ArticleGenes & development2011
SKIP counteracts p53-mediated apoptosis via selective regulation of p21Cip1 mRNA splicing.
Article in Genes & development, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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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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.
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Who cites it
53 citing papers in PubMed, 71 citations in OpenAlex.
- Article
- Article
- Unraveling the miR-144-3p/PUMA pathway: a novel regulator of FDX1-mediated cuproptosis in colorectal cancer.Cellular oncology (Dordrecht, Netherlands) · 2025Article
- Sustainable integrative cell biology: CENP-C is guilty by association.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2025Article
- Article
- Mutations in the spliceosomal gene SNW1 cause neurodevelopment disorders with microcephaly.The Journal of clinical investigation · 2025Article
- RNA modification writer-based immunological profile and genomic landscape of tumor microenvironment in lung adenocarcinoma.Discover oncology · 2025Article
- Phosphorylation of SNW1 protein associated with equine melanocytic neoplasm identified in serum and feces.Scientific reports · 2024Article
- Super-enhancer-driven LIF promotes the mesenchymal transition in glioblastoma by activating ITGB2 signaling feedback in microglia.Neuro-oncology · 2024Article
- Truncating the spliceosomal 'rope protein' Prp45 results in Htz1 dependent phenotypes.RNA biology · 2024Article
- Long non-coding RNA generated from CDKN1A gene by alternative polyadenylation regulates p21 expression during DNA damage response.Nucleic acids research · 2023Article
- A dual role of RBM42 in modulating splicing and translation of CDKN1A/p21 during DNA damage response.Nature communications · 2023Article
- The PRP19 Ubiquitin Ligase, Standing at the Cross-Roads of mRNA Processing and Genome Stability.Cancers · 2022Review
- Prp19 Facilitated p21-Dependent Senescence of Hepatocellular Carcinoma Cells.Journal of oncology · 2022Article
- Salt responsive alternative splicing of a RING finger E3 ligase modulates the salt stress tolerance by fine-tuning the balance of COP9 signalosome subunit 5A.PLoS genetics · 2021Article
- The Identification of RNA-Binding Proteins Functionally Associated with Tumor Progression in Gastrointestinal Cancer.Cancers · 2021Article
- Review
- Gene Expression Changes and Associated Pathways Involved in the Progression of Prostate Cancer Advanced Stages.Frontiers in genetics · 2020Article
- SKIP Silencing Decreased Disease Resistance AgainstFrontiers in plant science · 2020Article
- Activation of P-TEFb by cAMP-PKA signaling in autosomal dominant polycystic kidney disease.Science advances · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The Ski-interacting protein SKIP/SNW1 functions as both a splicing factor and a transcriptional coactivator for induced genes. We showed previously that transcription elongation factors such as SKIP are dispensable in cells subjected to DNA damage stress. However, we report here that SKIP is critical for both basal and stress-induced expression of the cell cycle arrest factor p21(Cip1). RNAi chromatin immunoprecipitation (RNAi-ChIP) and RNA immunoprecipitation (RNA-IP) experiments indicate that SKIP is not required for transcription elongation of the gene under stress, but instead is critical for splicing and p21(Cip1) protein expression. SKIP interacts with the 3' splice site recognition factor U2AF65 and recruits it to the p21(Cip1) gene and mRNA. Remarkably, SKIP is not required for splicing or loading of U2AF65 at other investigated p53-induced targets, including the proapoptotic gene PUMA. Consequently, depletion of SKIP induces a rapid down-regulation of p21(Cip1) and predisposes cells to undergo p53-mediated apoptosis, which is greatly enhanced by chemotherapeutic DNA damage agents. ChIP experiments reveal that SKIP is recruited to the p21(Cip1), and not PUMA, gene promoters, indicating that p21(Cip1) gene-specific splicing is predominantly cotranscriptional. The SKIP-associated factors DHX8 and Prp19 are also selectively required for p21(Cip1) expression under stress. Together, these studies define a new step that controls cancer cell apoptosis.
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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.