发布求助
文献互助 智能选刊 最新文献

JAK-STAT最新文献

筛选
英文 中文
How are STAT1 and cholesterol metabolism associated in antiviral responses? STAT1和胆固醇代谢如何与抗病毒反应相关?
JAK-STAT Pub Date : 2013-07-01 Epub Date: 2013-08-15 DOI: 10.4161/jkst.24189
Tomoh Matsumiya, Tadaatsu Imaizumi
{"title":"How are STAT1 and cholesterol metabolism associated in antiviral responses?","authors":"Tomoh Matsumiya,&nbsp;Tadaatsu Imaizumi","doi":"10.4161/jkst.24189","DOIUrl":"https://doi.org/10.4161/jkst.24189","url":null,"abstract":"<p><p>Sterol metabolites are known to be associated with immune responses. 25-Hydroxycholesterol (25HC) is a cholesterol metabolite that is produced by macrophages. The production of 25HC was reported to be TLR-dependent, indicating the involvement of 25HC in innate immunity. Now Blanc et al. show that macrophages synthesize 25HC to exert an antiviral effect. STAT1 was shown to be the most essential transcriptional factor involved in the induction of cholesterol 25-hydroxylase (Ch25h), the enzyme required to produce 25HC, indicating the importance of STAT1 in oxysterol-mediated innate immunity. </p>","PeriodicalId":89791,"journal":{"name":"JAK-STAT","volume":"2 3","pages":"e24189"},"PeriodicalIF":0.0,"publicationDate":"2013-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/jkst.24189","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31761344","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: 7
JAK-STAT in heterochromatin and genome stability. JAK-STAT在异染色质和基因组稳定性中的作用。
JAK-STAT Pub Date : 2013-07-01 Epub Date: 2013-08-08 DOI: 10.4161/jkst.26090
Louise Silver-Morse, Willis X Li
{"title":"JAK-STAT in heterochromatin and genome stability.","authors":"Louise Silver-Morse,&nbsp;Willis X Li","doi":"10.4161/jkst.26090","DOIUrl":"https://doi.org/10.4161/jkst.26090","url":null,"abstract":"<p><p>The canonical JAK-STAT signaling pathway transmits signals from the cell membrane to the nucleus, to regulate transcription of particular genes involved in development and many other physiological processes. It has been shown in Drosophila that JAK and STAT also function in a non-canonical mode, to regulate heterochromatin. This review discusses the non-canonical functioning of JAK and STAT, and its effects on biological processes. Decreased levels of activated JAK and increased levels of unphosphorylated STAT generate higher levels of heterochromatin. These higher heterochromatin levels result in suppression of hematopoietic tumor-like masses, increased resistance to DNA damage, and longer lifespan. </p>","PeriodicalId":89791,"journal":{"name":"JAK-STAT","volume":"2 3","pages":"e26090"},"PeriodicalIF":0.0,"publicationDate":"2013-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/jkst.26090","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31761732","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: 26
Transcriptional regulation by STAT1 and STAT2 in the interferon JAK-STAT pathway. 干扰素JAK-STAT通路中STAT1和STAT2的转录调控。
JAK-STAT Pub Date : 2013-07-01 Epub Date: 2013-06-18 DOI: 10.4161/jkst.23931
Nancy Au-Yeung, Roli Mandhana, Curt M Horvath
{"title":"Transcriptional regulation by STAT1 and STAT2 in the interferon JAK-STAT pathway.","authors":"Nancy Au-Yeung,&nbsp;Roli Mandhana,&nbsp;Curt M Horvath","doi":"10.4161/jkst.23931","DOIUrl":"https://doi.org/10.4161/jkst.23931","url":null,"abstract":"<p><p>STAT1 and STAT2 proteins are key mediators of type I and type III interferon (IFN) signaling, and are essential components of the cellular antiviral response and adaptive immunity. They associate with IFN regulatory factor 9 (IRF9) to form a heterotrimeric transcription factor complex known as ISGF3. The regulation of IFN-stimulated gene (ISG) expression has served as a model of JAK-STAT signaling and mammalian transcriptional regulation, but to date has primarily been analyzed at the single gene level. While many aspects of ISGF3-mediated gene regulation are thought to be common features applicable to several ISGs, there are also many reports of distinct cases of non-canonical STAT1 or STAT2 signaling events and distinct patterns of co-regulators that contribute to gene-specific transcription. Recent genome-wide studies have begun to uncover a more complete profile of ISG regulation, moving toward a genome-wide understanding of general mechanisms that underlie gene-specific behaviors. </p>","PeriodicalId":89791,"journal":{"name":"JAK-STAT","volume":"2 3","pages":"e23931"},"PeriodicalIF":0.0,"publicationDate":"2013-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/jkst.23931","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31761381","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: 225
JAK-STAT pathway and myogenic differentiation. JAK-STAT通路与肌源性分化。
JAK-STAT Pub Date : 2013-04-01 DOI: 10.4161/jkst.23282
You-Na Jang, Eun Joo Baik
{"title":"JAK-STAT pathway and myogenic differentiation.","authors":"You-Na Jang,&nbsp;Eun Joo Baik","doi":"10.4161/jkst.23282","DOIUrl":"https://doi.org/10.4161/jkst.23282","url":null,"abstract":"<p><p>Myogenic differentiation plays an important role in muscle regeneration and is regulated by two transcription factor families, MRFs and MEF2, which induce differentiation of myoblasts through expression of the muscle-specific gene, myogenin. In addition, many intracellular signaling pathways are also involved in myogenic differentiation, including p38 MAPK, ERK/MAPK and PI3K/AKT. The JAK-STAT pathway is activated by various cytokines and positively or negatively regulates the differentiation of myoblasts. JAK1 plays a notable role in proliferation; whereas, JAK2 and JAK3 function mainly in differentiation. The STATs, molecules downstream of JAK, regulate myogenesis. With JAK1, STAT1 promotes proliferation, while STAT3 has a dual effect on proliferation and differentiation. The JAK-STAT negative regulator, SOCS, is also associated with myogenesis; although, its role is controversial. In this review, we will discuss the role of the JAK-STAT pathway on myogenic differentiation. </p>","PeriodicalId":89791,"journal":{"name":"JAK-STAT","volume":"2 2","pages":"e23282"},"PeriodicalIF":0.0,"publicationDate":"2013-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/jkst.23282","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31752418","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: 96
The tumor suppressor function of STAT1 in breast cancer. STAT1在乳腺癌中的抑瘤功能。
JAK-STAT Pub Date : 2013-04-01 DOI: 10.4161/jkst.23353
Antonis E Koromilas, Veronika Sexl
{"title":"The tumor suppressor function of STAT1 in breast cancer.","authors":"Antonis E Koromilas,&nbsp;Veronika Sexl","doi":"10.4161/jkst.23353","DOIUrl":"https://doi.org/10.4161/jkst.23353","url":null,"abstract":"<p><p>The anti-tumor function of STAT1 through its capacity to control the immune system and promote tumor immune surveillance has been well understood. However, little is known about cell autonomous (i.e., tumor cell-specific) functions of STAT1 in tumor formation. Recent studies have provided strong evidence that STAT1 suppresses mouse mammary gland tumorigenesis by both, immune regulatory and tumor cell-specific functions of STAT1. Specifically, STAT1 deficiency in the mouse mammary gland inhibits ErbB2/Neu-mediated tumorigenesis and contributes to spontaneous formation of estrogen receptor α (ER α)-positive as well as ER α-negative tumors closely resembling human disease. Herein, we review the anti-tumor functions of STAT1 revealed from investigations of murine breast cancer models and from characterization of the signaling properties of STAT1 in human breast tumor cells. The significance of STAT1 in breast cancer is underscored by studies proposing a prognostic value for the expression and/or phosphorylation of STAT1 for specific molecular types of breast cancer. Furthermore, STAT1 dependent transcription is proposed to contribute to therapeutic responses by modulating the efficacy of chemotherapeutic drugs and the development of drug resistance. </p>","PeriodicalId":89791,"journal":{"name":"JAK-STAT","volume":"2 2","pages":"e23353"},"PeriodicalIF":0.0,"publicationDate":"2013-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/jkst.23353","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31752419","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: 85
Why should we care about fly tumors?: The case of JAK-STAT and EGFR cooperation in oncogenesis. 为什么我们要关心苍蝇的肿瘤?JAK-STAT和EGFR在肿瘤发生中的合作案例。
JAK-STAT Pub Date : 2013-04-01 DOI: 10.4161/jkst.23203
James Castelli-Gair Hombría, Florenci Serras
{"title":"Why should we care about fly tumors?: The case of JAK-STAT and EGFR cooperation in oncogenesis.","authors":"James Castelli-Gair Hombría,&nbsp;Florenci Serras","doi":"10.4161/jkst.23203","DOIUrl":"https://doi.org/10.4161/jkst.23203","url":null,"abstract":"<p><p>Drosophila is proving to be a valuable model for studying aggressive tumors induced by the combined activation of EGFR and JAK-STAT signaling. Here we summarize some of the most recent data showing that tissue damage and the modulation of common pathway regulators are at the heart tumor progression and metastasis. </p>","PeriodicalId":89791,"journal":{"name":"JAK-STAT","volume":"2 2","pages":"e23203"},"PeriodicalIF":0.0,"publicationDate":"2013-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/jkst.23203","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31751457","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: 4
STAT3 and the Hyper-IgE syndrome: Clinical presentation, genetic origin, pathogenesis, novel findings and remaining uncertainties. STAT3和高ige综合征:临床表现、遗传起源、发病机制、新发现和仍不确定因素
JAK-STAT Pub Date : 2013-04-01 DOI: 10.4161/jkst.23435
Trine H Mogensen
{"title":"STAT3 and the Hyper-IgE syndrome: Clinical presentation, genetic origin, pathogenesis, novel findings and remaining uncertainties.","authors":"Trine H Mogensen","doi":"10.4161/jkst.23435","DOIUrl":"https://doi.org/10.4161/jkst.23435","url":null,"abstract":"<p><p>During recent years a number of primary immunodeficiencies resulting from impaired function of JAK-STAT molecules have been described. One of these is the Hyper-IgE syndrome (HIES) characterized by elevated IgE levels, eczema, recurrent staphylococcal skin and pulmonary infections and pleiotropic somatic manifestations. In 2007 the genetic basis of HIES was revealed by identification of dominant negative STAT3 mutations in HIES patients. Subsequently impaired function of Tyk2 and DOCK8 have been implicated in milder forms of HIES. Since STAT3 acts as a central transcription factor downstream of multiple cytokine and growth factor receptors and thus regulates antimicrobial responses and cell survival, impaired STAT3 function results in immunodeficiency and in some cases tumorigenesis. However, as the immunological and molecular basis of HIES is being unraveled, important biological and immunological insight into JAK-STAT signaling is emerging that may have implications for our understanding of the pathogenesis and clinical management of patients with HIES. </p>","PeriodicalId":89791,"journal":{"name":"JAK-STAT","volume":"2 2","pages":"e23435"},"PeriodicalIF":0.0,"publicationDate":"2013-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/jkst.23435","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31752420","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: 94
CCL2 at the crossroad of cancer metastasis. CCL2在癌症转移的十字路口。
JAK-STAT Pub Date : 2013-04-01 DOI: 10.4161/jkst.23816
Robert Eferl
{"title":"CCL2 at the crossroad of cancer metastasis.","authors":"Robert Eferl","doi":"10.4161/jkst.23816","DOIUrl":"https://doi.org/10.4161/jkst.23816","url":null,"abstract":"<p><p>Primary tumors can affect organ functions, either mechanically when they grow to a considerable size or via production of hormones. However, mortality of cancer patients is in most cases due to formation of secondary growths.(1) (,) (2) Consequently, various drugs are currently employed in clinical trials to impair specific steps of cancer metastasis such as mesenchymal or amoeboid cell migration, intravasation and/or colonization.(2) From the clinical point of view, targeting late metastatic processes such as extravasation or colonization might be required for cancer patients that bear already dormant micrometastases in their capillaries which have left behind earlier metastatic steps. Development of such drugs needs characterization of molecular targets implicated in distinct steps of cancer metastasis. </p>","PeriodicalId":89791,"journal":{"name":"JAK-STAT","volume":"2 2","pages":"e23816"},"PeriodicalIF":0.0,"publicationDate":"2013-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/jkst.23816","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31752341","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: 10
Targeting the tumor microenvironment: JAK-STAT3 signaling. 靶向肿瘤微环境:JAK-STAT3信号传导。
JAK-STAT Pub Date : 2013-04-01 DOI: 10.4161/jkst.23828
Eirini Bournazou, Jacqueline Bromberg
{"title":"Targeting the tumor microenvironment: JAK-STAT3 signaling.","authors":"Eirini Bournazou,&nbsp;Jacqueline Bromberg","doi":"10.4161/jkst.23828","DOIUrl":"https://doi.org/10.4161/jkst.23828","url":null,"abstract":"<p><p>Persistent JAK-STAT3 signaling is implicated in many aspects of tumorigenesis. Apart from its tumor-intrinsic effects, STAT3 also exerts tumor-extrinsic effects, supporting tumor survival and metastasis. These involve the regulation of paracrine cytokine signaling, alterations in metastatic sites rendering these permissive for the growth of cancer cells and subversion of host immune responses to create an immunosuppressive environment. Targeting this signaling pathway is considered a novel promising therapeutic approach, especially in the context of tumor immunity. In this article, we will review to what extent JAK-STAT3-targeted therapies affect the tumor microenvironment and whether the observed effects underlie responsiveness to therapy. </p>","PeriodicalId":89791,"journal":{"name":"JAK-STAT","volume":"2 2","pages":"e23828"},"PeriodicalIF":0.0,"publicationDate":"2013-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/jkst.23828","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31752342","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: 18
Regulation of STATs by polycystin-1 and their role in polycystic kidney disease. 多囊蛋白-1调控STATs及其在多囊肾病中的作用。
JAK-STAT Pub Date : 2013-04-01 DOI: 10.4161/jkst.23650
Thomas Weimbs, Erin E Olsan, Jeffrey J Talbot
{"title":"Regulation of STATs by polycystin-1 and their role in polycystic kidney disease.","authors":"Thomas Weimbs,&nbsp;Erin E Olsan,&nbsp;Jeffrey J Talbot","doi":"10.4161/jkst.23650","DOIUrl":"https://doi.org/10.4161/jkst.23650","url":null,"abstract":"<p><p>Autosomal-dominant polycystic kidney disease (ADPKD) is a common genetic disease caused by mutations in the gene coding for polycystin-1 (PC1). PC1 can regulate STAT transcription factors by a novel, dual mechanism. STAT3 and STAT6 are aberrantly activated in renal cysts. Genetic and pharmacological approaches to inhibit STAT3 or STAT6 have led to promising results in ADPKD mouse models. Here, we review current findings that lead to a model of PC1 as a key regulator of STAT signaling in renal tubule cells. We discuss how PC1 may orchestrate appropriate epithelial responses to renal injury, and how this system may lead to aberrant STAT activation in ADPKD thereby causing inappropriate activation of tissue repair programs that culminate in renal cyst growth and fibrosis. </p>","PeriodicalId":89791,"journal":{"name":"JAK-STAT","volume":"2 2","pages":"e23650"},"PeriodicalIF":0.0,"publicationDate":"2013-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/jkst.23650","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31752421","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: 59
首页 上一页 下一页 尾页
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整，为了账户安全，请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
请完成安全验证×
相关产品
×
本文献相关产品
联系我们：info@booksci.cn Book学术提供免费学术资源搜索服务，方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号：604180095
Book学术官方微信
小红书