• 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

杜兴氏肌营养不良基因在培养的肌肉细胞中的表达。

Expression of the Duchenne's muscular dystrophy gene in cultured muscle cells.

作者信息

Lev A A, Feener C C, Kunkel L M, Brown R H

机构信息

Day Neuromuscular Research Center, Massachusetts General Hospital, Boston 02114.

出版信息

J Biol Chem. 1987 Nov 25;262(33):15817-20.

PMID:3680227
Abstract

A partial cDNA clone for the Duchenne's muscular dystrophy (DMD) locus was used to investigate the expression of this locus in human muscle in vitro. Hybridization to a 14-kilobase RNA transcript was demonstrated in both fetal and mature human skeletal muscle and four lines of human muscle cells in culture. The DMD transcript was not detected in cultured cells outside the muscle lineage. In cultured muscle cells, gene expression was evident only in myotubes both before and after innervation with mouse spinal cord. Primary cultures of human myoblasts did not show the presence of the DMD transcript prior to fusion to form myotubes. An in vitro model is potentially an excellent system in which to investigate factors controlling expression of the DMD gene in normal muscle and how this expression is altered in cultured DMD muscle.

摘要

利用杜兴氏肌营养不良(DMD)基因座的部分cDNA克隆,在体外研究该基因座在人肌肉中的表达。在胎儿和成熟的人骨骼肌以及四种培养的人肌肉细胞系中,均证实了与14千碱基RNA转录本的杂交。在肌肉谱系以外的培养细胞中未检测到DMD转录本。在培养的肌肉细胞中,仅在小鼠脊髓支配前后的肌管中基因表达明显。人成肌细胞的原代培养物在融合形成肌管之前未显示DMD转录本的存在。体外模型可能是一个极好的系统,可用于研究控制正常肌肉中DMD基因表达的因素,以及在培养的DMD肌肉中这种表达是如何改变的。

相似文献

1
Expression of the Duchenne's muscular dystrophy gene in cultured muscle cells.杜兴氏肌营养不良基因在培养的肌肉细胞中的表达。
J Biol Chem. 1987 Nov 25;262(33):15817-20.
2
Duchenne muscular dystrophy gene expression in normal and diseased human muscle.
Science. 1988 Mar 18;239(4846):1418-20. doi: 10.1126/science.2450401.
3
Analysis of dystrophin expression after activation of myogenesis in amniocytes, chorionic-villus cells, and fibroblasts. A new method for diagnosing Duchenne's muscular dystrophy.羊膜细胞、绒毛膜绒毛细胞和成纤维细胞中肌生成激活后肌营养不良蛋白表达的分析。一种诊断杜氏肌营养不良症的新方法。
N Engl J Med. 1993 Sep 23;329(13):915-20. doi: 10.1056/NEJM199309233291303.
4
Ultrastructure of muscle in fetal Duchenne's dystrophy.
Arch Pathol Lab Med. 1981 Aug;105(8):414-8.
5
Na(+)/Ca(2+) exchange in human myotubes: intracellular calcium rises in response to external sodium depletion are enhanced in DMD.人肌管中的钠/钙交换:杜氏肌营养不良症(DMD)患者中,细胞内钙因外部钠耗竭而升高的情况会增强。
Neuromuscul Disord. 2002 Oct;12(7-8):665-73. doi: 10.1016/s0960-8966(02)00022-6.
6
Dystrophin negative skeletal and myocardial muscle cells in a carrier of Duchenne's muscular dystrophy.杜氏肌营养不良症携带者中抗肌萎缩蛋白阴性的骨骼肌和心肌细胞
Eur Heart J. 1993 Jul;14(7):989-92. doi: 10.1093/eurheartj/14.7.989.
7
Myoblast transfer in the treatment of Duchenne's muscular dystrophy.成肌细胞移植治疗杜氏肌营养不良症。
N Engl J Med. 1995 Sep 28;333(13):832-8. doi: 10.1056/NEJM199509283331303.
8
Expression of the putative Duchenne muscular dystrophy gene in differentiated myogenic cell cultures and in the brain.假定的杜兴氏肌营养不良基因在分化的成肌细胞培养物和大脑中的表达。
Nature. 1988 Feb 18;331(6157):635-8. doi: 10.1038/331635a0.
9
Mosaic expression of dystrophin in symptomatic carriers of Duchenne's muscular dystrophy.杜兴氏肌营养不良症有症状携带者中抗肌萎缩蛋白的镶嵌表达。
N Engl J Med. 1989 Jan 19;320(3):138-42. doi: 10.1056/NEJM198901193200302.
10
Defective myoblasts identified in Duchenne muscular dystrophy.在杜兴氏肌肉营养不良症中发现的有缺陷的成肌细胞。
Proc Natl Acad Sci U S A. 1983 Aug;80(15):4856-60. doi: 10.1073/pnas.80.15.4856.

引用本文的文献

1
Tetraploidization of Immortalized Myoblasts Induced by Cell Fusion Drives Myogenic Sarcoma Development with Deletion.细胞融合诱导的永生化成肌细胞四倍体化驱动伴有缺失的成肌肉瘤发展。
Cancers (Basel). 2020 May 19;12(5):1281. doi: 10.3390/cancers12051281.
2
Bioinspired Three-Dimensional Human Neuromuscular Junction Development in Suspended Hydrogel Arrays.悬浮水凝胶阵列中仿生三维人类神经肌肉接头的发育。
Tissue Eng Part C Methods. 2018 Jun;24(6):346-359. doi: 10.1089/ten.TEC.2018.0062.
3
Intracellular Distribution and Nuclear Activity of Antisense Oligonucleotides After Unassisted Uptake in Myoblasts and Differentiated Myotubes In Vitro.
体外成肌细胞和分化肌管中反义寡核苷酸在非辅助摄取后的细胞内分布及核活性
Nucleic Acid Ther. 2017 Jun;27(3):144-158. doi: 10.1089/nat.2016.0641. Epub 2017 Apr 4.
4
Isolation of nuclei from skeletal muscle satellite cells and myofibers for use in chromatin immunoprecipitation assays.从骨骼肌卫星细胞和肌纤维中分离细胞核用于染色质免疫沉淀分析。
Methods Mol Biol. 2012;798:517-30. doi: 10.1007/978-1-61779-343-1_31.
5
A muscle-specific enhancer within intron 1 of the human dystrophin gene is functionally dependent on single MEF-1/E box and MEF-2/AT-rich sequence motifs.人类肌营养不良蛋白基因第1内含子中的一个肌肉特异性增强子在功能上依赖于单个MEF-1/E盒和MEF-2/富含AT序列基序。
Nucleic Acids Res. 1997 Apr 15;25(8):1618-25. doi: 10.1093/nar/25.8.1618.
6
A role for the dystrophin-glycoprotein complex as a transmembrane linker between laminin and actin.肌营养不良蛋白-糖蛋白复合物作为层粘连蛋白与肌动蛋白之间跨膜连接物的作用。
J Cell Biol. 1993 Aug;122(4):809-23. doi: 10.1083/jcb.122.4.809.
7
Mechanosensitive ion channels in skeletal muscle from normal and dystrophic mice.正常小鼠和营养不良小鼠骨骼肌中的机械敏感离子通道
J Physiol. 1994 Dec 1;481 ( Pt 2)(Pt 2):299-309. doi: 10.1113/jphysiol.1994.sp020440.
8
Successful histocompatible myoblast transplantation in dystrophin-deficient mdx mouse despite the production of antibodies against dystrophin.尽管产生了抗肌营养不良蛋白的抗体,但在肌营养不良蛋白缺陷的mdx小鼠中成功进行了组织相容性成肌细胞移植。
J Cell Biol. 1995 Nov;131(4):975-88. doi: 10.1083/jcb.131.4.975.
9
On the nature of the Duchenne muscular dystrophy locus: a portion of a complex of related gene clusters of recent pseudoautosomal origin?关于杜兴氏肌营养不良基因座的性质:它是近期假常染色体起源的相关基因簇复合体的一部分吗?
Mol Cell Biochem. 1988 Jun;81(2):103-19. doi: 10.1007/BF00219313.
10
Immunocytochemical study of dystrophin in muscle cultures from patients with Duchenne muscular dystrophy and unaffected control patients.对杜氏肌营养不良症患者和未受影响的对照患者的肌肉培养物中肌营养不良蛋白进行免疫细胞化学研究。
Am J Pathol. 1988 Sep;132(3):410-6.