Regulation of c‐myc expression by IFN‐γ through Stat1‐dependent and ‐independent pathways

By C. Ramana, N. Grammatikakis, M. Chernov, Hannah Nguyen, Kee Chuan Goh, Bryan R. G. Williams, G. Stark. 2000

303 citations recorded by the source corpus.

Subfields: Cancer Research, Oncology, Pharmacology

View Paper: https://www.semanticscholar.org/paper/94a4d9e0662f1734d9bab03d82a34f3a7a230e65

How researchers see this paper

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In Cancer Research

1. R. Jove
2. Hua Yu
3. R. Randall
4. S. Goodbourn

In Oncology

1. Hua Yu
2. R. Jove
3. R. Buettner
4. R. Randall
5. S. Goodbourn
6. D. Gabrilovich
7. M. Karin
8. A. Alcamí

Citations in the corpus

• Myc and cell cycle control. (2015, background): “Consistently, the response to antiproliferative cytokines as transforming growth factor β (TGFβ) or interferon-γ results in Myc down-regulation [53–56].”
• STAT proteins: From normal control of cellular events to tumorigenesis (2003, background): “The dimer translocates into the nucleus and induces the expression of target genes, which contain a regulatory sequence termed GAS (IFNg activation site) in the promoter region (Ramana et al., 2000) (Fig.”
• Activated STAT signaling in human tumors provides novel molecular targets for therapeutic intervention. (2002, background): “On the other hand, Stat1 can negatively regulate the expression of the c-Myc promoter in response to IFN- , consistent with its role as a mediator of growth suppression (39).”
• Interferons: cell signalling, immune modulation, antiviral response and virus countermeasures. (2000, background): “It has also recently been shown that PKRplays a role in Ser(#( phosphorylation (Ramana et al., 2000), but this is unlikely to be direct.”
• The eIF2α kinases: their structures and functions (2013, unknown): “As well as eIF2α, PKR phosphorylates p53 [33, 34], facilitates activation of the STAT transcription factors [40, 109, 161], in addition to promoting MAPK activity [61].”
• The STATs of cancer — new molecular targets come of age (2004, background): “Consistent with the anti-proliferative activity of STAT1, it has been shown that c-MYC expression is downregulated by IFN-γ, which activates STAT”