Recessive genetic deregulation abrogates c-myc suppression by interferon and is implicated in oncogenesis
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Summary
It was concluded that changes in the cis-acting sequences of c-myc were not involved in this type of relaxed regulation and that resistance resulted rather from inactivation or loss of postreceptor elements which operate in trans.
- Type
- article
- Published
- 1988-07-01
- Cited by
- 23
- References
- 43
- OpenAlex
- https://openalex.org/W3043196
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:25795414
Keywords
Medicine, Long QT syndrome, QT interval, Cardiology, Internal medicine
References
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- A reproducible microanalytical method for the detection of specific RNA sequences by dot-blot hybridization.
- Spontaneous mammary adenocarcinomas in transgenic mice that carry and express MTV/myc fusion genes.
- Chromatin structure around the c-myc gene in Burkitt lymphomas with upstream and downstream translocation points.
- A block to elongation is largely responsible for decreased transcription of c-myc in differentiated HL60 cells
- Post-transcriptional control of myc and p53 expression during differentiation of the embryonal carcinoma cell line F9
- Autocrine beta-related interferon controls c-myc suppression and growth arrest during hematopoietic cell differentiation.
- Effect of somatic mutation within translocated c-myc genes in Burkitt's lymphoma
- Expression of c-myc changes during differentiation of mouse erythroleukaemia cells
- Cellular oncogenes and multistep carcinogenesis.
- Increased rate of degradation of c-myc mRNA in interferon-treated Daudi cells.
- Differential expression of the translocated and the untranslocated c-myc oncogene in Burkitt lymphoma.
- Translocations among antibody genes in human cancer.
- Interferon regulates c-myc gene expression in Daudi cells at the post-transcriptional level.
Cited by
- Apoptosis induced by cancer chemotherapeutic drugs and its genetic suppression
- Antitumor activity of IFIX, a novel interferon-inducible HIN-200 gene, in breast cancer
- An in vitro model for cytogenetic conversion in CML. Interferon-alpha preferentially inhibits the outgrowth of malignant stem cells preserved in long-term culture.
- Cell cycle regulation of the double stranded RNA activated protein kinase, PKR
- Stress induced experimental colitis
- The interferon‐inducible gene, Ifi204, acquires malignant transformation capability upon mutation at the Rb‐binding sites
- Induction of protein-tyrosine-phosphatase activity by interleukin 6 in M1 myeloblastic cells and analysis of possible counteractions by the BCR-ABL oncogene.
- The polyoma virus T antigen interferes with interferon-inducible gene expression.
- Molecular mechanisms underlying interferon-α-induced G0/G1 arrest: CKI-mediated regulation of G1 Cdk-complexes and activation of pocket proteins
- Minimal extent of homology required for completion of meiotic recombination in Saccharomyces cerevisiae.
- Cytokine triggered molecular pathways that control cell cycle arrest
- Interleukin 6 induces DNA binding activity of AP1 in M1 myeloblastic cells but not in a growth resistant cell derivative.
- BALB/c-3T3 fibroblasts resistant to growth inhibition by beta interferon exhibit aberrant platelet-derived growth factor, epidermal growth factor, and fibroblast growth factor signal transduction
- Alpha interferon suppresses the cyclin D3 and cdc25A genes, leading to a reversible G0-like arrest
- Deregulated c-myc expression abrogates the interferon- and interleukin 6-mediated G0/G1 cell cycle arrest but not other inhibitory responses in M1 myeloblastic cells.
- Interferons and interleukin-6 suppress the DNA-binding activity of E2F in growth-sensitive hematopoietic cells
- Studies on a novel poly(ADP-ribosyl)ation polymerase PARP-10 and its functional interaction with c-Myc
- Perspectives in CancerResearch Oncogenes, Antioncogenes, and the Molecular Bases of Multistep Carcinogenesis1
- Perspectivesin CancerResearch Oncogenes , Antioncogenes , and the Molecular Bases of Multistep Carcinogenesis 1
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