ArticleNature communications2016
ELL targets c-Myc for proteasomal degradation and suppresses tumour growth.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 24 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Genetic variants of genes in the NER pathway associated with risk of breast cancer: A large-scale analysis of 14 published GWAS datasets in the DRIVE study.International journal of cancer · 2019Pooled it
- Integrating spatial and single-cell transcriptomics analysis reveals MYCN-UBE2C-TFRC signaling endows ferroptosis resistance in neuroectodermal tumors.Science China. Life sciences · 2026Article
- Akt-mediated RALY phosphorylation functions as a molecular switch governing c-Myc stability.Cell death and differentiation · 2026Article
- ISGylation of γH2AX retains MDC1 and facilitates homologous recombination repair causing radioresistance in esophageal adenocarcinoma.The Journal of biological chemistry · 2026Article
- NKD1 enhances colon cancer progression by inhibiting the autophagic degradation of MYC.Cell death & disease · 2025Article
- Prognostic model of ubiquitination-related genes in ovarian cancer based on transcriptomic analysis and experimental validation.Frontiers in immunology · 2025Article
- TRAIP suppresses bladder cancer progression by catalyzing K48-linked polyubiquitination of MYC.Oncogene · 2024Article
- Modes of Action of a Novel c-MYC Inhibiting 1,2,4-Oxadiazole Derivative in Leukemia and Breast Cancer Cells.Molecules (Basel, Switzerland) · 2023Article
- TRIM55 inhibits colorectal cancer development via enhancing protein degradation of c-Myc.Cancer medicine · 2023Article
- ZebrafishJournal of virology · 2023Article
- Telotristat Etiprate alleviates rheumatoid arthritis by targeting LGALS3 and affecting MAPK signaling.Intractable & rare diseases research · 2023Article
- Targeting metabolism: A potential strategy for hematological cancer therapy.World journal of clinical cases · 2022Review
- EST12 regulates Myc expression and enhances anti-mycobacterial inflammatory responseFrontiers in immunology · 2022Article
- Targeting c-Myc to Overcome Acquired Resistance of EGFR Mutant NSCLC Cells to the Third-Generation EGFR Tyrosine Kinase Inhibitor, Osimertinib.Cancer research · 2021Article
- Targeting the MYC Ubiquitination-Proteasome Degradation Pathway for Cancer Therapy.Frontiers in oncology · 2021Review
- Identification of Vitamin D-related gene signature to predict colorectal cancer prognosis.PeerJ · 2021Article
- E2 ubiquitin-conjugating enzyme UBE2L6 promotes Senecavirus A proliferation by stabilizing the viral RNA polymerase.PLoS pathogens · 2020Article
- Writing and erasing MYC ubiquitination and SUMOylation.Genes & diseases · 2019Review
- ELL2 Influences Transcription Elongation, Splicing, Ig Secretion and Growth.Journal of mucosal immunology research · 2019Article
- Aberrant activation of non-coding RNA targets of transcriptional elongation complexes contributes to TDP-43 toxicity.Nature communications · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increasing evidence supports that ELL (eleven-nineteen lysine-rich leukaemia) is a key regulator of transcriptional elongation, but the physiological function of Ell in mammals remains elusive. Here we show that ELL functions as an E3 ubiquitin ligase and targets c-Myc for proteasomal degradation. In addition, we identify that UbcH8 serves as a ubiquitin-conjugating enzyme in this pathway. Cysteine 595 of ELL is an active site of the enzyme; its mutation to alanine (C595A) renders the protein unable to promote the ubiquitination and degradation of c-Myc. ELL-mediated c-Myc degradation inhibits c-Myc-dependent transcriptional activity and cell proliferation, and also suppresses c-Myc-dependent xenograft tumour growth. In contrast, the ELL(C595A) mutant not only loses the ability to inhibit cell proliferation and xenograft tumour growth, but also promotes tumour metastasis. Thus, our work reveals a previously unrecognized function for ELL as an E3 ubiquitin ligase for c-Myc and a potential tumour suppressor.
Indexed as
Identifiers
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.