果蝇生长发育中PI3K_Akt_dTOR信号通路的研究进展_查佶_百度文库
两大类热门资源免费畅读
续费一年阅读会员，立省24元！
果蝇生长发育中PI3K_Akt_dTOR信号通路的研究进展_查佶
上传于||暂无简介
阅读已结束，如果下载本文需要使用2下载券
想免费下载本文？
下载文档到电脑，查找使用更方便
还剩1页未读，继续阅读
你可能喜欢扫扫二维码，随身浏览文档
手机或平板扫扫即可继续访问
PI3K_Akt_mTOR信号通路及临床相关肿瘤抑制剂
举报该文档为侵权文档。
举报该文档含有违规或不良信息。
反馈该文档无法正常浏览。
举报该文档为重复文档。
推荐理由：
将文档分享至：
分享完整地址
文档地址：
粘贴到BBS或博客
flash地址：
支持嵌入FLASH地址的网站使用
html代码：
&embed src='/DocinViewer--144.swf' width='100%' height='600' type=application/x-shockwave-flash ALLOWFULLSCREEN='true' ALLOWSCRIPTACCESS='always'&&/embed&
450px*300px480px*400px650px*490px
支持嵌入HTML代码的网站使用
您的内容已经提交成功
您所提交的内容需要审核后才能发布，请您等待！
3秒自动关闭窗口 上传我的文档
 下载
 收藏
该文档贡献者很忙，什么也没留下。
 下载此文档
正在努力加载中...
PI3K AKT信号通路在维持血糖平衡中的作用
下载积分：1000
内容提示：PI3K AKT信号通路在维持血糖平衡中的作用
文档格式：PDF|
浏览次数：12|
上传日期： 18:35:33|
文档星级：
该用户还上传了这些文档
PI3K AKT信号通路在维持血糖平衡中的作用
官方公共微信PI3K / Akt Signaling Pathway | Cell Signaling Technology
PI3K / Akt Signaling Pathway
PI3K / Akt Signaling Pathway
Use this Pathway for:
Pathway Description: Since its initial discovery as a proto-oncogene, the serine/threonine kinase Akt (also known as protein kinase B or PKB) has become a major focus of attention because of its critical role in regulating diverse cellular functions including metabolism, growth, proliferation, survival, transcription and protein synthesis. The Akt signaling cascade is activated by receptor tyrosine kinases, integrins, B and T cell receptors, cytokine receptors, G-protein-coupled receptors and other stimuli that induce production of phospha- tidylinositol (3,4,5) trisphosphates (PIP3) by phosphoinositide 3-kinase (PI3K). These lipids serve as plasma membrane docking sites for proteins that harbor pleckstrin-homol- ogy (PH) domains, including Akt and its upstream activator PDK1. At the membrane PDK1 phosphorylates Akt at Thr308 leading to partial activation of Akt. Phosphorylation of Akt at Ser473 by mTORC2 stimulates full enzymatic activity. Members of the PI3K-related kinase (PIKK) family, including DNA-PK, can also phosphorylate Akt at Ser473. Akt is dephosphorylated by protein phosphatase 2A (PP2A) and the PH-domain leucine-rich-repeat-containing protein phosphatases (PHLPP1/2). In addition, the tumor suppres- sor phosphatase and tensin homolog (PTEN) inhibits Akt activity by dephosphorylating PIP3. Dysregulation of the PI3K/Akt pathway is implicated in a number of human diseases including cancer, diabetes, cardiovascular disease and neurological diseases. In cancer, two mutations that increase the intrinsic kinase activity of PI3K have been identified. In addition, PTEN is frequently mutated or lost in human tumors. Activating mutations in Akt have also been described. The frequency with which dysregulated Akt signaling contributes to human disease has culminated in the aggressive development of small molecule inhibitors of PI3K and Akt. There are three highly related isoforms of Akt (Akt1, Akt2 and Akt3), which phosphorylate substrates containing the consensus phosphorylation motif RxRxxS/T. Akt isoforms share many substrates but isoform-specific Akt substrates have also been identified. For example, all Akt isoforms are able to phosphorylate PRAS40 (proline-rich Akt sub- strate of 40 kDa) but only Akt1 can phosphorylate the actin-associated protein palladin. Akt regulates cell growth through its effects on the TSC1/TSC2 complex and mTORC signaling. Akt contributes to cell proliferation via phosphorylation of the CDK inhibitors p21 and p27. Akt is a major mediator of cell survival through direct inhibition of pro-apoptotic proteins like Bad or inhibition of pro-apoptotic signals generated by transcription factors like FoxO. Akt is critically involved in the regulation of metabolism through activation of AS160 and PFKFB2. In addition, Akt has been shown to regulate proteins involved in neuronal function including the GABA receptor, ataxin-1 and huntingtin proteins. Akt contributes to cell migration and invasion via phosphorylation of palladin and vimentin. Akt also regulates NF-κB signaling by phosphorylating IKKα and Tpl2. Due to the critical role of Akt/PKB in regulating diverse cellular functions it is an important therapeutic target for the treatment of human disease.Selected Reviews:
Bhaskar PT, Hay N (2007)
Dev. Cell 12(4), 487–502.
Bozulic L, Hemmings BA (2009)
Curr. Opin. Cell Biol. 21(2), 256–61.
Brugge J, Hung MC, Mills GB (2007)
Cancer Cell 12(2), 104–7.
Carnero A, Blanco-Aparicio C, Renner O, Link W, Leal JF (2008)
Curr Cancer Drug Targets 8(3), 187–98.
Hers I, Vincent EE, Tavaré JM (2011)
Cell. Signal. 23(10), 1515–27.
Liu P, Cheng H, Roberts TM, Zhao JJ (2009)
Nat Rev Drug Discov 8(8), 627–44.
Manning BD, Cantley LC (2007)
Cell 129(7), 1261–74.
Salmena L, Carracedo A, Pandolfi PP (2008)
Cell 133(3), 403–14.
We would like to thank Kristin Brown and Prof. Alex Toker, Beth Israel Deaconess Medical Center, Harvard Medical School for reviewing this diagram. created September 2007 revised June 2014
SIGN UP FOR NEWS
VISIT US AT您所在位置： &
&nbsp&&nbsp&nbsp&&nbsp
PI3K-Akt信号转导通路和肿瘤.pdf5页
本文档一共被下载：
次 ,您可全文免费在线阅读后下载本文档。
文档加载中...广告还剩秒
需要金币：150 &&
PI3K-Akt信号转导通路和肿瘤.pdf
你可能关注的文档：
··········
··········
P13K／Akt信号转导通路和肿瘤 翳
解友邦 李建平 冯建明 吴天一 顾玉海 【摘要】磷脂酰肌醇3激酶在肿瘤细胞信号转导中起着重要的调节作用，许多因子可以使磷脂酰
肌醇3一激酶活化，引起蛋白激酶B与细胞膜的结合，在磷酸肌醇依赖激酶的参与下，蛋白激酶B和苏氨
酸和丝氨酸残基发生磷酸化而活化，进入胞质和胞核，激活细胞内酶促级联反应，从而产生生物学效应，
其与肿瘤细胞恶性增殖、血管新生和糖酵解有密切的关系。 【关键词】P13K／Akt；信号通路；肿瘤 transductionandtumorXie
P13K／Aktsignal Youbang+，Li pathway Jianping，FengJianming，Wu 810007，China
Tianyi，GuYuhai．+QinghaiUniversity，Xining
CorrP5po”dingauthor：WuTianyi，Email：wutianyiqh@hotmail．COrn；GuYuhai，Email：qhguyuhai@
j63．∞m [Abstract] an roleinthe
and Phosphatidylinositol3-kinase P13K playsimportant
regulation transductionoftumorcells．P13Kisactivated
factors，whichleadsto kinaseB
signal bymany protein PKBor tOcellmembrane．Withthe ofthe kinaseinthe Akt binding help
phosphoinositide-dependent is withthreonine and
P13K／Akttransduction andserine，activated signal pathway，Aktphosphorylated
and mediates
cascadereactiontO effects． nucleus，which cytoplasm enzymatic producebiological
Itis with and of related tumorcells． closely proliferation，angiogenesisglycolysismalignant [Keywords]P13K／Akt；Signalpathway；Tumor P13K／Akt信号转导通路和肿瘤有着密切的关系，可激
活下游基因或蛋白的表达引起细胞增殖，调控下游凋亡或抗
凋亡基因，介导造血和血管生成，通过调控糖的转运和糖酵 在哺乳动物细胞中存在。调节亚单位p85从N端到c端依
解的相关酶增加肿瘤细胞对氧的利用，同时调节血管生成。 次有SH3结构域、RHO结合域／断裂点簇
正在加载中，请稍后...