ArticleCell2010
Myc-nick: a cytoplasmic cleavage product of Myc that promotes alpha-tubulin acetylation and cell differentiation.
Article in Cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 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
130 citing papers in PubMed, 219 citations in OpenAlex.
- ARNT2 repression disrupts neuronal identity and promotes glioblastoma growth.Cell communication and signaling : CCS · 2026Article
- c-Myc transactivates CFL1 to induce senescence-like phenotype and potentiate the bystander effects for the migration and proliferation in lung cancer cells.Cell death discovery · 2026Article
- Enforced MYC expression directs a distinct transcriptional state during plasma cell differentiation.Life science alliance · 2025Article
- Impaired myogenesis in limb girdle muscular dystrophy type 2B.Scientific reports · 2025Article
- Muscle fiber Myc is dispensable for muscle growth and its forced expression severely perturbs homeostasis.Nature communications · 2025Article
- Microtubule regulation in cancer cells.Frontiers in cell and developmental biology · 2025Article
- Tubulin Acetylation: A Critical Regulator of Microtubule Function.Results and problems in cell differentiation · 2025Review
- Histone deacetylase 6 inhibition promotes microtubule acetylation and facilitates autophagosome-lysosome fusion in dystrophin-deficient mdx mice.Acta physiologica (Oxford, England) · 2025Article
- Mouse and human embryonic genome activation initiate at the one-cell stage.Frontiers in cell and developmental biology · 2025Article
- c-Myc and FOXO3a-The Everlasting Decision Between Neural Regeneration and Degeneration.International journal of molecular sciences · 2024Review
- Mycb and Mych stimulate Müller glial cell reprogramming and proliferation in the uninjured and injured zebrafish retina.Development (Cambridge, England) · 2024Article
- Acetylation of c-Myc at Lysine 148 Protects Neurons After Ischemia.Neuromolecular medicine · 2024Article
- The neuronal transcription factor MEIS2 is a calpain-2 protease target.Journal of cell science · 2024Article
- ATAC and SAGA co-activator complexes utilize co-translational assembly, but their cellular localization properties and functions are distinct.Cell reports · 2023Article
- ATAC and SAGA coactivator complexes utilize co-translational assembly, but their cellular localization properties and functions are distinct.bioRxiv : the preprint server for biology · 2023Article
- Review
- Demystifying the Druggability of the MYC Family of Oncogenes.Journal of the American Chemical Society · 2023Review
- Effect of 3D Spheroid Culturing on NF-κB Signaling Pathway and Neurogenic Potential in Human Amniotic Fluid Stem Cells.International journal of molecular sciences · 2023Article
- Integrative single-cell RNA-seq and ATAC-seq analysis of myogenic differentiation in pig.BMC biology · 2023Article
- MYC function and regulation in physiological perspective.Frontiers in cell and developmental biology · 2023Review
70 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
3 authors at 1 institution in 1 country.
Funding
Abstract
The Myc oncoprotein family comprises transcription factors that control multiple cellular functions and are widely involved in oncogenesis. Here we report the identification of Myc-nick, a cytoplasmic form of Myc generated by calpain-dependent proteolysis at lysine 298 of full-length Myc. Myc-nick retains conserved Myc box regions but lacks nuclear localization signals and the bHLHZ domain essential for heterodimerization with Max and DNA binding. Myc-nick induces alpha-tubulin acetylation and altered cell morphology by recruiting histone acetyltransferase GCN5 to microtubules. During muscle differentiation, while the levels of full-length Myc diminish, Myc-nick and acetylated alpha-tubulin levels are increased. Ectopic expression of Myc-nick accelerates myoblast fusion, triggers the expression of myogenic markers, and permits Myc-deficient fibroblasts to transdifferentiate in response to MyoD. We propose that the cleavage of Myc by calpain abrogates the transcriptional inhibition of differentiation by full-length Myc and generates Myc-nick, a driver of cytoplasmic reorganization and differentiation.
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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.