ArticlePloS one2011
C-KIT signaling depends on microphthalmia-associated transcription factor for effects on cell proliferation.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 68 citations in OpenAlex.
- Epidermal Growth Factor Receptor/KIT-Linked Proliferative Bias in Normal Breast Lobules from Matched Non-Hispanic Black and White Women Is Rapidly Reversible by Receptor Tyrosine Kinase Inhibition.The American journal of pathology · 2026Article
- Emerging perspectives on the selective autophagy of melanosomes: melanophagy.Experimental & molecular medicine · 2025Review
- Melanocyte differentiation and mechanosensation are differentially modulated by distinct extracellular matrix proteins.EMBO reports · 2025Article
- Three NovelAnimals : an open access journal from MDPI · 2025Article
- Article
- NOTCH1- and CD117-Positive Stem Cells in Human Endometriosis and Adenomyosis Lesions.Diagnostics (Basel, Switzerland) · 2024Article
- The Influence of Blue Light Exposure on Reconstructed 3-Dimensional Skin Model: Molecular Changes and Gene Expression Profile.JID innovations : skin science from molecules to population health · 2024Article
- Population Analysis Identifies 15 Multi-VariantAnimals : an open access journal from MDPI · 2024Article
- Spotting the Pattern: A Review on White Coat Color in the Domestic Horse.Animals : an open access journal from MDPI · 2024Review
- Microbes, macrophages, and melanin: a unifying theory of disease as exemplified by cancer.Frontiers in immunology · 2024Review
- Lung-specific MCEMP1 functions as an adaptor for KIT to promote SCF-mediated mast cell proliferation.Nature communications · 2023Article
- Plants as Modulators of Melanogenesis: Role of Extracts, Pure Compounds and Patented Compositions in Therapy of Pigmentation Disorders.International journal of molecular sciences · 2022Review
- A 9‑gene expression signature to predict stage development in resectable stomach adenocarcinoma.BMC gastroenterology · 2022Article
- MITF in Normal Melanocytes, Cutaneous and Uveal Melanoma: A Delicate Balance.International journal of molecular sciences · 2022Review
- KIT gene mutation causes deafness and hypopigmentation in Bama miniature pigs.American journal of translational research · 2020Article
- Stem Cell Factor-Inducible MITF-M Expression in Therapeutics for Acquired Skin Hyperpigmentation.Theranostics · 2020Article
- Feeder-free Derivation of Melanocytes from Human Pluripotent Stem Cells.Journal of visualized experiments : JoVE · 2016Article
- A molecular systems approach to modelling human skin pigmentation: identifying underlying pathways and critical components.BMC research notes · 2015Article
- KIT in melanoma: many shades of gray.The Journal of investigative dermatology · 2015Article
- The role of human cervical cancer oncogene in cancer progression.International journal of clinical and experimental medicine · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
The development of melanocytes is regulated by the tyrosine kinase receptor c-KIT and the basic-helix-loop-helix-leucine zipper transcription factor Mitf. These essential melanocyte survival regulators are also well known oncogenic factors in malignant melanoma. Despite their importance, not much is known about the regulatory mechanisms and signaling pathways involved. In this study, we therefore sought to identify the signaling pathways and mechanisms involved in c-KIT mediated regulation of Mitf. We report that c-KIT stimulation leads to the activation of Mitf specifically through the c-KIT phosphorylation sites Y721 (PI3 kinase binding site), Y568 and Y570 (Src binding site). Our study not only confirms the involvement of Ras-Erk signaling pathway in the activation of Mitf, but also establishes that Src kinase binding to Y568 and Y570 of c-KIT is required. Using specific inhibitors we observe and verify that c-KIT induced activation of Mitf is dependent on PI3-, Akt-, Src-, p38- or Mek kinases. Moreover, the proliferative effect of c-KIT is dependent on Mitf in HEK293T cells. In contrast, c-KIT Y568F and Y721F mutants are less effective in driving cell proliferation, compared to wild type c-KIT. Our results reveal novel mechanisms by which c-KIT signaling regulates Mitf, with implications for understanding both melanocyte development and melanoma.
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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.