Transcriptional and posttranscriptional regulation of interferon-induced gene expression in human cells

Regulation of IFN‐α/β genes: evidence for a dual function of the transcription factor complex ISGF3 in the production and action of IFN‐α/β

“…In this regard, an interesting sequence similarity was noted between the IRF-1 binding site, termed IRF-E (consensus sequence, G(A)AAA G / C T / C GAAA G / C T / C ) and another element, ISRE, which is found in the promoters of various IFN-inducible genes (consensus sequence, A / G NGAAANNGAAACT) (Friedman et al 1984;Tanaka et al 1993;Darnell et al 1994).…”

Divergent roles of STAT1 and STAT5 in malignancy as revealed by gene disruptions in mice

“…The motivation for these studies derives from evidence that IFNa and IFNg induced rapid but largely distinct changes in gene expression in target cells (Fan et al, 1988(Fan et al, , 1989Friedman et al, 1984;Larner et al, 1984;Revel and Chebath, 1986), re¯ecting their largely distinct biology of inducing direct antiviral action versus modulation of immune cell function, respectively. The discovery of a family of transcription factors that could be activated by a cell surface receptor and deliver information directly to the nucleus to modulate gene expression with the same speci®city inherent in the ligand-receptor interaction, provided an appealing explanation of how speci®city is maintained during signal transduction (Levy and Darnell, 1990).…”

Metallothionein RNA levels in HL‐60 cells Effect of cadmium, differentiation, and protein kinase C activation

“…MT gene expression is predominantly regulated at the level of transcription [5][6][7][8][9]. Though the mechanism of regulation is poorly understood, rapid induction occurs upon exposure to metals [5] and, in mammalian cells, to various circulating factors such as glucocorticoid hormones [6], ainterferon [7], and interleukin-1 and other mediators of the inflammatory response [8,9].…”

“…Though the mechanism of regulation is poorly understood, rapid induction occurs upon exposure to metals [5] and, in mammalian cells, to various circulating factors such as glucocorticoid hormones [6], ainterferon [7], and interleukin-1 and other mediators of the inflammatory response [8,9]. It has been suggested that a common pathway for MT induction involves protein kinase C (PKC) activation since MT levels increase in serum-starved cells after treatment with growth factors and TPA, agents which function in part through PKC activation [10,11].…”