ArticleCell2019
Pharmacological Targeting of STK19 Inhibits Oncogenic NRAS-Driven Melanomagenesis.
Article in Cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 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
57 citing papers in PubMed, 93 citations in OpenAlex.
- To be or not to be a protein coding mutation, that's the question!NAR genomics and bioinformatics · 2025Review
- CRISPR/Cas9 library screening reveals that STK19 has synergistic antitumor effects when combined with cisplatin on tongue squamous cell carcinoma.Journal of translational medicine · 2025Article
- Single-Cell Transcriptomic Landscape Deciphers Intratumoral Heterogeneity and Subtypes of Acral and Mucosal Melanomas.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Article
- Review
- Global trends and emerging insights in BRAF and MEK inhibitor resistance in melanoma: a bibliometric analysis.Frontiers in molecular biosciences · 2025Article
- Dissecting the pathogenic effects of smoking in blood DNA methylation on allergic diseases.The World Allergy Organization journal · 2024Article
- STK19 is a transcription-coupled repair factor that participates in UVSSA ubiquitination and TFIIH loading.Nucleic acids research · 2024Article
- Pharmacological targeting of casein kinase 1δ suppresses oncogenic NRAS-driven melanoma.Nature communications · 2024Article
- Mutations found in cancer patients compromise DNA binding of the winged helix protein STK19.Scientific reports · 2024Article
- A synthetic lethal dependency on casein kinase 2 in response to replication-perturbing therapeutics in RB1-deficient cancer cells.Science advances · 2024Article
- STK19 is a DNA/RNA-binding protein critical for DNA damage repair and cell proliferation.The Journal of cell biology · 2024Article
- Review
- Article
- The nuclear GYF protein CD2BP2/U5-52K is required for T cell homeostasis.Frontiers in immunology · 2024Article
- ADP-dependent glucokinase controls metabolic fitness in prostate cancer progression.Military Medical Research · 2023Article
- CCDC50 promotes tumor growth through regulation of lysosome homeostasis.EMBO reports · 2023Article
- Regulation of Ras Signaling by S-Nitrosylation.Antioxidants (Basel, Switzerland) · 2023Review
- Breast Sarcomas, Phyllodes Tumors, and Desmoid Tumors: Turning the Magnifying Glass on Rare and Aggressive Entities.Cancers · 2023Review
- Article
- Molecular basis and genetic testing strategies for diagnosing 21-hydroxylase deficiency, including CAH-X syndrome.Annals of pediatric endocrinology & metabolism · 2023Article
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Authors and funding
21 authors at 11 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activating mutations in NRAS account for 20%-30% of melanoma, but despite decades of research and in contrast to BRAF, no effective anti-NRAS therapies have been forthcoming. Here, we identify a previously uncharacterized serine/threonine kinase STK19 as a novel NRAS activator. STK19 phosphorylates NRAS to enhance its binding to its downstream effectors and promotes oncogenic NRAS-mediated melanocyte malignant transformation. A recurrent D89N substitution in STK19 whose alterations were identified in 25% of human melanomas represents a gain-of-function mutation that interacts better with NRAS to enhance melanocyte transformation. STK19
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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.