• 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

相似文献

1
Sm22α transcription occurs at the early onset of the cardiovascular system and the intron 1 is dispensable for its transcription in smooth muscle cells during mouse development.Sm22α转录发生在心血管系统发育早期,在小鼠发育过程中,内含子1对于其在平滑肌细胞中的转录并非必需。
Int J Physiol Pathophysiol Pharmacol. 2010;2(1):12-9. Epub 2009 Nov 22.
2
Analysis of SM22alpha-deficient mice reveals unanticipated insights into smooth muscle cell differentiation and function.对SM22α基因敲除小鼠的分析揭示了平滑肌细胞分化和功能方面意想不到的见解。
Mol Cell Biol. 2001 Feb;21(4):1336-44. doi: 10.1128/MCB.2001.21.4.1336-1344.2001.
3
Smooth muscle--specific expression of CYP4A1 induces endothelial sprouting in renal arterial microvessels.细胞色素P450 4A1(CYP4A1)在平滑肌中的特异性表达可诱导肾动脉微血管内皮细胞出芽。
Circ Res. 2004 Feb 6;94(2):167-74. doi: 10.1161/01.RES.0000111523.12842.FC. Epub 2003 Dec 11.
4
SM22α suppresses cytokine-induced inflammation and the transcription of NF-κB inducing kinase (Nik) by modulating SRF transcriptional activity in vascular smooth muscle cells.SM22α通过调节血管平滑肌细胞中血清反应因子(SRF)的转录活性,抑制细胞因子诱导的炎症反应以及NF-κB诱导激酶(Nik)的转录。
PLoS One. 2017 Dec 28;12(12):e0190191. doi: 10.1371/journal.pone.0190191. eCollection 2017.
5
Evidence for serum response factor-mediated regulatory networks governing SM22alpha transcription in smooth, skeletal, and cardiac muscle cells.血清反应因子介导的调控网络在平滑肌、骨骼肌和心肌细胞中调控SM22α转录的证据。
Dev Biol. 1997 Jul 15;187(2):311-21. doi: 10.1006/dbio.1997.8621.
6
Arterial injury promotes medial chondrogenesis in Sm22 knockout mice.动脉损伤促进 Sm22 敲除小鼠的中膜软骨形成。
Cardiovasc Res. 2011 Apr 1;90(1):28-37. doi: 10.1093/cvr/cvq378. Epub 2010 Dec 22.
7
A serum response factor-dependent transcriptional regulatory program identifies distinct smooth muscle cell sublineages.一种血清反应因子依赖性转录调控程序可识别不同的平滑肌细胞亚系。
Mol Cell Biol. 1997 Apr;17(4):2266-78. doi: 10.1128/MCB.17.4.2266.
8
Human SM22 alpha BAC encompasses regulatory sequences for expression in vascular and visceral smooth muscles at fetal and adult stages.
Am J Physiol Heart Circ Physiol. 2003 Apr;284(4):H1398-407. doi: 10.1152/ajpheart.00737.2002. Epub 2003 Jan 9.
9
SM22 alpha, a marker of adult smooth muscle, is expressed in multiple myogenic lineages during embryogenesis.SM22α是一种成人平滑肌标志物,在胚胎发育过程中在多个肌源性谱系中表达。
Circ Res. 1996 Feb;78(2):188-95. doi: 10.1161/01.res.78.2.188.
10
A critical developmental role for tgfbr2 in myogenic cell lineages is revealed in mice expressing SM22-Cre, not SMMHC-Cre.在表达SM22-Cre而非SMMHC-Cre的小鼠中,揭示了tgfbr2在生肌细胞谱系中的关键发育作用。
J Mol Cell Cardiol. 2006 Oct;41(4):724-31. doi: 10.1016/j.yjmcc.2006.06.067. Epub 2006 Aug 2.

引用本文的文献

1
TGFβ1 Regulates Cellular Composition of In Vitro Cardiac Perivascular Niche Based on Cardiospheres.TGFβ1 根据心脏球状体调节体外心脏血管周龛细胞组成。
Bull Exp Biol Med. 2024 May;177(1):115-123. doi: 10.1007/s10517-024-06142-8. Epub 2024 Jul 4.
2
SM22α deficiency: promoting vascular fibrosis via SRF-SMAD3-mediated activation of transcription following arterial injury.平滑肌22α缺乏:通过血清反应因子-信号转导和转录激活因子3介导的动脉损伤后转录激活促进血管纤维化。
Res Sq. 2024 Feb 27:rs.3.rs-3941602. doi: 10.21203/rs.3.rs-3941602/v1.
3
Deletion of SM22α disrupts the structure and function of caveolae and T-tubules in cardiomyocytes, contributing to heart failure.SM22α 的缺失破坏了心肌细胞中 caveolae 和 T-tubules 的结构和功能,导致心力衰竭。
PLoS One. 2022 Jul 18;17(7):e0271578. doi: 10.1371/journal.pone.0271578. eCollection 2022.
4
Multiple genotype-phenotype association study reveals intronic variant pair on SIDT2 associated with metabolic syndrome in a Korean population.多基因型-表型关联研究揭示 SIDT2 内含子变异对与韩国人群代谢综合征的关联。
Hum Genomics. 2018 Nov 1;12(1):48. doi: 10.1186/s40246-018-0180-4.
5
SM22α suppresses cytokine-induced inflammation and the transcription of NF-κB inducing kinase (Nik) by modulating SRF transcriptional activity in vascular smooth muscle cells.SM22α通过调节血管平滑肌细胞中血清反应因子(SRF)的转录活性,抑制细胞因子诱导的炎症反应以及NF-κB诱导激酶(Nik)的转录。
PLoS One. 2017 Dec 28;12(12):e0190191. doi: 10.1371/journal.pone.0190191. eCollection 2017.
6
Insulin-independent GLUT4 translocation in proliferative vascular smooth muscle cells involves SM22α.增殖性血管平滑肌细胞中不依赖胰岛素的葡萄糖转运蛋白4转位涉及SM22α。
J Mol Med (Berl). 2017 Feb;95(2):181-192. doi: 10.1007/s00109-016-1468-2. Epub 2016 Sep 8.
7
Systematic selection of small molecules to promote differentiation of embryonic stem cells and experimental validation for generating cardiomyocytes.用于促进胚胎干细胞分化并生成心肌细胞的小分子的系统筛选及实验验证。
Cell Death Discov. 2016 Feb 8;2:16007. doi: 10.1038/cddiscovery.2016.7. eCollection 2016.
8
α5 and αv integrins cooperate to regulate vascular smooth muscle and neural crest functions in vivo.α5和αv整合素在体内协同调节血管平滑肌和神经嵴功能。
Development. 2015 Feb 15;142(4):797-808. doi: 10.1242/dev.117572.
9
The murine allantois: a model system for the study of blood vessel formation.鼠类尿囊:血管生成研究的模型系统。
Blood. 2012 Sep 27;120(13):2562-72. doi: 10.1182/blood-2012-03-390070. Epub 2012 Jul 31.
10
Construction of vascular tissues with macro-porous nano-fibrous scaffolds and smooth muscle cells enriched from differentiated embryonic stem cells.构建具有大孔纳米纤维支架的血管组织和从分化的胚胎干细胞中富集的平滑肌细胞。
PLoS One. 2012;7(4):e35580. doi: 10.1371/journal.pone.0035580. Epub 2012 Apr 24.

本文引用的文献

1
Landmarks and lineages in the developing heart.发育中心脏的标志性结构和细胞谱系。
Circ Res. 2009 Jun 5;104(11):1235-7. doi: 10.1161/CIRCRESAHA.109.199729.
2
Actin cytoskeletal dynamics in smooth muscle: a new paradigm for the regulation of smooth muscle contraction.平滑肌中的肌动蛋白细胞骨架动力学:平滑肌收缩调节的新范式
Am J Physiol Cell Physiol. 2008 Sep;295(3):C576-87. doi: 10.1152/ajpcell.00253.2008. Epub 2008 Jul 2.
3
Transgelin: an actin-binding protein and tumour suppressor.转胶蛋白:一种肌动蛋白结合蛋白和肿瘤抑制因子。
Int J Biochem Cell Biol. 2009 Mar;41(3):482-6. doi: 10.1016/j.biocel.2008.02.011. Epub 2008 Mar 10.
4
Physiologic properties and regulation of the actin cytoskeleton in vascular smooth muscle.血管平滑肌中肌动蛋白细胞骨架的生理特性与调控
J Cardiovasc Pharmacol Ther. 2008 Jun;13(2):130-40. doi: 10.1177/1074248407313737. Epub 2008 Jan 22.
5
SM22alpha is required for agonist-induced regulation of contractility: evidence from SM22alpha knockout mice.SM22α是激动剂诱导的收缩性调节所必需的:来自SM22α基因敲除小鼠的证据。
Mol Cells. 2007 Apr 30;23(2):175-81.
6
Multiple repressor pathways contribute to phenotypic switching of vascular smooth muscle cells.多种阻遏物途径促成血管平滑肌细胞的表型转换。
Am J Physiol Cell Physiol. 2007 Jan;292(1):C59-69. doi: 10.1152/ajpcell.00394.2006. Epub 2006 Sep 6.
7
Building the mammalian heart from two sources of myocardial cells.利用两种心肌细胞来源构建哺乳动物心脏。
Nat Rev Genet. 2005 Nov;6(11):826-35. doi: 10.1038/nrg1710.
8
Myocardin enhances Smad3-mediated transforming growth factor-beta1 signaling in a CArG box-independent manner: Smad-binding element is an important cis element for SM22alpha transcription in vivo.心肌素以不依赖CArG盒的方式增强Smad3介导的转化生长因子-β1信号传导:Smad结合元件是体内SM22α转录的重要顺式元件。
Circ Res. 2005 Nov 11;97(10):983-91. doi: 10.1161/01.RES.0000190604.90049.71. Epub 2005 Oct 13.
9
5' CArG degeneracy in smooth muscle alpha-actin is required for injury-induced gene suppression in vivo.平滑肌α-肌动蛋白中的5' CArG简并性是体内损伤诱导基因抑制所必需的。
J Clin Invest. 2005 Feb;115(2):418-27. doi: 10.1172/JCI22648.
10
SM22alpha modulates vascular smooth muscle cell phenotype during atherogenesis.SM22α在动脉粥样硬化形成过程中调节血管平滑肌细胞表型。
Circ Res. 2004 Apr 16;94(7):863-5. doi: 10.1161/01.RES.0000126417.38728.F6. Epub 2004 Mar 25.

Sm22α转录发生在心血管系统发育早期,在小鼠发育过程中,内含子1对于其在平滑肌细胞中的转录并非必需。

Sm22α transcription occurs at the early onset of the cardiovascular system and the intron 1 is dispensable for its transcription in smooth muscle cells during mouse development.

作者信息

Yang Maozhou, Jiang Hong, Li Li

出版信息

Int J Physiol Pathophysiol Pharmacol. 2010;2(1):12-9. Epub 2009 Nov 22.

PMID:20428474
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2860299/
Abstract

SM22α, also known as SM22, has been widely used as a smooth muscle cell (SMC) marker and is known to be expressed in the embryonic heart. The intron 1 of Sm22 contains multiple important and evolutionarily conserved regulatory elements. To determine the role of the intron 1 in Sm22 transcriptional regulation and the function of SM22 during development, we generated a Sm22 knockout mouse by replacing the intron 1 and the translation initiation with a nuclear localized LacZ (nLacZ) reporter. The resulting Sm22 knockout mice (Sm22(-)/(-)) were viable and fertile without any apparent developmental defects. Using X-gal staining assay, we found that Sm22 transcription was detectable in the chorion formation region and in the heart field before formation of the heart tube at E7.5, namely much earlier than the looped heart stage where it had been previously reported. The expression of lacZ progressively expanded throughout the heart tube by E8.5. LacZ was transiently expressed in the heart and somites and then became restricted to the vascular and visceral SMC organs. These results indicate that SM22 is not required for mouse basal homeostatic function and that the intron 1 is dispensable for Sm22 transcription during development. Given the importance of vasculature in organogenesis and in diseases, this mouse line may be a valuable tool to trace the development and pathology of the cardiovascular system.

摘要

SM22α,也被称为SM22,已被广泛用作平滑肌细胞(SMC)标志物,并且已知在胚胎心脏中表达。Sm22的内含子1包含多个重要且在进化上保守的调控元件。为了确定内含子1在Sm22转录调控中的作用以及SM22在发育过程中的功能,我们通过用核定位的LacZ(nLacZ)报告基因替换内含子1和翻译起始位点,构建了一只Sm22基因敲除小鼠。所得到的Sm22基因敲除小鼠(Sm22(-)/(-))能够存活且可育,没有任何明显的发育缺陷。通过X-gal染色分析,我们发现在胚胎第7.5天心脏管形成之前,在绒毛膜形成区域和心脏场中可检测到Sm22转录,即比之前报道的环状心脏阶段要早得多。到胚胎第8.5天时,lacZ的表达在整个心脏管中逐渐扩展。LacZ在心脏和体节中短暂表达,然后局限于血管和内脏SMC器官。这些结果表明,SM22对于小鼠基础稳态功能并非必需,并且内含子1在发育过程中对于Sm22转录是可有可无的。鉴于脉管系统在器官发生和疾病中的重要性,该小鼠品系可能是追踪心血管系统发育和病理学的一个有价值的工具。