ArticleOncotarget2014
In vivo quantification and perturbation of Myc-Max interactions and the impact on oncogenic potential.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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
19 citing papers in PubMed, 29 citations in OpenAlex.
- IL-15 Priming Alters IFN-γ Regulation in Murine NK Cells.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Strategies to target the cancer driver MYC in tumor cells.Frontiers in oncology · 2023Review
- MYCMI-7: A Small MYC-Binding Compound that Inhibits MYC: MAX Interaction and Tumor Growth in a MYC-Dependent Manner.Cancer research communications · 2022Article
- Targeted degradation of transcription factors by TRAFTACs: TRAnscription Factor TArgeting Chimeras.Cell chemical biology · 2021Article
- Taking the Myc out of cancer: toward therapeutic strategies to directly inhibit c-Myc.Molecular cancer · 2021Review
- MYC Analysis in Cancer and Evolution.Methods in molecular biology (Clifton, N.J.) · 2021Article
- The Diarylheptanoid Curcumin Induces MYC Inhibition and Cross-Links This Oncoprotein to the Coactivator TRRAP.Frontiers in oncology · 2021Article
- The brain acid-soluble protein 1 (BASP1) interferes with the oncogenic capacity of MYC and its binding to calmodulin.Molecular oncology · 2020Article
- Modulation of Disordered Proteins with a Focus on Neurodegenerative Diseases and Other Pathologies.International journal of molecular sciences · 2019Review
- A selective high affinity MYC-binding compound inhibits MYC:MAX interaction and MYC-dependent tumor cell proliferation.Scientific reports · 2018Article
- Interleukin-1Journal of the American Society of Nephrology : JASN · 2018Article
- Calcium-dependent binding of Myc to calmodulin.Oncotarget · 2017Article
- ChIP-on-chip analysis of thyroid hormone-regulated genes and their physiological significance.Oncotarget · 2016Article
- OncoBinder facilitates interpretation of proteomic interaction data by capturing coactivation pairs in cancer.Oncotarget · 2016Article
- The Quest for Targets Executing MYC-Dependent Cell Transformation.Frontiers in oncology · 2016Review
- Article
- Stopping MYC in its tracks.Aging · 2015Article
- In-vivo detection of binary PKA network interactions upon activation of endogenous GPCRs.Scientific reports · 2015Article
- MYC and RAF: Key Effectors in Cellular Signaling and Major Drivers in Human Cancer.Current topics in microbiology and immunologyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
The oncogenic bHLH-LZ transcription factor Myc forms binary complexes with its binding partner Max. These and other bHLH-LZ-based protein-protein interactions (PPI) in the Myc-Max network are essential for the physiological and oncogenic activities of Myc. We have generated a genetically determined and highly specific protein-fragment complementation assay based on Renilla luciferase to analyze the dynamic interplay of bHLH-LZ transcription factors Myc, Max, and Mxd1 in vivo. We also applied this PPI reporter to quantify alterations of nuclear Myc-Max complexes in response to mutational events, competitive binding by the transcriptional repressor Mxd1, or perturbations by small-molecule Myc inhibitors, including recently identified potent PPI inhibitors from a Kröhnke pyridine library. We show that the specificity of Myc-Max PPI reduction by the pyridine inhibitors directly correlates with their efficient and highly specific potential to interfere with the proliferation of human and avian tumor cells displaying deregulated Myc expression. In a direct comparison with known Myc inhibitors using human and avian cell systems, the pyridine compounds reveal a unique inhibitory potential even at sub-micromolar concentrations combined with remarkable specificity for the inhibition of Myc-driven tumor cell proliferation. Furthermore, we show in direct comparisons using defined avian cell systems that different Max PPI profiles for the variant members of the Myc protein family (c-Myc, v-Myc, N-Myc, L-Myc) correlate with their diverse oncogenic potential and their variable sensitivity to the novel pyridine inhibitors.
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.