ReviewOncogene1999
New Myc-interacting proteins: a second Myc network emerges.
Review in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 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
71 citing papers in PubMed, 1 synthesis or guideline pooled it, 179 citations in OpenAlex.
- MicroRNAs role in telomere length maintenance and telomerase activity in tumor cells.Journal of molecular medicine (Berlin, Germany) · 2024Pooled it
- Review
- 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
- The Mechanistic Role of Bridging Integrator 1 (BIN1) in Alzheimer's Disease.Cellular and molecular neurobiology · 2021Review
- The Long Noncoding RNA LINC00665 Facilitates c-Myc Transcriptional ActivityFrontiers in oncology · 2021Article
- The therapeutic potential of exosomal miR-22 for cervical cancer radiotherapy.Cancer biology & therapy · 2020Article
- MicroRNA-22 enhances radiosensitivity in cervical cancer cell lines via direct inhibition of c-Myc binding protein, and the subsequent reduction in hTERT expression.Oncology letters · 2020Article
- CAMKV Is a Candidate Immunotherapeutic Target inFrontiers in oncology · 2020Article
- The functions and mechanisms of prefoldin complex and prefoldin-subunits.Cell & bioscience · 2020Review
- Emerging Roles of C-Myc in Cancer Stem Cell-Related Signaling and Resistance to Cancer Chemotherapy: A Potential Therapeutic Target Against Colorectal Cancer.International journal of molecular sciences · 2019Review
- Overexpression of MYC binding protein promotes invasion and migration in gastric cancer.Oncology letters · 2018Article
- Article
- Direct HPV E6/Myc interactions induce histone modifications, Pol II phosphorylation, and hTERT promoter activation.Oncotarget · 2017Article
- Review
- Transactivation Domain of Human c-Myc Is Essential to Alleviate Poly(Q)-Mediated Neurotoxicity in Drosophila Disease Models.Journal of molecular neuroscience : MN · 2017Article
- Therapeutic Interventions of Cancers Using Intrinsically Disordered Proteins as Drug Targets: c-Myc as Model System.Cancer informatics · 2017Review
- p63α modulates c-Myc activity via direct interaction and regulation of MM1 protein stability.Oncotarget · 2016Article
- Developments in Burkitt's lymphoma: novel cooperations in oncogenic MYC signaling.Cancer management and research · 2014Review
- Small molecules targeting c-Myc oncogene: promising anti-cancer therapeutics.International journal of biological sciences · 2014Review
- STK38 is a critical upstream regulator of MYC's oncogenic activity in human B-cell lymphoma.Oncogene · 2013Article
11 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
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite its intensive investigation for almost two decades, c-Myc remains a fascinating and enigmatic subject. A large and compelling body of evidence indicates that c-Myc is a transcription factor with central roles in the regulation of cell proliferation, differentiation, and apoptosis, but its exact function has remained elusive. In this review we survey recent advances in the identification and analysis of c-Myc-binding proteins, which suggest insights into the transcriptional roles of c-Myc but which also extend the existing functional paradigms. The C-terminal domain (CTD) of c-Myc mediates interaction with Max and physiological recognition of DNA target sequences, events needed for all biological actions. Recently described interactions between the CTD and other cellular proteins, including YY-1, AP-2, BRCA-1, TFII-I, and Miz-1, suggest levels of regulatory complexity beyond Max in controlling DNA recognition by c-Myc. The N-terminal domain (NTD), which includes the evolutionarily conserved and functionally crucial Myc Box sequences (MB1 and MB2), contains the transcription activation domain (TAD) of c-Myc as well as regions required for transcriptional repression, cell cycle regulation, transformation, and apoptosis. In addition to interaction with the retinoblastoma family protein p107, the NTD has been shown to interact with alpha-tubulin and the novel adaptor proteins Binl, MM-1, Pam, TRRAP, and AMY-1. The structure of these proteins and their effects on c-Myc actions suggest links to the transcriptional regulatory machinery as well as to cell cycle regulation, chromatin modeling, and apoptosis. Investigations of this emerging NTD-based network may reveal how c-Myc is regulated and how it affects cell fate, as well as providing tools to distinguish the physiological roles of various Myc target genes.
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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.