ArticleMolecular and cellular biology1989
Posttranscriptional regulation of cellular gene expression by the c-myc oncogene.
Article in Molecular and cellular biology, 1989. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 106 citations in OpenAlex.
- MYC and the art of microRNA maintenance.Cold Spring Harbor perspectives in medicine · 2014Review
- Occupancy classification of position weight matrix-inferred transcription factor binding sites.PloS one · 2011Article
- Influence of immune privilege on ocular tumor development.Ocular immunology and inflammation · 2010Review
- Immunotherapeutic suppression of indoleamine 2,3-dioxygenase and tumor growth with ethyl pyruvate.Cancer research · 2010Article
- Distinct patterns of hypoxic expression of carbonic anhydrase IX (CA IX) in human malignant glioma cell lines.Journal of neuro-oncology · 2007Article
- Transformation-selective apoptotic program triggered by farnesyltransferase inhibitors requires Bin1.Oncogene · 2003Article
- mRNA instability in the nucleus due to a novel open reading frame element is a major determinant of the narrow tissue specificity of folate receptor alpha.Molecular and cellular biology · 2003Article
- The c-Myc-interacting adaptor protein Bin1 activates a caspase-independent cell death program.Oncogene · 2000Article
- Antisense delivery using protamine-oligonucleotide particles.Nucleic acids research · 2000Article
- Mechanism for elimination of a tumor suppressor: aberrant splicing of a brain-specific exon causes loss of function of Bin1 in melanoma.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
- New Myc-interacting proteins: a second Myc network emerges.Oncogene · 1999Review
- Cell growth inhibition by farnesyltransferase inhibitors is mediated by gain of geranylgeranylated RhoB.Molecular and cellular biology · 1999Article
- Is plasminogen activator inhibitor-1 the molecular switch that governs urokinase receptor-mediated cell adhesion and release?The Journal of cell biology · 1996Article
- Myc-Max heterodimers activate a DEAD box gene and interact with multiple E box-related sites in vivo.The EMBO journal · 1996Article
- Two distinct phases of apoptosis in mammary gland involution: proteinase-independent and -dependent pathways.Development (Cambridge, England) · 1996Article
- Nuclear proto-oncogene products transactivate the human papillomavirus type 16 promoter.British journal of cancer · 1995Article
- Effects of c-myc expression on cell cycle progression.Molecular and cellular biology · 1994Article
- Increased expression of eukaryotic translation initiation factors eIF-4E and eIF-2 alpha in response to growth induction by c-myc.Proceedings of the National Academy of Sciences of the United States of America · 1993Article
- B-myc inhibits neoplastic transformation and transcriptional activation by c-myc.Molecular and cellular biology · 1993Article
- Coordinated expression of extracellular matrix-degrading proteinases and their inhibitors regulates mammary epithelial function during involution.The Journal of cell biology · 1992Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The c-myc oncogene has been implicated in the development of many different cancers, yet the mechanism by which the c-myc protein alters cellular growth control has proven elusive. We used a cDNA hybridization difference assay to isolate two genes, mr1 and mr2, that were constitutively expressed (i.e., deregulated) in rodent fibroblast cell lines immortalized by transfection of a viral promoter-linked c-myc gene. Both cDNAs were serum inducible in quiescent G0 fibroblasts, suggesting that they are functionally related to cellular proliferative processes. Although there were significant differences in cytoplasmic mRNA levels between myc-immortalized and control cells, the rates of transcription and mRNA turnover of both genes were similar, suggesting that c-myc regulates mr1 and mr2 expression by some nuclear posttranscriptional mechanism. mr1 was also rapidly (within 2 h) and specifically induced by dexamethasone in BALB/c cell lines expressing a mouse mammary tumor virus long terminal repeat-driven myc gene, under conditions where other growth factor-inducible genes were unaffected. A frameshift mutation in the mouse mammary tumor virus myc gene destroyed the dexamethasone stimulation of mr1, indicating that c-myc protein is required for the effect. As in the myc-immortalized cells, the induction of mr1 by c-myc occurred without detectable changes in mr1 transcription or cytoplasmic mRNA stability, implicating regulation, either direct or indirect, through a nuclear posttranscriptional mechanism. These results provide evidence that c-myc can rapidly modulate cellular gene expression and suggest that c-myc may function in gene regulation at the level of RNA export, splicing, or nuclear RNA turnover.
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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.