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STAT2 phosphorylation and signaling. STAT2磷酸化和信号传导。
JAK-STAT Pub Date : 2013-10-01 Epub Date: 2013-08-12 DOI: 10.4161/jkst.25790
Håkan C Steen, Ana M Gamero
{"title":"STAT2 phosphorylation and signaling.","authors":"Håkan C Steen,&nbsp;Ana M Gamero","doi":"10.4161/jkst.25790","DOIUrl":"https://doi.org/10.4161/jkst.25790","url":null,"abstract":"<p><p>STAT2 is an essential transcription factor in type I IFN mediated anti-viral and anti-proliferative signaling. STAT2 function is regulated by tyrosine phosphorylation, which is the trigger for STAT-dimerization, subsequent nuclear translocation, and transcriptional activation of IFN stimulated genes. Evidence of additional STAT2 phosphorylation sites has emerged as well as novel roles for STAT2 separate from the classical ISGF3-signaling. This review aims to summarize knowledge of phosphorylation-mediated STAT2-regulation and future avenues of related STAT2 research. </p>","PeriodicalId":89791,"journal":{"name":"JAK-STAT","volume":"2 4","pages":"e25790"},"PeriodicalIF":0.0,"publicationDate":"2013-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/jkst.25790","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32023644","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 53
The Drosophila JAK-STAT pathway. 果蝇JAK-STAT通路。
JAK-STAT Pub Date : 2013-07-01 Epub Date: 2013-08-01 DOI: 10.4161/jkst.25353
Martin P Zeidler, Nina Bausek
{"title":"The Drosophila JAK-STAT pathway.","authors":"Martin P Zeidler,&nbsp;Nina Bausek","doi":"10.4161/jkst.25353","DOIUrl":"https://doi.org/10.4161/jkst.25353","url":null,"abstract":"<p><p>The conservation of signaling cascades between humans and Drosophila, over more than 500 million years of evolutionary time, means that the genetic tractability of the fly can be used to its full advantage to understand the functional requirements for JAK-STAT pathway signaling across species. Here we review the background to how the pathway was first identified and the first characterization of JAK-STAT pathway phenotypes in the Drosophila system, highlighting the molecular, functional, and disease-related conservation of the pathway. </p>","PeriodicalId":89791,"journal":{"name":"JAK-STAT","volume":"2 3","pages":"e25353"},"PeriodicalIF":0.0,"publicationDate":"2013-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/jkst.25353","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31761234","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 41
The Drosophila JAK-STAT pathway in blood cell formation and immunity. 果蝇JAK-STAT通路在血细胞形成和免疫中的作用。
JAK-STAT Pub Date : 2013-07-01 Epub Date: 2013-07-15 DOI: 10.4161/jkst.25700
Ismaël Morin-Poulard, Alain Vincent, Michèle Crozatier
{"title":"The Drosophila JAK-STAT pathway in blood cell formation and immunity.","authors":"Ismaël Morin-Poulard,&nbsp;Alain Vincent,&nbsp;Michèle Crozatier","doi":"10.4161/jkst.25700","DOIUrl":"https://doi.org/10.4161/jkst.25700","url":null,"abstract":"<p><p>Genetic alterations affecting the JAK-STAT signaling pathway are linked to several malignancies and hematological disorders in humans. Despite being one of the most extensively studied pathways, there remain many gaps to fill. JAK-STAT components are widely conserved during evolution. Here, we review the known roles of the JAK-STAT pathway in Drosophila immunity: controlling the different steps of hematopoiesis, both under physiological conditions and in response to immune challenge, and contributing to antiviral responses. We then summarize what is currently known about JAK-STAT signaling in renewal of the adult intestine, under physiological conditions or in response to ingestion of pathogenic bacteria. </p>","PeriodicalId":89791,"journal":{"name":"JAK-STAT","volume":"2 3","pages":"e25700"},"PeriodicalIF":0.0,"publicationDate":"2013-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/jkst.25700","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31761238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 68
Sphingosine-1-phosphate: Driver of NFκB and STAT3 persistent activation in chronic intestinal inflammation and colitis-associated cancer. 鞘氨醇-1-磷酸:慢性肠道炎症和结肠炎相关癌症中NFκB和STAT3持续激活的驱动因素
JAK-STAT Pub Date : 2013-07-01 Epub Date: 2013-08-15 DOI: 10.4161/jkst.24150
Arianne L Theiss
{"title":"Sphingosine-1-phosphate: Driver of NFκB and STAT3 persistent activation in chronic intestinal inflammation and colitis-associated cancer.","authors":"Arianne L Theiss","doi":"10.4161/jkst.24150","DOIUrl":"https://doi.org/10.4161/jkst.24150","url":null,"abstract":"<p><p>Inflammatory bowel disease is associated with an increased risk of colorectal cancer. Colitis-associated cancer is a classical inflammation-driven cancer in which constitutive NFκB and STAT3 activation drive tumorigenesis. Recent findings published by Liang et al. in Cancer Cell demonstrate that sphingosine kinase 1 (SphK1)-mediated upregulation of sphingosine-1-phosphate (S1P) drives a persistent NFκB/IL-6/STAT3/sphingosine-1-phosphate receptor 1 (S1PR1) amplification loop that is critical to the development of chronic colitis and colitis-associated cancer. FTY720, an antagonist of S1PR1, abolished persistent NFκB/IL-6/STAT3 signaling and reduced the development and progression of colitis-associated cancer. Targeting SphK1/S1P/S1PR1 may provide a therapeutic option to prevent the progression of colitis to cancer. </p>","PeriodicalId":89791,"journal":{"name":"JAK-STAT","volume":"2 3","pages":"e24150"},"PeriodicalIF":0.0,"publicationDate":"2013-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/jkst.24150","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31761342","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 23
STAT3 as a new autophagy regulator. STAT3作为一种新的自噬调节因子。
JAK-STAT Pub Date : 2013-07-01 Epub Date: 2013-08-15 DOI: 10.4161/jkst.24353
Barbara Jonchère, Audrey Bélanger, Catherine Guette, Benjamin Barré, Olivier Coqueret
{"title":"STAT3 as a new autophagy regulator.","authors":"Barbara Jonchère,&nbsp;Audrey Bélanger,&nbsp;Catherine Guette,&nbsp;Benjamin Barré,&nbsp;Olivier Coqueret","doi":"10.4161/jkst.24353","DOIUrl":"https://doi.org/10.4161/jkst.24353","url":null,"abstract":"<p><p>Signal transducers and activators of transcription 3 (STAT3) proteins are cytoplasmic transcription factors that translocate into the nucleus to induce transcription following growth factor or cytokine stimulation. Besides their normal functions, these proteins play an important role in cancer cells through the abnormal activation of cell cycle progression and the deregulation of survival and senescence pathways. New data obtained from the laboratory of Guido Kroemer identifies STAT3 as a new autophagy regulator. In the cytoplasm, in the absence of conventional phosphorylation on the tyrosine 705 residue, STAT3 interacts with the PKR kinase to inhibit eIF2A phosphorylation and so reduce autophagic pathways. This new and nonconventional function of STAT3 has an important role in normal cells but we suggest that it might also affect cancer cells and the response to chemotherapy treatment. </p>","PeriodicalId":89791,"journal":{"name":"JAK-STAT","volume":"2 3","pages":"e24353"},"PeriodicalIF":0.0,"publicationDate":"2013-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/jkst.24353","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31761347","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 42
Computational models of the JAK1/2-STAT1 signaling. JAK1/2-STAT1信号的计算模型。
JAK-STAT Pub Date : 2013-07-01 Epub Date: 2013-04-15 DOI: 10.4161/jkst.24672
Anna Gambin, Agata Charzyńska, Aleksandra Ellert-Miklaszewska, Mikołaj Rybiński
{"title":"Computational models of the JAK1/2-STAT1 signaling.","authors":"Anna Gambin,&nbsp;Agata Charzyńska,&nbsp;Aleksandra Ellert-Miklaszewska,&nbsp;Mikołaj Rybiński","doi":"10.4161/jkst.24672","DOIUrl":"https://doi.org/10.4161/jkst.24672","url":null,"abstract":"<p><p>Despite a conceptually simple mechanism of signaling, the JAK-STAT pathway exhibits considerable behavioral complexity. Computational pathway models are tools to investigate in detail signaling process. They integrate well with experimental studies, helping to explain molecular dynamics and to state new hypotheses, most often about the structure of interactions. A relatively small amount of experimental data is available for a JAK1/2-STAT1 variant of the pathway, hence, only several computational models were developed. Here we review a dominant approach of kinetic modeling of the JAK1/2-STAT1 pathway, based on ordinary differential equations. We also give a brief overview of attempts to computationally infer topology of this pathway. </p>","PeriodicalId":89791,"journal":{"name":"JAK-STAT","volume":"2 3","pages":"e24672"},"PeriodicalIF":0.0,"publicationDate":"2013-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/jkst.24672","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31761349","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 31
STATs and macrophage fusion. STATs和巨噬细胞融合。
JAK-STAT Pub Date : 2013-07-01 Epub Date: 2013-04-23 DOI: 10.4161/jkst.24777
Takeshi Miyamoto
{"title":"STATs and macrophage fusion.","authors":"Takeshi Miyamoto","doi":"10.4161/jkst.24777","DOIUrl":"https://doi.org/10.4161/jkst.24777","url":null,"abstract":"<p><p>Macrophages play a pivotal role in host defense against multiple foreign materials such as bacteria, parasites and artificial devices. Some macrophage lineage cells, namely osteoclasts and foreign body giant cells (FBGCs), form multi-nuclear giant cells by the cell-cell fusion of mono-nuclear cells. Osteoclasts are bone-resorbing cells, and are formed in the presence of RANKL on the surface of bones, while FBGCs are formed in the presence of IL-4 or IL-13 on foreign materials such as artificial joints, catheters and parasites. Recently, fusiogenic mechanisms and the molecules required for the cell-cell fusion of these macrophage lineage cells were, at least in part, clarified. Dendritic cell specific transmembrane protein (DC-STAMP) and osteoclast stimulatory transmembrane protein (OC-STAMP), both of which comprise seven transmembrane domains, are required for both osteoclast and FBGC cell-cell fusion. STAT6 was demonstrated to be required for the cell-cell fusion of FBGCs but not osteoclasts. In this review, advances in macrophage cell-cell fusion are discussed. </p>","PeriodicalId":89791,"journal":{"name":"JAK-STAT","volume":"2 3","pages":"e24777"},"PeriodicalIF":0.0,"publicationDate":"2013-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/jkst.24777","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31761232","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 17
JAK2-V617F-induced MAPK activity is regulated by PI3K and acts synergistically with PI3K on the proliferation of JAK2-V617F-positive cells. jak2 - v617f诱导的MAPK活性受PI3K调控，并与PI3K协同作用于jak2 - v617f阳性细胞的增殖。
JAK-STAT Pub Date : 2013-07-01 Epub Date: 2013-04-08 DOI: 10.4161/jkst.24574
Alexandra Wolf, René Eulenfeld, Karoline Gäbler, Catherine Rolvering, Serge Haan, Iris Behrmann, Bernd Denecke, Claude Haan, Fred Schaper
{"title":"JAK2-V617F-induced MAPK activity is regulated by PI3K and acts synergistically with PI3K on the proliferation of JAK2-V617F-positive cells.","authors":"Alexandra Wolf,&nbsp;René Eulenfeld,&nbsp;Karoline Gäbler,&nbsp;Catherine Rolvering,&nbsp;Serge Haan,&nbsp;Iris Behrmann,&nbsp;Bernd Denecke,&nbsp;Claude Haan,&nbsp;Fred Schaper","doi":"10.4161/jkst.24574","DOIUrl":"https://doi.org/10.4161/jkst.24574","url":null,"abstract":"<p><p>The identification of a constitutively active JAK2 mutant, namely JAK2-V617F, was a milestone in the understanding of Philadelphia chromosome-negative myeloproliferative neoplasms. The JAK2-V617F mutation confers cytokine hypersensitivity, constitutive activation of the JAK-STAT pathway, and cytokine-independent growth. In this study we investigated the mechanism of JAK2-V617F-dependent signaling with a special focus on the activation of the MAPK pathway. We observed JAK2-V617F-dependent deregulated activation of the multi-site docking protein Gab1 as indicated by constitutive, PI3K-dependent membrane localization and tyrosine phosphorylation of Gab1. Furthermore, we demonstrate that PI3K signaling regulates MAPK activation in JAK2-V617F-positve cells. This cross-regulation of the MAPK pathway by PI3K affects JAK2-V617F-specific target gene induction, erythroid colony formation, and regulates proliferation of JAK2-V617F-positive patient cells in a synergistically manner. </p>","PeriodicalId":89791,"journal":{"name":"JAK-STAT","volume":"2 3","pages":"e24574"},"PeriodicalIF":0.0,"publicationDate":"2013-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/jkst.24574","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31761348","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 27
JAK-STAT pathway in Drosophila morphogenesis: From organ selector to cell behavior regulator. 果蝇形态发生中的JAK-STAT通路:从器官选择到细胞行为调节。
JAK-STAT Pub Date : 2013-07-01 Epub Date: 2013-08-08 DOI: 10.4161/jkst.26089
James Castelli-Gair Hombría, Sol Sotillos
{"title":"JAK-STAT pathway in Drosophila morphogenesis: From organ selector to cell behavior regulator.","authors":"James Castelli-Gair Hombría,&nbsp;Sol Sotillos","doi":"10.4161/jkst.26089","DOIUrl":"https://doi.org/10.4161/jkst.26089","url":null,"abstract":"<p><p>One of the main contributions of Drosophila to the JAK-STAT field is the study of morphogenesis. JAK-STAT signaling controls the formation of many different structures through surprisingly different morphogenetic behaviors that include induction of cell rearrangements, invagination, folding of tissues, modulation of cell shape, and migration. This variability may be explained by the many transcription factors and signaling molecules STAT regulates at early stages of development. But is STAT just acting as an upstream inducer of morphogenesis or does it have a more direct role in controlling cell behaviors? Here we review what is known about how the canonical phosphorylation of STAT contributes to shaping the embryonic and imaginal structures. </p>","PeriodicalId":89791,"journal":{"name":"JAK-STAT","volume":"2 3","pages":"e26089"},"PeriodicalIF":0.0,"publicationDate":"2013-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/jkst.26089","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31761239","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 9
CDK8 as the STAT1 serine 727 kinase? CDK8作为STAT1丝氨酸727激酶?
JAK-STAT Pub Date : 2013-07-01 Epub Date: 2013-08-15 DOI: 10.4161/jkst.24275
Julia Staab, Christoph Herrmann-Lingen, Thomas Meyer
{"title":"CDK8 as the STAT1 serine 727 kinase?","authors":"Julia Staab,&nbsp;Christoph Herrmann-Lingen,&nbsp;Thomas Meyer","doi":"10.4161/jkst.24275","DOIUrl":"https://doi.org/10.4161/jkst.24275","url":null,"abstract":"<p><p>Whereas cytokine-induced tyrosine phosphorylation of STAT (signal transducer and activator of transcription) proteins by JAK kinases has been well studied, much less is known about STAT-specific serine kinases and their signal-dependent regulation. The paper by Joanna Bancerek and colleagues published recently in Immunity reports that upon interferon-γ (IFNγ) stimulation of cells the chromatin-associated cyclin-dependent kinase 8 (CDK8) phosphorylates the regulatory serine residue 727 in the transactivation domain of STAT1. The authors state that the CDK8 module of the Mediator complex is a key component in the STAT1 signal pathway, linking serine phosphorylation to gene-specific transcriptional events. </p>","PeriodicalId":89791,"journal":{"name":"JAK-STAT","volume":"2 3","pages":"e24275"},"PeriodicalIF":0.0,"publicationDate":"2013-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/jkst.24275","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31761345","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 12
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