• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

Integrative Analysis of PRKAG2 Cardiomyopathy iPS and Microtissue Models Identifies AMPK as a Regulator of Metabolism, Survival, and Fibrosis.

作者信息

Hinson J Travis, Chopra Anant, Lowe Andre, Sheng Calvin C, Gupta Rajat M, Kuppusamy Rajarajan, O'Sullivan John, Rowe Glenn, Wakimoto Hiroko, Gorham Joshua, Burke Michael A, Zhang Kehan, Musunuru Kiran, Gerszten Robert E, Wu Sean M, Chen Christopher S, Seidman Jonathan G, Seidman Christine E

出版信息

Cell Rep. 2017 Jun 13;19(11):2410. doi: 10.1016/j.celrep.2017.05.038.

DOI:10.1016/j.celrep.2017.05.038
PMID:28614725
Abstract
摘要

相似文献

1
Integrative Analysis of PRKAG2 Cardiomyopathy iPS and Microtissue Models Identifies AMPK as a Regulator of Metabolism, Survival, and Fibrosis.PRKAG2心肌病诱导多能干细胞和微组织模型的综合分析确定AMPK为代谢、存活和纤维化的调节因子。
Cell Rep. 2017 Jun 13;19(11):2410. doi: 10.1016/j.celrep.2017.05.038.
2
Integrative Analysis of PRKAG2 Cardiomyopathy iPS and Microtissue Models Identifies AMPK as a Regulator of Metabolism, Survival, and Fibrosis.PRKAG2心肌病诱导多能干细胞和微组织模型的综合分析确定AMPK为代谢、存活和纤维化的调节因子。
Cell Rep. 2016 Dec 20;17(12):3292-3304. doi: 10.1016/j.celrep.2016.11.066.
3
Increased alpha2 subunit-associated AMPK activity and PRKAG2 cardiomyopathy.α2亚基相关的AMPK活性增加与PRKAG2心肌病。
Circulation. 2005 Nov 15;112(20):3140-8. doi: 10.1161/CIRCULATIONAHA.105.550806. Epub 2005 Nov 7.
4
Molecular cloning, genomic organization, and mapping of PRKAG2, a heart abundant gamma2 subunit of 5'-AMP-activated protein kinase, to human chromosome 7q36.5'-AMP激活蛋白激酶的心脏高丰度γ2亚基PRKAG2的分子克隆、基因组结构及定位到人染色体7q36。
Genomics. 2000 Dec 1;70(2):258-63. doi: 10.1006/geno.2000.6376.
5
DNA polymorphisms and transcript abundance of PRKAG2 and phosphorylated AMP-activated protein kinase in the rumen are associated with gain and feed intake in beef steers.瘤胃中PRKAG2的DNA多态性、转录丰度以及磷酸化的AMP激活蛋白激酶与肉牛的增重和采食量相关。
Anim Genet. 2014 Aug;45(4):461-72. doi: 10.1111/age.12151. Epub 2014 Apr 15.
6
Transgenic mice overexpressing mutant PRKAG2 define the cause of Wolff-Parkinson-White syndrome in glycogen storage cardiomyopathy.过表达突变型PRKAG2的转基因小鼠确定了糖原贮积性心肌病中预激综合征的病因。
Circulation. 2003 Jun 10;107(22):2850-6. doi: 10.1161/01.CIR.0000075270.13497.2B. Epub 2003 Jun 2.
7
Glycogen storage diseases presenting as hypertrophic cardiomyopathy.表现为肥厚型心肌病的糖原贮积病。
N Engl J Med. 2005 Jan 27;352(4):362-72. doi: 10.1056/NEJMoa033349.
8
Constitutively active AMP kinase mutations cause glycogen storage disease mimicking hypertrophic cardiomyopathy.组成型激活的AMP激酶突变导致类似肥厚型心肌病的糖原贮积病。
J Clin Invest. 2002 Feb;109(3):357-62. doi: 10.1172/JCI14571.
9
Activation of cardiac hypertrophic signaling pathways in a transgenic mouse with the human PRKAG2 Thr400Asn mutation.在携带人类PRKAG2基因Thr400Asn突变的转基因小鼠中,心脏肥厚信号通路的激活。
Biochim Biophys Acta. 2010 Feb;1802(2):284-91. doi: 10.1016/j.bbadis.2009.12.001. Epub 2009 Dec 11.
10
Increased glycogen stores due to gamma-AMPK overexpression protects against ischemia and reperfusion damage.由于γ-AMPK过表达导致糖原储备增加,可保护机体免受缺血再灌注损伤。
Biochem Pharmacol. 2008 Apr 1;75(7):1482-91. doi: 10.1016/j.bcp.2007.12.011. Epub 2008 Jan 5.

引用本文的文献

1
Three-Dimensional iPSC-Based In Vitro Cardiac Models for Biomedical and Pharmaceutical Research Applications.基于三维 iPSC 的体外心脏模型在生物医学和药物研发中的应用。
Int J Mol Sci. 2024 Oct 4;25(19):10690. doi: 10.3390/ijms251910690.
2
Human Induced Pluripotent Stem Cell as a Disease Modeling and Drug Development Platform-A Cardiac Perspective.人类诱导多能干细胞作为疾病建模和药物开发平台——心脏视角。
Cells. 2021 Dec 9;10(12):3483. doi: 10.3390/cells10123483.
3
Poison Exon Splicing Regulates a Coordinated Network of SR Protein Expression during Differentiation and Tumorigenesis.
毒蕈碱型乙酰胆碱受体调控网络与阿尔茨海默病的研究进展
Mol Cell. 2020 Nov 19;80(4):648-665.e9. doi: 10.1016/j.molcel.2020.10.019. Epub 2020 Nov 10.
4
Troponin destabilization impairs sarcomere-cytoskeleton interactions in iPSC-derived cardiomyocytes from dilated cardiomyopathy patients.肌钙蛋白不稳定会损害扩张型心肌病患者诱导多能干细胞衍生的心肌细胞中的肌节-细胞骨架相互作用。
Sci Rep. 2020 Jan 14;10(1):209. doi: 10.1038/s41598-019-56597-3.
5
Human Induced Pluripotent Stem-Cell-Derived Cardiomyocytes as Models for Genetic Cardiomyopathies.人诱导多能干细胞衍生心肌细胞作为遗传性心肌病模型。
Int J Mol Sci. 2019 Sep 6;20(18):4381. doi: 10.3390/ijms20184381.
6
Functional Prediction of Chronic Kidney Disease Susceptibility Gene PRKAG2 by Comprehensively Bioinformatics Analysis.通过综合生物信息学分析对慢性肾脏病易感基因PRKAG2进行功能预测
Front Genet. 2018 Dec 3;9:573. doi: 10.3389/fgene.2018.00573. eCollection 2018.
7
Modelling inherited cardiac disease using human induced pluripotent stem cell-derived cardiomyocytes: progress, pitfalls, and potential.利用人诱导多能干细胞衍生的心肌细胞进行遗传性心脏疾病建模:进展、陷阱和潜力。
Cardiovasc Res. 2018 Dec 1;114(14):1828-1842. doi: 10.1093/cvr/cvy208.
8
Genetic Infiltrative Cardiomyopathies.遗传性浸润性心肌病
Heart Fail Clin. 2018 Apr;14(2):215-224. doi: 10.1016/j.hfc.2017.12.003.