, the molecular mass of KIT is 140-160 kD. KIT is normally expressed on the surface of hematopoietic stem and progenitor cells, mast cells, melanocytes, germ cells, and interstitial cells of Cajal. There are both transmembrane and soluble forms of KIT; however, the transmembrane form is believed to be biologically active, while the role of soluble KIT is poorly understood. The ligand for KIT is stem cell factor (SCF), also known as steel factor or mast cell growth factor. Both soluble and membrane-bound forms of SCF exist, resulting from alternative splicing of exon 6 (Broudy, Blood 90:1345-1364, 1997; Heinrich et al., J Clin Oncol 20:1692-1703, 2002; Lennartsson and Ronnstrand, Curr Cancer Drug Targets 6:65-75, 2006).

    Original languageEnglish (US)
    Title of host publicationCancer Therapeutic Targets
    PublisherSpringer New York
    Pages683-692
    Number of pages10
    Volume2-2
    ISBN (Electronic)9781441907172
    ISBN (Print)9781441907165
    DOIs
    StatePublished - Jan 1 2017

    Fingerprint

    Stem Cell Factor
    Hematopoietic Stem Cells
    fms-Like Tyrosine Kinase 3
    Colony-Stimulating Factor Receptors
    Cells
    Interstitial Cells of Cajal
    Platelet-Derived Growth Factor alpha Receptor
    Platelet-Derived Growth Factor beta Receptor
    Glycosylation
    Chromosomes, Human, Pair 4
    Macrophage Colony-Stimulating Factor
    Melanocytes
    Alternative Splicing
    Receptor Protein-Tyrosine Kinases
    Molecular mass
    Chromosomes
    Mast Cells
    Germ Cells
    Exons
    Blood

    Keywords

    • ABL
    • BCR-ABL
    • JAK/STAT
    • KIT
    • MAP kinase
    • MetaGIST study
    • PI3-K
    • Platelet-derived growth factor receptor alpha (PDGFRa)
    • Platelet-derived growth factor receptor alpha (PDGFRa)
    • Stem cell factor (SCF)

    ASJC Scopus subject areas

    • Medicine(all)
    • Biochemistry, Genetics and Molecular Biology(all)
    • Pharmacology, Toxicology and Pharmaceutics(all)

    Cite this

    MacLeod, A. C., Klug, L. R., & Heinrich, M. (2017). CKIT. In Cancer Therapeutic Targets (Vol. 2-2, pp. 683-692). Springer New York. https://doi.org/10.1007/978-1-4419-0717-2_25

    CKIT. / MacLeod, Alison C.; Klug, Lillian R.; Heinrich, Michael.

    Cancer Therapeutic Targets. Vol. 2-2 Springer New York, 2017. p. 683-692.

    Research output: Chapter in Book/Report/Conference proceedingChapter

    MacLeod, AC, Klug, LR & Heinrich, M 2017, CKIT. in Cancer Therapeutic Targets. vol. 2-2, Springer New York, pp. 683-692. https://doi.org/10.1007/978-1-4419-0717-2_25
    MacLeod AC, Klug LR, Heinrich M. CKIT. In Cancer Therapeutic Targets. Vol. 2-2. Springer New York. 2017. p. 683-692 https://doi.org/10.1007/978-1-4419-0717-2_25
    MacLeod, Alison C. ; Klug, Lillian R. ; Heinrich, Michael. / CKIT. Cancer Therapeutic Targets. Vol. 2-2 Springer New York, 2017. pp. 683-692
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