ArticleCell2020
Evidence That STK19 Is Not an NRAS-dependent Melanoma Driver.
Article in Cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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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
21 citing papers in PubMed, 33 citations in OpenAlex.
- Mechanisms of transcription-coupled repair and DNA damage surveillance in health and disease.Nature reviews. Molecular cell biology · 2026Review
- Antibody-drug conjugates for infectious and neglected tropical diseases: chemical design principles, target biology, and translational challenges.Frontiers in chemistry · 2026Review
- To be or not to be a protein coding mutation, that's the question!NAR genomics and bioinformatics · 2025Review
- Transcription-coupled repair: tangled up in convoluted repair.The FEBS journal · 2025Review
- Reannotation of cancer mutations based on expressed RNA transcripts reveals functional non-coding mutations in melanoma.American journal of human genetics · 2025Article
- Molecular model of TFIIH recruitment to the transcription-coupled repair machinery.Nature communications · 2025Article
- Article
- STK19 facilitates the clearance of lesion-stalled RNAPII during transcription-coupled DNA repair.Cell · 2024Article
- STK19 is a transcription-coupled repair factor that participates in UVSSA ubiquitination and TFIIH loading.Nucleic acids research · 2024Article
- STK19 positions TFIIH for cell-free transcription-coupled DNA repair.bioRxiv : the preprint server for biology · 2024Article
- Mutations found in cancer patients compromise DNA binding of the winged helix protein STK19.Scientific reports · 2024Article
- STK19 is a DNA/RNA-binding protein critical for DNA damage repair and cell proliferation.The Journal of cell biology · 2024Article
- Review
- Detecting recurrent passenger mutations in melanoma by targeted UV damage sequencing.Nature communications · 2023Article
- RAS pathway regulation in melanoma.Disease models & mechanisms · 2022Review
- Targeting RAS phosphorylation in cancer therapy: Mechanisms and modulators.Acta pharmaceutica Sinica. B · 2021Review
- The landscape of driver mutations in cutaneous squamous cell carcinoma.NPJ genomic medicine · 2021Article
- Many Distinct Ways Lead to Drug Resistance inLife (Basel, Switzerland) · 2021Review
- MHC Class III RNA Binding Proteins and Immunity.RNA biology · 2021Review
- A Missense Mutation rs781536408 (c.2395G>A) ofFrontiers in genetics · 2021Article
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11 authors at 1 institution in 1 country.
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Abstract
STK19 was proposed to be a cancer driver, and recent work by Yin et al. (2019) in Cell suggested that the frequently recurring STK19 D89N substitution represents a gain-of-function change, allowing increased phosphorylation of NRAS to enhance melanocyte transformation. Here we show that the STK19 gene has been incorrectly annotated, and that the expressed protein is 110 amino acids shorter than indicated by current databases. The "cancer driving" STK19 D89N substitution is thus outside the coding region. We also fail to detect evidence of the mutation affecting STK19 expression; instead, it is a UV signature mutation, found in the promoter of other genes as well. Furthermore, STK19 is exclusively nuclear and chromatin-associated, while no evidence for it being a kinase was found. The data in this Matters Arising article raise fundamental questions about the recently proposed role for STK19 in melanoma progression via a function as an NRAS kinase, suggested by Yin et al. (2019) in Cell. See also the response by Yin et al. (2020), published in this issue.
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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.