2003
DOI: 10.1182/blood-2003-01-0100
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IGF-1 down-regulates IFN-γR2 chain surface expression and desensitizes IFN-γ/STAT-1 signaling in human T lymphocytes

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Cited by 45 publications
(57 citation statements)
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“…The first evidence for a role in transcription came from studies in yeast in which the fusion of the COOH-terminal domain of BRCA1 to a Gal4 DNA binding domain resulted in the activation of a Gal4 reporter construct. This activation was abrogated on the introduction of diseaserelated mutations in the COOH-terminal domain as well as the deletion of the last 11 amino acids of BRCA1 (6)(7)(8). These results were supported by the observation that the BRCA1 COOHterminal domain was highly acidic, a common feature of transcription factors (9).…”
Section: Introductionsupporting
confidence: 75%
“…The first evidence for a role in transcription came from studies in yeast in which the fusion of the COOH-terminal domain of BRCA1 to a Gal4 DNA binding domain resulted in the activation of a Gal4 reporter construct. This activation was abrogated on the introduction of diseaserelated mutations in the COOH-terminal domain as well as the deletion of the last 11 amino acids of BRCA1 (6)(7)(8). These results were supported by the observation that the BRCA1 COOHterminal domain was highly acidic, a common feature of transcription factors (9).…”
Section: Introductionsupporting
confidence: 75%
“…Despite the prolonged STAT1 activation elicited by IFN-g in ST4-S1 cells, MHC I molecules induction was unchanged, suggesting that low levels of active STAT1 are sufficient to achieve maximal induction. This observation fits with the data showing that IFN-g optimally induces the upregulation of MHC I in human malignant T cells cultured in the presence of serum, 23 an experimental condition that promotes IFN-gR2 internalization and weak and transient STAT1 activation by IFN-g. 18,21,24 Importantly, IL-6 was able to induce apoptosis in ST4-S1 cells more efficiently than IFN-g, correlating with the growth inhibition activity observed in vivo. Indeed, although IFN-g did not affect tumor growth, IL-6 treatment could delay the growth of ST4-S1 cells in SCID mice and in some cases even completely prevent it.…”
Section: Discussionmentioning
confidence: 74%
“…IFN-gdependent apoptosis is known to be strictly linked to the levels of IFN-gR2 expression. 15,18,24 In ST4-S1 cells, IFN-gR2 expression levels were as low as those of the ST4-WT and ST4-C control cells (data not shown), correlating with the limited Figure 4 Interleukin (IL)-6 can inhibit in vivo growth of ST4-S1 cells. Severe combined immunodeficient mice were inoculated subcutaneously with 10 Â 10 6 ST4-C (a) or ST4-S1 cells (b).…”
Section: Discussionmentioning
confidence: 75%
“…Serum starvation enhances IFN-γR1 expression in T cells [54], and enhances IFN-γR2 cell surface expression in a variety of hematopoietic cell lines; this latter effect may be due to deprivation of IGF-1 [87]. Notably, enhanced activation of Stat1 occurred with the upregulation of IFN-γR2 and an IFN-γ-induced proapoptotic fate during serum starvation, establishing a three-way correlation, but how these pathways are linked was not certain.…”
Section: Discussionmentioning
confidence: 99%