Molecular cloning of APRF, a novel IFN-stimulated gene factor 3 p91-related transcription factor involved in the gp130-mediated signaling pathway

Akira, Shizuo; Nishio, Yukihiro; Inoue, Masahiro; Wang, Xuejie; We, Shi; Matsusaka, Taiji; Yoshida, Kanji; Sudo, Tetsuo; Naruto, Masanobu; Kishimoto, Tadamitsu

doi:10.1016/0092-8674(94)90235-6

Cited by 957 publications

(651 citation statements)

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“…STAT3 was originally discovered as a transcription factor activated by IL-6 family cytokines through gp130 [56,57]. The IL-6 receptor system consists of two chains: the 80 kD IL-6 receptor for ligand binding and a 130 kD co-receptor (gp130) for signal transduction.…”

Section: Stat3 Initiation Of Inflammation and Mammalian Disorders Inmentioning

confidence: 99%

STAT3 in immune responses and inflammatory bowel diseases

2006

Cell Res

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214npg STAT3 has been known as a mediator for gene expression induced by many important cytokines. Recent studies have suggested that STAT3 has important functions in regulation of both innate and adaptive immunity. Loss of STAT3 in immune cells caused severe inflammation in response to pathogens. This review discusses the recent progress and suggests directions for the future research on this interesting molecule.

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Section: Stat3 Initiation Of Inflammation and Mammalian Disorders Inmentioning

confidence: 99%

STAT3 in immune responses and inflammatory bowel diseases

2006

Cell Res

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“…Several Signal Transducer and Transcriptional Activator (Stat) proteins are phosphorylated in response to IL-6 including gp130-bound Stat3/APRF (Akira et al, 1994;Harroch et al, 1994b;Zhong et al, 1994;Stahl et al, 1995) as well as Stat1 (Harroch et al, 1994a,b;Zhong et al, 1994) and Stat5b (Ripperger et al, 1995). The various Stat proteins compose nuclear transcription complexes of di ering a nities for a group of enhancers designated as palindromic Inter-feron Regulated Elements (pIRE) since they are also activated by Interferons (Sims et al, 1993;Harroch et al, 1994a,b).…”

Section: Introductionmentioning

confidence: 99%

Unmasking by soluble IL-6 receptor of IL-6 effect on metastatic melanoma: growth inhibition and differentiation of B16-F10.9 tumor cells

Katz

Harroch

et al. 1997

Oncogene

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Interleukin-6 (IL-6) inhibits the growth of melanocytes and of early stage melanoma cells, but not that of advanced melanoma cells. The in vitro IL-6 response can be restored in the highly metastatic melamona B16-F10.9 by addition of recombinant soluble IL-6 receptor a-chain (sIL-6R). The F10.9 cells then undergo irreversible growth-arrest and show increased adherence with changes from epithelioid to spindleoid morphology. The sIL-6R is required for IL-6 to induce a sustained activation of the various Stat transcription factors which bind to speci®c IL-6 inducible enhancers. The sIL-6R and IL-6 combination causes an increase in the level of the anti-oncogenic transcription factor IRF-1 protein and DNA-binding, which remain elevated for 24 h. The promoter activity of the anti-oncogenic p21/Waf-1/Cip-1 gene is induced and accumulation of the p21 protein is observed. These results illustrate the potent agonist activity of sIL-6R on molecular pathways which could mediate the growth-arrest and di erentiation of the metastatic melanoma cells. Previously observed antimetastatic e ects of IL-6 therapy in mice bearing F10.9 tumors may be at least partly due to direct growth inhibition and di erentiation elicited by sIL-6R present in biological¯uids.

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“…Rather, Akira's work consumed him. In a 1994 study 3 on the immunesignalling protein STAT3, he used 6,000 mice in 6 months. By the end of the project, Kishimoto says, the mice dealers were telling him, "There are no mice left in Japan".…”

Section: Back To Basicsmentioning

confidence: 99%