ArticleOncogene1999
Bin1 functionally interacts with Myc and inhibits cell proliferation via multiple mechanisms.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
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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.
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
60 citing papers in PubMed, 119 citations in OpenAlex.
- Bridging autophagy and endolysosomal dysfunction: Role of bridging integrator 1 in Alzheimer's disease.Neural regeneration research · 2026Article
- Bend it like BIN1: how a membrane-curving adaptor protein shapes cardiac physiology.American journal of physiology. Heart and circulatory physiology · 2025Review
- BIN1 inhibited tumor growth, metastasis and stemness by ALDH1/NOTCH pathway in bladder carcinoma.Hereditas · 2025Article
- Rapid flow-based synthesis of post-translationally modified peptides and proteins: a case study on MYC's transactivation domain.Chemical science · 2024Article
- Repression of developmental transcription factor networks triggers aging-associated gene expression in human glial progenitor cells.Nature communications · 2024Article
- The nexus of long noncoding RNAs, splicing factors, alternative splicing and their modulations.RNA biology · 2024Review
- BIN1 in cancer: biomarker and therapeutic target.Journal of cancer research and clinical oncology · 2023Review
- High Indoleamine 2,3-Dioxygenase Expression along with Low Bridging Integrator-1 Expression in Hepatocellular Carcinoma Patients.Asian Pacific journal of cancer prevention : APJCP · 2023Article
- A comprehensive single cell data analysis of lymphoblastoid cells reveals the role of super-enhancers in maintaining EBV latency.Journal of medical virology · 2023Article
- New Synthetic Lethality Re-Sensitizing Platinum-Refractory Cancer Cells to Cisplatin In Vitro: The Rationale to Co-Use PARP and ATM Inhibitors.International journal of molecular sciences · 2021Article
- The Mechanistic Role of Bridging Integrator 1 (BIN1) in Alzheimer's Disease.Cellular and molecular neurobiology · 2021Review
- MYC: a multipurpose oncogene with prognostic and therapeutic implications in blood malignancies.Journal of hematology & oncology · 2021Review
- A Proteomic Study for the Discovery of Beef Tenderness Biomarkers and Prediction of Warner-Bratzler Shear Force Measured onFoods (Basel, Switzerland) · 2021Article
- Transcriptomic and proteomic analysis of Hemidactylus frenatus during initial stages of tail regeneration.Scientific reports · 2021Article
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- The CARM1-p300-c-Myc-Max (CPCM) transcriptional complex regulates the expression ofInternational journal of biological sciences · 2020Article
- The splicing factor RBM25 controls MYC activity in acute myeloid leukemia.Nature communications · 2019Article
- CDK5 neutralizes the tumor suppressing effect of BIN1 via mediating phosphorylation of c-MYC at Ser-62 site in NSCLC.Cancer cell international · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumor suppressor Bin1 was identified through its interaction with the N-terminal region of Myc which harbors its transcriptional activation domain. Here we show that Bin1 and Myc physically and functionally associate in cells and that Bin1 inhibits cell proliferation through both Myc-dependent and Myc-independent mechanisms. Bin1 specifically inhibited transactivation by Myc as assayed from artificial promoters or from the Myc target genes ornithine decarboxylase (ODC) and alpha prothymosin (pT). Inhibition of ODC but not pT required the presence of the Myc binding domain (MBD) of Bin1 suggesting two mechanisms of action. Consistent with this possibility, a non-MBD region of Bin1 was sufficient to recruit a repression function to DNA that was unrelated to histone deacetylase. Regions outside the MBD required for growth inhibition were mapped in Ras cotransformation or HepG2 hepatoma cell growth assays. Bin1 required the N-terminal BAR domain to suppress focus formation by Myc whereas the C-terminal U1 and SH3 domains were required to inhibit adenovirus E1A or mutant p53, respectively. All three domains contributed to Bin1 suppression of tumor cell growth but BAR-C was most crucial. These findings supported functional interaction between Myc and Bin1 in cells and indicated that Bin1 could inhibit malignant cell growth through multiple mechanisms.
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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.