ArticleOncogene2013
Dual regulation of Myc by Abl.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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
22 citing papers in PubMed, 29 citations in OpenAlex.
- Phosphosite-centric regulatory network of ATAD2 and its involvement in transcriptional networks.Molecular genetics and genomics : MGG · 2026Article
- Article
- The ABL-MYC axis controls WIPI1-enhanced autophagy in lifespan extension.Communications biology · 2023Article
- The acquisition order of leukemic drug resistance mutations is directed by the selective fitness associated with each resistance mechanism.Scientific reports · 2023Article
- Targeting mitochondrial respiration and the BCL2 family in high-grade MYC-associated B-cell lymphoma.Molecular oncology · 2022Article
- Bafetinib Suppresses the Transcription of PD-L1 Through c-Myc in LungFrontiers in pharmacology · 2022Article
- 8-Hydroxydaidzein Downregulates JAK/STAT, MMP, Oxidative Phosphorylation, and PI3K/AKT Pathways in K562 Cells.Biomedicines · 2021Article
- Metabolic convergence on lipogenesis in RAS, BCR-ABL, and MYC-driven lymphoid malignancies.Cancer & metabolism · 2021Article
- ABL1, Overexpressed in Hepatocellular Carcinomas, Regulates Expression of NOTCH1 and Promotes Development of Liver Tumors in Mice.Gastroenterology · 2020Article
- Pinning Down the Transcription: A Role for Peptidyl-ProlylFrontiers in cell and developmental biology · 2020Review
- PIN1 Provides Dynamic Control of MYC in Response to Extrinsic Signals.Frontiers in cell and developmental biology · 2020Article
- The impact of phosphatases on proliferative and survival signaling in cancer.Cellular and molecular life sciences : CMLS · 2018Review
- Aurora A Kinase Inhibitor AKI603 Induces Cellular Senescence in Chronic Myeloid Leukemia Cells Harboring T315I Mutation.Scientific reports · 2016Article
- Pin1 is required for sustained B cell proliferation upon oncogenic activation of Myc.Oncotarget · 2016Article
- Charting Immune Signaling Proteomes En Route to New Therapeutic Strategies.Cancer immunology research · 2015Review
- FBXO32 Targets c-Myc for Proteasomal Degradation and Inhibits c-Myc Activity.The Journal of biological chemistry · 2015Article
- Growth factor receptor/steroid receptor cross talk in trastuzumab-treated breast cancer.Oncogene · 2015Article
- MYC degradation.Cold Spring Harbor perspectives in medicine · 2014Review
- Regulation of transcription factor activity by interconnected post-translational modifications.Trends in pharmacological sciences · 2014Review
- Genomic quantitative real-time PCR proves residual disease positivity in more than 30% samples with negative mRNA-based qRT-PCR in Chronic Myeloid Leukemia.Oncoscience · 2014Article
Corrections and comments
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Authors and funding
16 authors at 7 institutions in 3 countries.
Funding
Abstract
The tyrosine kinase c-Abl (or Abl) and the prolyl-isomerase Pin1 cooperatively activate the transcription factor p73 by enhancing recruitment of the acetyltransferase p300. As the transcription factor c-Myc (or Myc) is a known target of Pin1 and p300, we hypothesized that it might be regulated in a similar manner. Consistent with this hypothesis, overexpression of Pin1 augmented the interaction of Myc with p300 and transcriptional activity. The action of Abl, however, was more complex than predicted. On one hand, Abl indirectly enhanced phosphorylation of Myc on Ser 62 and Thr 58, its association with Pin1 and p300 and its acetylation by p300. These effects of Abl were exerted through phosphorylation of substrate(s) other than Myc itself. On the other hand, Abl interacted with the C-terminal domain of Myc and phosphorylated up to five tyrosine residues in its N-terminus, the principal of which was Y74. Indirect immunofluorescence or immunohistochemical staining suggested that the Y74-phosphorylated form of Myc (Myc-pY74) localized to the cytoplasm and coexisted either with active Abl in a subset of mammary carcinomas or with Bcr-Abl in chronic myeloid leukemia. In all instances, Myc-pY74 constituted a minor fraction of the cellular Myc protein. Thus, our data unravel two potential effects of Abl on Myc: first, Abl signaling can indirectly augment acetylation of Myc by p300, and most likely also its transcriptional activity in the nucleus; second, Abl can directly phosphorylate Myc on tyrosine: the resulting form of Myc appears to be cytoplasmic, and its presence correlates with Abl activation in cancer.
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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.