ArticleThe EMBO journal2012
The SNF2-like helicase HELLS mediates E2F3-dependent transcription and cellular transformation.
Article in The EMBO journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
What it found
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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.
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Who cites it
59 citing papers in PubMed, 80 citations in OpenAlex.
- Evaluation of the subtype-specific epigenetic prognostic association of HELLS in non-small cell lung cancer: integrated clinical and molecular insights.Translational cancer research · 2026Article
- Prognostic and Functional Role of HELLS in Prostate Cancer: Implications for Tumor Progression and Immune Microenvironment.Applied biochemistry and biotechnology · 2026Article
- CDCA7 targets LSH to DNA maintenance methylation in S phase and transcription regulation in interphase via two distinct DNA-binding modes.Nucleic acids research · 2026Article
- Article
- Integrative single-cell transcriptomic and multi-dimensional bioinformatic analysis reveals proliferation-associated gene expression signatures and cellular heterogeneity in hepatocellular carcinoma.Discover oncology · 2026Article
- Photoclick chemistry led to the identification of HELLS as a helicase for DNA G-quadruplexes.Nucleic acids research · 2026Article
- Histone variant macroH2A1 regulates synchronous firing of replication origins in the inactive X chromosome.Nucleic acids research · 2024Article
- Immunological function and prognostic value of lymphoid-specific helicase in liver hepatocellular carcinoma.Cancer biomarkers : section A of Disease markers · 2023Article
- Review
- The Chromatin Remodeler HELLS: A New Regulator in DNA Repair, Genome Maintenance, and Cancer.International journal of molecular sciences · 2022Review
- The chromatin remodelling protein LSH/HELLS regulates the amount and distribution of DNA hydroxymethylation in the genome.Epigenetics · 2022Article
- Lymphoid-specific helicase in epigenetics, DNA repair and cancer.British journal of cancer · 2022Review
- HELLS Is Negatively Regulated by Wild-Type P53 in Liver Cancer by a Mechanism Involving P21 and FOXM1.Cancers · 2022Article
- Mammalian Resilience Revealed by a Comparison of Human Diseases and Mouse Models Associated With DNA Helicase Deficiencies.Frontiers in molecular biosciences · 2022Review
- Differential Expression of E2F Transcription Factors and Their Functional and Prognostic Roles in Human Prostate Cancer.Frontiers in cell and developmental biology · 2022Article
- Regulation of Oncogenic Targets by Tumor-SuppressiveBiomedicines · 2021Article
- Review
- The DNA-helicase HELLS drives ALKCell death & disease · 2021Article
- LSH mediates gene repression through macroH2A deposition.Nature communications · 2020Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
The activating E2F-transcription factors are best known for their dependence on the Retinoblastoma protein and their role in cellular proliferation. E2F3 is uniquely amplified in specific human tumours where its expression is inversely correlated with the survival of patients. Here, E2F3B interaction partners were identified by mass spectrometric analysis. We show that the SNF2-like helicase HELLS interacts with E2F3A in vivo and cooperates with its oncogenic functions. Depletion of HELLS severely perturbs the induction of E2F-target genes, hinders cell-cycle re-entry and growth. Using chromatin immmunoprecipitation coupled to sequencing, we identified genome-wide targets of HELLS and E2F3A/B. HELLS binds promoters of active genes, including the trithorax-related MLL1, and co-regulates E2F3-dependent genes. Strikingly, just as E2F3, HELLS is overexpressed in human tumours including prostate cancer, indicating that either factor may contribute to the malignant progression of tumours. Our work reveals that HELLS is important for E2F3 in tumour cell proliferation.
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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.