ArticleCancer research2011
Phosphorylation regulates c-Myc's oncogenic activity in the mammary gland.
Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 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.
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Who cites it
126 citing papers in PubMed, 165 citations in OpenAlex.
- A Multistep Immune-Competent Genetically Engineered Mouse Model Reveals Phenotypic Plasticity in Uveal Melanoma.Cancer research · 2026Article
- Targeting mitochondrial α-ketoglutarate sequestration disables dual oncogenic drivers and metabolic adaptability in pancreatic ductal adenocarcinoma.Cell death & disease · 2026Article
- WEE1 stabilizes MYC to promote therapeutic resistance in esophageal adenocarcinoma.Cancer letters · 2026Article
- MYC-driven gliosis impairs neuron-glia communication in amyotrophic lateral sclerosis.Brain : a journal of neurology · 2026Article
- The protein phosphatase 2A-B56α complex regulates N-Myc degradation in neuroblastoma.The Journal of biological chemistry · 2026Article
- Methionine metabolism and the NOP2 methyltransferase are essential for MYC-Driven liver tumorigenesis.bioRxiv : the preprint server for biology · 2026Article
- G-protein-coupled receptor ADGRG1 drives a protective microglial state in Alzheimer's disease through MYC activation.Neuron · 2025Article
- Ubiquitination of transcription factors in cancer: unveiling therapeutic potential.Molecular oncology · 2025Review
- A flexible, high-throughput system for studying live mRNA translation with HiBiT technology.Nucleic acids research · 2025Article
- Discovery of a Pyrazolopyridinone-Based MYC Inhibitor That Selectively Engages Intracellular c-MYC and Disrupts MYC-MAX Heterodimerization.Journal of medicinal chemistry · 2025Article
- Tuft cells transdifferentiate to neural-like progenitor cells in the progression of pancreatic cancer.Developmental cell · 2025Article
- Roles of Post-Translational Modifications of Transcription Factors Involved in Breast Cancer Hypoxia.Molecules (Basel, Switzerland) · 2025Review
- CRL2Oncogene · 2024Article
- A germline point mutation in the MYC-FBW7 phosphodegron initiates hematopoietic malignancies.Genes & development · 2024Article
- Single-cell mapping identifies MSICancer cell · 2023Article
- MYC Deregulation and PTEN Loss Model Tumor and Stromal Heterogeneity of Aggressive Triple-Negative Breast Cancer.Nature communications · 2023Article
- Unraveling MYC's Role in Orchestrating Tumor Intrinsic and Tumor Microenvironment Interactions Driving Tumorigenesis and Drug Resistance.Pathophysiology : the official journal of the International Society for Pathophysiology · 2023Review
- Calcineurin-mediated dephosphorylation enhances the stability and transactivation of c-Myc.Scientific reports · 2023Article
- MYC regulates CSF1 expression via microRNA 17/20a to modulate tumor-associated macrophages in osteosarcoma.JCI insight · 2023Article
- MNT suppresses T cell apoptosis via BIM and is critical for T lymphomagenesis.Cell death and differentiation · 2023Article
66 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
Abstract
Expression of the c-Myc oncoprotein is affected by conserved threonine 58 (T58) and serine 62 (S62) phosphorylation sites that help to regulate c-Myc protein stability, and altered ratios of T58 and S62 phosphorylation have been observed in human cancer. Here, we report the development of 3 unique c-myc knock-in mice that conditionally express either c-Myc(WT) or the c-Myc(T58A) or c-Myc(S62A) phosphorylation mutant from the constitutively active ROSA26 locus in response to Cre recombinase to study the role of these phosphorylation sites in vivo. Using a mammary-specific Cre model, we found that expression of c-Myc(WT) resulted in increased mammary gland density, but normal morphology and no tumors at the level expressed from the ROSA promoter. In contrast, c-Myc(T58A) expression yielded enhanced mammary gland density, hyperplastic foci, cellular dysplasia, and mammary carcinoma, associated with increased genomic instability and suppressed apoptosis relative to c-Myc(WT). Alternatively, c-Myc(S62A) expression reduced mammary gland density relative to control glands, and this was associated with increased genomic instability and normal apoptotic function. Our results indicate that specific activities of c-Myc are differentially affected by T58 and S62 phosphorylation. This model provides a robust platform to interrogate the role that these phosphorylation sites play in c-Myc function during development and tumorigenesis.
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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.