ArticleOncogene1999
Isoforms of c-KIT differ in activation of signalling pathways and transformation of NIH3T3 fibroblasts.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 98 citations in OpenAlex.
- Article
- SRSF10 is essential for progenitor spermatogonia expansion by regulating alternative splicing.eLife · 2022Article
- Role and significance of c-KIT receptor tyrosine kinase in cancer: A review.Bosnian journal of basic medical sciences · 2022Review
- A novel anti-c-Kit antibody-drug conjugate to treat wild-type and activating-mutant c-Kit-positive tumors.Molecular oncology · 2022Article
- CD117/c-kit defines a prostate CSC-like subpopulation driving progression and TKI resistance.Scientific reports · 2021Article
- Canine sarcomas as a surrogate for the human disease.Pharmacology & therapeutics · 2018Review
- Review
- The stem cell factor (SCF)/c-KIT signalling in testis and prostate cancer.Journal of cell communication and signaling · 2017Article
- Identification of the two KIT isoforms and their expression status in canine hemangiosarcomas.BMC veterinary research · 2016Article
- Receptor tyrosine kinase (c-Kit) inhibitors: a potential therapeutic target in cancer cells.Drug design, development and therapy · 2016Review
- Expression and localisation of c-kit and KITL in the adult human ovary.Journal of ovarian research · 2015Article
- KIT GNNK splice variants: expression in systemic mastocytosis and influence on the activating potential of the D816V mutation in mast cells.Experimental hematology · 2013Article
- Structural and functional properties of platelet-derived growth factor and stem cell factor receptors.Cold Spring Harbor perspectives in biology · 2013Review
- Review
- Systemic mast cell activation disease: the role of molecular genetic alterations in pathogenesis, heritability and diagnostics.Immunology · 2012Review
- Prognostic significance of c-KIT in vulvar cancer: bringing this molecular marker from bench to bedside.Journal of translational medicine · 2012Article
- c-Kit is required for growth and survival of the cells of origin of Brca1-mutation-associated breast cancer.Oncogene · 2012Article
- Article
- An unusual and potentially misleading phenotypic change in a primary gastrointestinal stromal tumour (GIST) under imatinib mesylate therapy.Virchows Archiv : an international journal of pathology · 2011Article
- Therapy-refractory gastrointestinal motility disorder in a child with c-kit mutations.World journal of gastroenterology · 2010Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alternate splicing of mRNA encoding c-KIT results in isoforms which differ in the presence or absence of four amino acids (GNNK) in the juxtamembrane region of the extracellular domain of the receptor. In this study we show that these isoforms of human c-KIT, expressed at similar levels in NIH3T3 cells, display differential effects on various attributes of transformation. The GNNK- isoform strongly promoted anchorage independent growth (colony formation in semi-solid medium), loss of contact inhibition (focus formation), and led to tumorigenicity in nude mice. In contrast, the GNNK+ isoform elicited colony formation but relatively poor focus formation and no tumorigenicity. Saturation binding analysis indicated that the isoforms do not differ significantly in their affinity for the KIT ligand, Steel Factor (SLF). Negligible ligand-independent receptor phosphorylation was observed in either case but, after ligand stimulation, the GNNK- isoform displayed more rapid and extensive tyrosine autophosphorylation and faster internalization. Both isoforms recruited the p85 subunit of phosphatidylinositol 3-kinase and led to similar phosphorylation of its downstream effector c-Akt, but the GNNK- isoform gave rise to more MAP kinase phosphorylation. Thus the c-KIT isoforms display different signalling characteristics and have different transforming activity in NIH3T3 cells.
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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.