ArticleMolecular and cellular biology2000
Disruption of Myc-tubulin interaction by hyperphosphorylation of c-Myc during mitosis or by constitutive hyperphosphorylation of mutant c-Myc in Burkitt's lymphoma.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 49 citations in OpenAlex.
- Pan-cancer Myc modulator that targets Myc-α-tubulin interaction to drive selective mitotic catastrophe.Scientific reports · 2025Article
- Targeting the MYC interaction network in B-cell lymphoma via histone deacetylase 6 inhibition.Oncogene · 2022Article
- Bioinformatic analysis linking genomic defects to chemosensitivity and mechanism of action.PloS one · 2021Article
- Downregulated genes by silencingAging · 2020Article
- Identification of MYC as an antinecroptotic protein that stifles RIPK1-RIPK3 complex formation.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- The microtubule-associated histone methyltransferase SET8, facilitated by transcription factor LSF, methylates α-tubulin.The Journal of biological chemistry · 2020Article
- Disruption of Microtubules Post-Virus Entry Enhances Adeno-Associated Virus Vector Transduction.Human gene therapy · 2016Article
- A role for c-Myc in regulating anti-mycobacterial responses.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Post-translational control of Myc function during differentiation.Cell cycle (Georgetown, Tex.) · 2011Article
- Myc-nick: the force behind c-Myc.Science signaling · 2010Article
- Enhanced growth inhibition by combined DNA methylation/HDAC inhibitors in lung tumor cells with silenced CDKN2A.International journal of oncology · 2010Article
- Article
- Helicobacter pylori induces ERK-dependent formation of a phospho-c-Fos c-Jun activator protein-1 complex that causes apoptosis in macrophages.The Journal of biological chemistry · 2010Article
- Article
- A target selection of somatic hypermutations is regulated similarly between T and B cells upon activation-induced cytidine deaminase expression.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Review
- Article
- EBNA-LP associates with cellular proteins including DNA-PK and HA95.Journal of virology · 2001Article
- The Max network gone mad.Molecular and cellular biology · 2001Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Somatic mutations at Thr-58 of c-Myc have been detected in Burkitt's lymphoma (BL) tumors and have been shown to affect the transforming potential of the Myc oncoprotein. In addition, the N-terminal domain of c-Myc has been shown to interact with microtubules in vivo, and the binding of c-Myc to alpha-tubulin was localized to amino acids 48 to 135 within the c-Myc protein. We demonstrate that c-Myc proteins harboring a naturally occurring mutation at Thr-58 from BL cell lines have increased stability and are constitutively hyperphosphorylated, which disrupts the in vivo interaction of c-Myc with alpha-tubulin. In addition, we show that wild-type c-Myc-alpha-tubulin interactions are also disrupted during a transient mitosis-specific hyperphosphorylation of c-Myc, which resembles the constitutive hyperphosphorylation pattern of Thr-58 in BL cells.
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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.