ArticleNature communications2016
BPTF is required for c-MYC transcriptional activity and in vivo tumorigenesis.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 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
88 citing papers in PubMed, 1 synthesis or guideline pooled it, 180 citations in OpenAlex.
- Shared neuroimaging and molecular profiles in type 2 diabetes mellitus and major depressive disorder: an integrative analysis of genetic, transcriptomic, and neuroimaging data.Translational psychiatry · 2025Pooled it
- Developmental and MAPK-responsive transcription factors regulate distinct malignant cell states and associated genetic dependencies in pancreatic cancer.Nature genetics · 2026Article
- BPTF is essential for vaccine-induced germinal center B cell responses.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Prostate Cancer: Dissecting Novel Immunosuppressive Mechanisms Through Context-Specific Transcriptomic Programs and MDSC Cells.International journal of molecular sciences · 2026Article
- MYC as a key target for melanoma therapy.Frontiers in cell and developmental biology · 2026Review
- Nucleolus as a cornerstone linking proliferation and metabolism to cellular responses to stress: involvement of transcription factors MYC and p53.Frontiers in molecular biosciences · 2026Review
- BPTF regulates androgen receptor activity by enhancing chromatin accessibility and stabilizing the AR-FOXA1 interaction.Nature communications · 2025Article
- Genomic characterization of host gene alterations in Theileria annulata-transformed leukocytes.Communications biology · 2025Article
- BPTF-665aa mediate chromatin remodeling drives chemoresistance in T-LBL/ALL.Journal of experimental & clinical cancer research : CR · 2025Article
- HypoxamiRs in pancreatic cancer: master regulators of the hypoxic tumor microenvironment.Cell biology and toxicology · 2025Review
- Loss of BPTF restores estrogen response and suppresses metastasis of mammary tumors.Nature communications · 2025Article
- The Role of Non-Coding RNAs in MYC-Mediated Metabolic Regulation: Feedback Loops and Interactions.Non-coding RNA · 2025Review
- BPTF promotes glioma development through USP34-mediated de-ubiquitination of FOXC1.Histology and histopathology · 2025Article
- TGF-β signaling-related signature for predicting prognosis and therapeutic response in lower-grade glioma.Translational cancer research · 2024Article
- CRISPR-based dissection of microRNA-23a ~ 27a ~ 24-2 cluster functionality in hepatocellular carcinoma.Oncogene · 2024Article
- Bromodomain inhibition targeting BPTF in the treatment of melanoma and other solid tumors.Clinical & experimental metastasis · 2024Review
- NUP98-BPTF promotes oncogenic transformation through PIM1 upregulation.Cancer medicine · 2024Article
- Monkey multi-organ cell atlas exposed to estrogen.Life medicine · 2024Article
- Targeting MYC at the intersection between cancer metabolism and oncoimmunology.Frontiers in immunology · 2024Review
- An alternative NURF complex sustains acute myeloid leukemia by regulating the accessibility of insulator regions.The EMBO journal · 2023Article
28 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
c-MYC oncogene is deregulated in most human tumours. Histone marks associated with transcriptionally active genes define high-affinity c-MYC targets. The mechanisms involved in their recognition by c-MYC are unknown. Here we report that c-MYC interacts with BPTF, a core subunit of the NURF chromatin-remodelling complex. BPTF is required for the activation of the full c-MYC transcriptional programme in fibroblasts. BPTF knockdown leads to decreased c-MYC recruitment to DNA and changes in chromatin accessibility. In Bptf-null MEFs, BPTF is necessary for c-MYC-driven proliferation, G1-S progression and replication stress, but not for c-MYC-driven apoptosis. Bioinformatics analyses unveil that BPTF levels correlate positively with c-MYC-driven transcriptional signatures. In vivo, Bptf inactivation in pre-neoplastic pancreatic acinar cells significantly delays tumour development and extends survival. Our findings uncover BPTF as a crucial c-MYC co-factor required for its biological activity and suggest that the BPTF-c-MYC axis is a potential therapeutic target in cancer.
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.