ArticleMolecular and cellular biology1995
A link between increased transforming activity of lymphoma-derived MYC mutant alleles, their defective regulation by p107, and altered phosphorylation of the c-Myc transactivation domain.
Article in Molecular and cellular biology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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
52 citing papers in PubMed, 140 citations in OpenAlex.
- Single-cell gain-of-function mapping reveals latent regulatory programs governing CD8Research square · 2026Article
- Latent Regulatory Programs Generate Synthetic T Cell States with Enhanced Therapeutic Potential.bioRxiv : the preprint server for biology · 2026Article
- Missense Mutations in Myc Box I Influence Nucleocytoplasmic Transport to Promote Leukemogenesis.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
- MYC Modulation around the CDK2/p27/SKP2 Axis.Genes · 2017Review
- Epstein-Barr Virus: Diseases Linked to Infection and Transformation.Frontiers in microbiology · 2016Review
- FBXO32 Targets c-Myc for Proteasomal Degradation and Inhibits c-Myc Activity.The Journal of biological chemistry · 2015Article
- Sin3b interacts with Myc and decreases Myc levels.The Journal of biological chemistry · 2014Article
- Article
- Developments in Burkitt's lymphoma: novel cooperations in oncogenic MYC signaling.Cancer management and research · 2014Review
- Cyclin A1 is essential for setting the pluripotent state and reducing tumorigenicity of induced pluripotent stem cells.Stem cells and development · 2012Article
- CD19 is a major B cell receptor-independent activator of MYC-driven B-lymphomagenesis.The Journal of clinical investigation · 2012Article
- Myc proteins in brain tumor development and maintenance.Upsala journal of medical sciences · 2012Article
- Point mutations in c-Myc uncouple neoplastic transformation from multiple other phenotypes in rat fibroblasts.PloS one · 2010Article
- TRRAP and GCN5 are used by c-Myc to activate RNA polymerase III transcription.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Retinoblastoma gene family expression in lymphoid tissues.Oncogene · 2006Review
- Article
- Stimulation of Myc transactivation by the TATA binding protein in promoter-reporter assays.BMC biochemistry · 2005Article
- 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
- Viral mutations enhance the Max binding properties of the vMyc b-HLH-LZ domain.Nucleic acids research · 2005Article
- Diffuse large B-cell lymphoma: insights gained from gene expression profiling.International journal of hematology · 2003Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 2 countries.
Funding
Abstract
The c-Myc protein is a transcription factor with an N-terminal transcriptional regulatory domain and C-terminal oligomerization and DNA-binding motifs. Previous studies have demonstrated that p107, a protein related to the retinoblastoma protein, binds to the c-Myc transcriptional activation domain and suppresses its activity. We sought to characterize the transforming activity and transcriptional properties of lymphoma-derived mutant MYC alleles. Alleles encoding c-Myc proteins with missense mutations in the transcriptional regulatory domain were more potent than wild-type c-Myc in transforming rodent fibroblasts. Although the mutant c-Myc proteins retained their binding to p107 in in vitro and in vivo assays, p107 failed to suppress their transcriptional activation activities. Many of the lymphoma-derived MYC alleles contain missense mutations that result in substitution for the threonine at codon 58 or affect sequences flanking this amino acid. We observed that in vivo phosphorylation of Thr-58 was absent in a lymphoma cell line with a mutant MYC allele containing a missense mutation flanking codon 58. Our in vitro studies suggest that phosphorylation of Thr-58 in wild-type c-Myc was dependent on cyclin A and required prior phosphorylation of Ser-62 by a p107-cyclin A-CDK complex. In contrast, Thr-58 remained unphosphorylated in two representative mutant c-Myc transactivation domains in vitro. Our studies suggest that missense mutations in MYC may be selected for during lymphomagenesis, because the mutant MYC proteins have altered functional interactions with p107 protein complexes and fail to be phosphorylated at Thr-58.
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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.