The v-myc oncogene

Lee, Clement; Reddy, E. Premkumar

doi:10.1038/sj.onc.1202786

Cited by 44 publications

(32 citation statements)

References 59 publications

(48 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…MYC is the viral homolog of c-myc transduced by several acute transforming retroviruses (Lee and Reddy 1999). MYC expression is driven by the retroviral long terminal repeat in case of retroviral transduction (Lee and Reddy 1999). Studies (Crouch and others 2005) showed that the activity of MYC can be potentiated by virally derived mutations.…”

Section: Discussionmentioning

confidence: 99%

“…In addition to upregulated gene expression, IFN-ls could also downregulate expression of several genes in macrophages, such as V-myc avian myelocytomatosis viral oncogene homolog (MYC) and platelet-derived growth factor receptor, alpha polypeptide (PDGFRA). MYC is the viral homolog of c-myc transduced by several acute transforming retroviruses (Lee and Reddy 1999). MYC expression is driven by the retroviral long terminal repeat in case of retroviral transduction (Lee and Reddy 1999).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Comparison of Antiviral Activity of Lambda-Interferons Against HIV Replication in Macrophages

Wang

Li²,

Wang³

et al. 2015

Journal of Interferon & Cytokine Research

View full text Add to dashboard Cite

Lambda-interferons (IFN-ls) have been demonstrated as having the ability to inhibit HIV replication in macrophages. However, specific differences in signaling transduction and anti-HIV activity in macrophages between different IFN-ls are unclear. Here, we showed that although all 3 members of (IFN-l1, l2, and l3) IFN-l family induced the expression of a number of genes of janus kinase/signal transducers and activators of transcription ( JAK/STAT) signaling pathway in monocyte-derived macrophages, IFN-l1 or IFN-l3 induced higher levels of antiviral IFN-stimulated genes (ISGs) expression than did IFN-l2. In addition, IFN-l1 or IFN-l3 induced higher levels of several pattern recognition receptors (PPRs) than did IFN-l2. Incubation of IFN-ls with HIV-infected macrophages showed that IFN-l1 or IFN-l3 is more potent in anti-HIV activity than IFN-l2. We also showed that IFN-l treatment before HIV infection was more potent in HIV inhibition than that after HIV infection. Further investigations showed that the inductions of ISGs and PPRs expression by IFN-ls were largely compromised by HIV infection. These findings provide further experimental evidence that IFN-ls have therapeutic potential in treatment of HIV infection.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Comparison of Antiviral Activity of Lambda-Interferons Against HIV Replication in Macrophages

Wang

Li²,

Wang³

et al. 2015

Journal of Interferon & Cytokine Research

View full text Add to dashboard Cite

show abstract

“…When these genes are reinserted into the host genome (via reverse transcription) they have been converted into oncogenes (106). Often these oncogenes encode growth factors that promote cell growth and proliferation (107). Overexpression of these viral oncogenes is caused by various mechanisms, including the addition of enhancers and promoters, and by gene amplification (e.g., (108)).…”

Section: Transposable Genetic Elementsmentioning

confidence: 99%

Intragenomic conflict and cancer

2002

View full text Add to dashboard Cite

Summary Intragenomic conflict occurs when some elements within the genome produce effects that enhance their own probability of replication or transmission at the expense of other elements within the same genome. Here it is proposed that mutations involved in intragenomic conflict are particularly likely to be co-opted by evolving lineages of cancer cells, and hence should be associated with the occurrence of cancer. We discuss several types of intragenomic conflict that are associated with various forms of cancer. ª

show abstract

“…Deregulated expression of c-Myc or expression of retrovirally encoded versions of the protein (referred to as v-Myc; for review see: Lee and Reddy, 1999) perturbs the balance between these processes and leads to neoplastic transformation of the cells. A large body of evidence has shown that Myc proteins exert their biological effects through activation and repression of specific sets of target genes.…”

Section: Introductionmentioning

confidence: 99%