细胞因子信号抑制因子1
肿瘤抑制因子
贾纳斯激酶
白血病抑制因子
Janus激酶1
JAK-STAT信号通路
癌症研究
细胞因子信号抑制因子
细胞因子
睫状神经营养因子
STAT蛋白
白细胞介素6
生物
细胞生物学
SOCS3
糖蛋白130
免疫学
信号转导
车站3
受体
酪氨酸激酶
神经营养因子
癌症
抑制器
生物化学
遗传学
作者
Peter C. Heinrich,Iris Behrmann,Serge Haan,Heike M. Hermanns,Gerhard Müller‐Newen,Fred Schaper
摘要
The IL (interleukin)-6-type cytokines IL-6, IL-11, LIF (leukaemia inhibitory factor), OSM (oncostatin M), ciliary neurotrophic factor, cardiotrophin-1 and cardiotrophin-like cytokine are an important family of mediators involved in the regulation of the acute-phase response to injury and infection. Besides their functions in inflammation and the immune response, these cytokines play also a crucial role in haematopoiesis, liver and neuronal regeneration, embryonal development and fertility. Dysregulation of IL-6-type cytokine signalling contributes to the onset and maintenance of several diseases, such as rheumatoid arthritis, inflammatory bowel disease, osteoporosis, multiple sclerosis and various types of cancer (e.g. multiple myeloma and prostate cancer). IL-6-type cytokines exert their action via the signal transducers gp (glycoprotein) 130, LIF receptor and OSM receptor leading to the activation of the JAK/STAT (Janus kinase/signal transducer and activator of transcription) and MAPK (mitogen-activated protein kinase) cascades. This review focuses on recent progress in the understanding of the molecular mechanisms of IL-6-type cytokine signal transduction. Emphasis is put on the termination and modulation of the JAK/STAT signalling pathway mediated by tyrosine phosphatases, the SOCS (suppressor of cytokine signalling) feedback inhibitors and PIAS (protein inhibitor of activated STAT) proteins. Also the cross-talk between the JAK/STAT pathway with other signalling cascades is discussed.
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