ArticleMolecular and cellular biology2000
c-Myc proteolysis by the ubiquitin-proteasome pathway: stabilization of c-Myc in Burkitt's lymphoma cells.
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 243 papers.
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Who cites it
243 citing papers in PubMed.
- Spatial expression of myocardin protein in normal and disease states.American journal of physiology. Cell physiology · 2026Article
- A Protein Editing Method to Modify Proteins in Live Mammalian Cells.Current protocols · 2026Article
- Chemical Induction of MYC Protein Degradation via MYC-MAX Disruption and 20S Proteasome Activation.ACS chemical biology · 2026Article
- MYC serine 62 phosphorylation promotes its association with DNA double-strand breaks to facilitate repair and cell survival under genotoxic stress.Genes & development · 2026Article
- Article
- PLAAT2 suppresses gastric cancer progression by facilitating cMyc ubiquitination and inhibiting MEK/ERK signaling.Cell death & disease · 2026Article
- Proteasomal control of transcription factors: mechanisms, regulation and dysregulation.Cellular and molecular life sciences : CMLS · 2026Review
- The Yin-Yang balance of SIRT1 and SIRT2 in cancer metabolic remodeling.International journal of biological sciences · 2026Review
- c-Myc: an emerging participant in heart failure.Frontiers in cardiovascular medicine · 2026Review
- Degrons: defining the rules of protein degradation.Nature reviews. Molecular cell biology · 2025Review
- Pentagamavunone-1 targets excessive MYCN/NCYM expression mediated by mitotic arrest to suppress hepatocellular carcinoma proliferation.Cancer gene therapy · 2025Article
- MYC Point Mutations in Cancer: A Reboot and a Sequel.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Review
- ERH regulates type II interferon immune signaling through post-transcriptional regulation of JAK2 mRNA.Nucleic acids research · 2025Article
- A flexible, high-throughput system for studying live mRNA translation with HiBiT technology.Nucleic acids research · 2025Article
- MYC in cancer: from undruggable target to clinical trials.Nature reviews. Drug discovery · 2025Review
- Intracellular protein editing enables incorporation of noncanonical residues in endogenous proteins.Science (New York, N.Y.) · 2025Article
- TRIM52 maintains cellular fitness and is under tight proteolytic control by multiple giant E3 ligases.Nature communications · 2025Article
- Temporal myc dynamics permit mitotic bypass, promoting polyploid phenotypes.Cancer letters · 2025Review
- Enitociclib, a selective CDK9 inhibitor: in vitro and in vivo preclinical studies in multiple myeloma.Blood neoplasia · 2025Article
- Metabolic Signaling in the Tumor Microenvironment.Cancers · 2025Review
183 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors.
Funding
Abstract
The c-Myc oncoprotein is a transcription factor which is a critical regulator of cellular proliferation. Deregulated expression of c-Myc is associated with many human cancers, including Burkitt's lymphoma. The c-Myc protein is normally degraded very rapidly with a half-life of 20 to 30 min. Here we demonstrate that proteolysis of c-Myc in vivo is mediated by the ubiquitin-proteasome pathway. Inhibition of proteasome activity blocks c-Myc degradation, and c-Myc is a substrate for ubiquitination in vivo. Furthermore, an increase in c-Myc stability occurs in mitotic cells and is associated with inhibited c-Myc ubiquitination. Deletion analysis was used to identify regions of the c-Myc protein which are required for rapid proteolysis. We found that a centrally located PEST sequence, amino acids 226 to 270, is necessary for rapid c-Myc degradation, but not for ubiquitination. Also, N-terminal sequences, located within the first 158 amino acids of c-Myc, are necessary for both efficient c-Myc ubiquitination and subsequent degradation. We found that c-Myc is significantly stabilized (two- to sixfold) in many Burkitt's lymphoma-derived cell lines, suggesting that aberrant c-Myc proteolysis may play a role in the pathogenesis of Burkitt's lymphoma. Finally, mutation of Thr-58, a major phosphorylation site in c-Myc and a mutational hot spot in Burkitt's lymphoma, increases c-Myc stability; however, mutation of c-Myc is not essential for stabilization in Burkitt's lymphoma cells.
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Registered trials
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