ArticleThe Journal of biological chemistry2014
Sin3b interacts with Myc and decreases Myc levels.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed.
- Targeting MYC-Driven Cancers: From Oncogenic Addiction to Therapeutic Vulnerability.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026Review
- Targeting MYC at the intersection between cancer metabolism and oncoimmunology.Frontiers in immunology · 2024Review
- MYC acetylated lysine residues drive oncogenic cell transformation and regulate select genetic programs for cell adhesion-independent growth and survival.Genes & development · 2023Article
- Chromatin-Associated SIN3B Protects Cancer Cells from Genotoxic Stress-Induced Apoptosis and Dictates DNA Damage Repair Pathway Choice.Molecular cancer research : MCR · 2023Article
- MYC function and regulation in physiological perspective.Frontiers in cell and developmental biology · 2023Review
- Article
- Targeting Myc Interacting Proteins as a Winding Path in Cancer Therapy.Frontiers in pharmacology · 2021Review
- Role for carbohydrate response element-binding protein (ChREBP) in high glucose-mediated repression of long noncoding RNA Tug1.The Journal of biological chemistry · 2020Article
- The transcription factors aryl hydrocarbon receptor and MYC cooperate in the regulation of cellular metabolism.The Journal of biological chemistry · 2020Article
- The MNT transcription factor autoregulates its expression and supports proliferation in MYC-associated factor X (MAX)-deficient cells.The Journal of biological chemistry · 2020Article
- SIN3B promotes integrin αV subunit gene transcription and cell migration of hepatocellular carcinoma.Journal of molecular cell biology · 2019Article
- Review
- Therapeutic Inhibition of Myc in Cancer. Structural Bases and Computer-Aided Drug Discovery Approaches.International journal of molecular sciences · 2018Review
- The aryl hydrocarbon receptor regulates nucleolar activity and protein synthesis in MYC-expressing cells.Genes & development · 2018Article
- The potential of targeting Sin3B and its associated complexes for cancer therapy.Expert opinion on therapeutic targets · 2017Review
- Zebrafish sin3b mutants are viable but have size, skeletal, and locomotor defects.Developmental dynamics : an official publication of the American Association of Anatomists · 2017Article
- MYC Modulation around the CDK2/p27/SKP2 Axis.Genes · 2017Review
- Multiple Roles of MYC in Integrating Regulatory Networks of Pluripotent Stem Cells.Frontiers in cell and developmental biology · 2017Review
- Article
- ChromNet: Learning the human chromatin network from all ENCODE ChIP-seq data.Genome biology · 2016Article
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myc expression is deregulated in many human cancers. A yeast two-hybrid screen has revealed that the transcriptional repressor Sin3b interacts with Myc protein. Endogenous Myc and Sin3b co-localize and interact in the nuclei of human and rat cells, as assessed by co-immunoprecipitation, immunofluorescence, and proximity ligation assay. The interaction is Max-independent. A conserved Myc region (amino acids 186-203) is required for the interaction with Sin3 proteins. Histone deacetylase 1 is recruited to Myc-Sin3b complexes, and its deacetylase activity is required for the effects of Sin3b on Myc. Myc and Sin3a/b co-occupied many sites on the chromatin of human leukemia cells, although the presence of Sin3 was not associated with gene down-regulation. In leukemia cells and fibroblasts, Sin3b silencing led to Myc up-regulation, whereas Sin3b overexpression induced Myc deacetylation and degradation. An analysis of Sin3b expression in breast tumors revealed an association between low Sin3b expression and disease progression. The data suggest that Sin3b decreases Myc protein levels upon Myc deacetylation. As Sin3b is also required for transcriptional repression by Mxd-Max complexes, our results suggest that, at least in some cell types, Sin3b limits Myc activity through two complementary activities: Mxd-dependent gene repression and reduction of Myc levels.
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.