• 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

锡兵功能对脊椎动物心脏发育至关重要:通过与锡兵相关基因XNkx2-3和XNkx2-5的显性抑制突变体消除心脏分化。

Tinman function is essential for vertebrate heart development: elimination of cardiac differentiation by dominant inhibitory mutants of the tinman-related genes, XNkx2-3 and XNkx2-5.

作者信息

Grow M W, Krieg P A

机构信息

Department of Zoology, University of Texas at Austin, Austin, Texas, 78712, USA.

出版信息

Dev Biol. 1998 Dec 1;204(1):187-96. doi: 10.1006/dbio.1998.9080.

DOI:10.1006/dbio.1998.9080
PMID:9851852
Abstract

In Drosophila, the tinman gene is absolutely required for development of the dorsal vessel, the insect equivalent of the heart. In vertebrates, the tinman gene is represented by a small family of tinman-related sequences, some of which are expressed during embryonic heart development. At present however, the precise importance of this gene family for vertebrate heart development is unclear. Using the Xenopus embryo, we have employed a dominant inhibitory strategy to interfere with the function of the endogenous tinman-related genes. In these experiments, suppression of tinman gene function can result in the complete elimination of myocardial gene expression and the absence of cell movements associated with embryonic heart development. This inhibition can be rescued by expression of wild-type tinman sequences. These experiments indicate that function of tinman family genes is essential for development of the vertebrate heart.

摘要

在果蝇中,tinman基因对于背血管(相当于昆虫的心脏)的发育是绝对必需的。在脊椎动物中,tinman基因由一小类与tinman相关的序列代表,其中一些在胚胎心脏发育过程中表达。然而目前,这个基因家族对脊椎动物心脏发育的确切重要性尚不清楚。利用非洲爪蟾胚胎,我们采用了显性抑制策略来干扰内源性tinman相关基因的功能。在这些实验中,tinman基因功能的抑制可导致心肌基因表达完全消除,以及与胚胎心脏发育相关的细胞运动缺失。这种抑制可通过野生型tinman序列的表达来挽救。这些实验表明,tinman家族基因的功能对于脊椎动物心脏的发育至关重要。

相似文献

1
Tinman function is essential for vertebrate heart development: elimination of cardiac differentiation by dominant inhibitory mutants of the tinman-related genes, XNkx2-3 and XNkx2-5.锡兵功能对脊椎动物心脏发育至关重要:通过与锡兵相关基因XNkx2-3和XNkx2-5的显性抑制突变体消除心脏分化。
Dev Biol. 1998 Dec 1;204(1):187-96. doi: 10.1006/dbio.1998.9080.
2
Vertebrate tinman homologues XNkx2-3 and XNkx2-5 are required for heart formation in a functionally redundant manner.脊椎动物tinman同源物XNkx2 - 3和XNkx2 - 5以功能冗余的方式参与心脏形成过程。
Development. 1998 Nov;125(22):4439-49. doi: 10.1242/dev.125.22.4439.
3
Transient cardiac expression of the tinman-family homeobox gene, XNkx2-10.
Mech Dev. 2000 Mar 1;91(1-2):369-73. doi: 10.1016/s0925-4773(99)00291-9.
4
A new tinman-related gene, nkx2.7, anticipates the expression of nkx2.5 and nkx2.3 in zebrafish heart and pharyngeal endoderm.一个新的与锡人相关的基因nkx2.7,在斑马鱼心脏和咽内胚层中先于nkx2.5和nkx2.3表达。
Dev Biol. 1996 Dec 15;180(2):722-31. doi: 10.1006/dbio.1996.0341.
5
Vertebrate tinman homologues and cardiac differentiation.脊椎动物tinman同源物与心脏分化
Semin Cell Dev Biol. 1999 Feb;10(1):73-83. doi: 10.1006/scdb.1999.0282.
6
Regulation of the tinman homologues in Xenopus embryos.非洲爪蟾胚胎中心脏特异性转录因子同源物的调控
Dev Biol. 2000 Nov 1;227(1):65-79. doi: 10.1006/dbio.2000.9891.
7
D-mef2 is a target for Tinman activation during Drosophila heart development.在果蝇心脏发育过程中,D-mef2是Tinman激活的一个靶点。
EMBO J. 1997 Feb 3;16(3):515-22. doi: 10.1093/emboj/16.3.515.
8
tinman-related genes expressed during heart development in Xenopus.在非洲爪蟾心脏发育过程中表达的与锡心人相关的基因。
Dev Genet. 1998;22(3):230-8. doi: 10.1002/(SICI)1520-6408(1998)22:3<230::AID-DVG5>3.0.CO;2-7.
9
Reduction of XNkx2-10 expression leads to anterior defects and malformation of the embryonic heart.XNkx2 - 10表达的降低会导致胚胎心脏前部缺陷和畸形。
Mech Dev. 2006 Oct;123(10):719-29. doi: 10.1016/j.mod.2006.07.008. Epub 2006 Jul 26.
10
Differential rescue of visceral and cardiac defects in Drosophila by vertebrate tinman-related genes.脊椎动物tinman相关基因对果蝇内脏和心脏缺陷的差异拯救作用。
Proc Natl Acad Sci U S A. 1998 Aug 4;95(16):9366-71. doi: 10.1073/pnas.95.16.9366.

引用本文的文献

1
NKX2-5 congenital heart disease mutations show diverse loss and gain of epigenomic, biochemical and chromatin search functions underpinning pathogenicity.NKX2 - 5先天性心脏病突变在表观基因组、生化和染色质搜索功能方面呈现出多样的功能丧失和获得,这些功能是致病性的基础。
bioRxiv. 2025 Jun 20:2025.06.20.659510. doi: 10.1101/2025.06.20.659510.
2
Use of Frogs as a Model to Study the Etiology of HLHS.使用青蛙作为研究左心发育不全综合征病因的模型。
J Cardiovasc Dev Dis. 2023 Jan 29;10(2):51. doi: 10.3390/jcdd10020051.
3
Activation of Nkx2.5 transcriptional program is required for adult myocardial repair.
激活 Nkx2.5 转录程序是成年心肌修复所必需的。
Nat Commun. 2022 May 27;13(1):2970. doi: 10.1038/s41467-022-30468-4.
4
Nkx genes establish second heart field cardiomyocyte progenitors at the arterial pole and pattern the venous pole through Isl1 repression.Nkx基因在动脉极建立第二心脏场心肌祖细胞,并通过抑制Isl1来调控静脉极的模式。
Development. 2018 Feb 5;145(3):dev161497. doi: 10.1242/dev.161497.
5
Characterization of human bone morphogenetic protein gene variants for possible roles in congenital heart disease.人类骨形态发生蛋白基因变异体在先天性心脏病中可能作用的特征分析。
Mol Med Rep. 2016 Aug;14(2):1459-64. doi: 10.3892/mmr.2016.5428. Epub 2016 Jun 23.
6
An early requirement for nkx2.5 ensures the first and second heart field ventricular identity and cardiac function into adulthood.nkx2.5的早期需求确保了第一和第二心脏区域的心室特征以及成年期的心脏功能。
Dev Biol. 2015 Apr 1;400(1):10-22. doi: 10.1016/j.ydbio.2014.12.019. Epub 2014 Dec 20.
7
A mouse model of human congenital heart disease: high incidence of diverse cardiac anomalies and ventricular noncompaction produced by heterozygous Nkx2-5 homeodomain missense mutation.一种人类先天性心脏病的小鼠模型:杂合性Nkx2-5同源结构域错义突变导致多种心脏异常和心室致密化不全的高发生率。
Circ Cardiovasc Genet. 2014 Aug;7(4):423-433. doi: 10.1161/CIRCGENETICS.113.000281. Epub 2014 Jul 15.
8
Nkx genes are essential for maintenance of ventricular identity.Nkx 基因对于维持心室身份至关重要。
Development. 2013 Oct;140(20):4203-13. doi: 10.1242/dev.095562. Epub 2013 Sep 11.
9
A recessive mutation resulting in a disabling amino acid substitution (T194R) in the LHX3 homeodomain causes combined pituitary hormone deficiency.一种隐性突变导致 LHX3 同源域中一个失活的氨基酸取代(T194R),从而导致垂体激素联合缺乏。
Horm Res Paediatr. 2012;77(1):41-51. doi: 10.1159/000335929. Epub 2012 Jan 26.
10
Mechanisms of cardiogenesis in cardiovascular progenitor cells.心血管祖细胞中的心脏发生机制。
Int Rev Cell Mol Biol. 2012;293:195-267. doi: 10.1016/B978-0-12-394304-0.00012-9.