• 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
Dystroglycan is not required for maintenance of the luminal epithelial basement membrane or cell polarity in the mouse prostate.肌营养不良蛋白聚糖对于维持小鼠前列腺管腔上皮基底膜或细胞极性不是必需的。
Prostate. 2010 May 15;70(7):777-87. doi: 10.1002/pros.21110.
2
Dystroglycan and perlecan provide a basal cue required for epithelial polarity during energetic stress.在能量应激期间,肌营养不良聚糖和基底膜聚糖为上皮极性提供了所需的基础信号。
Dev Cell. 2009 Jan;16(1):83-92. doi: 10.1016/j.devcel.2008.11.006.
3
Distribution of dystroglycan in normal adult mouse tissues.抗肌萎缩蛋白聚糖在正常成年小鼠组织中的分布。
J Histochem Cytochem. 1998 Apr;46(4):449-57. doi: 10.1177/002215549804600404.
4
Integrin and dystroglycan compensate each other to mediate laminin-dependent basement membrane assembly and epiblast polarization.整合素和肌营养不良蛋白聚糖相互补偿,以介导层粘连蛋白依赖性基底膜组装和外胚层极化。
Matrix Biol. 2017 Jan;57-58:272-284. doi: 10.1016/j.matbio.2016.07.005. Epub 2016 Jul 20.
5
Perlecan and Dystroglycan act at the basal side of the Drosophila follicular epithelium to maintain epithelial organization.基底膜聚糖和肌营养不良聚糖在果蝇卵泡上皮细胞的基底侧发挥作用,以维持上皮组织的结构。
Development. 2006 Oct;133(19):3805-15. doi: 10.1242/dev.02549. Epub 2006 Aug 30.
6
Oriented basement membrane fibrils provide a memory for F-actin planar polarization via the Dystrophin-Dystroglycan complex during tissue elongation.定向基底膜原纤维通过 Dystrophin-Dystroglycan 复合物在组织延伸过程中为 F-actin 平面极化提供记忆。
Development. 2020 Apr 8;147(7):dev186957. doi: 10.1242/dev.186957.
7
The microstructure of laminin-111 compensates for dystroglycan loss in mammary epithelial cells in downstream expression of milk proteins.层粘连蛋白-111 的微观结构补偿了细胞层粘连蛋白-111 在乳蛋白下游表达中对细胞内肌聚糖缺失的补偿作用。
Biomaterials. 2019 Oct;218:119337. doi: 10.1016/j.biomaterials.2019.119337. Epub 2019 Jul 9.
8
Normal and tumor-derived myoepithelial cells differ in their ability to interact with luminal breast epithelial cells for polarity and basement membrane deposition.正常和肿瘤来源的肌上皮细胞在与管腔型乳腺上皮细胞相互作用以形成极性和基底膜沉积方面存在差异。
J Cell Sci. 2002 Jan 1;115(Pt 1):39-50. doi: 10.1242/jcs.115.1.39.
9
Reduced expression of dystroglycan in breast and prostate cancer.乳腺和前列腺癌中肌营养不良聚糖表达降低。
Hum Pathol. 2001 Aug;32(8):791-5. doi: 10.1053/hupa.2001.26468.
10
Intracellular polarity protein PAR-1 regulates extracellular laminin assembly by regulating the dystroglycan complex.细胞内极性蛋白PAR-1通过调节肌营养不良蛋白聚糖复合物来调控细胞外层粘连蛋白的组装。
Genes Cells. 2009 Jul;14(7):835-50. doi: 10.1111/j.1365-2443.2009.01315.x. Epub 2009 Jun 22.

引用本文的文献

1
Involvement of abnormal dystroglycan expression and matriglycan levels in cancer pathogenesis.异常的肌营养不良聚糖表达和基质聚糖水平在癌症发病机制中的作用。
Cancer Cell Int. 2022 Dec 9;22(1):395. doi: 10.1186/s12935-022-02812-7.
2
The microstructure of laminin-111 compensates for dystroglycan loss in mammary epithelial cells in downstream expression of milk proteins.层粘连蛋白-111 的微观结构补偿了细胞层粘连蛋白-111 在乳蛋白下游表达中对细胞内肌聚糖缺失的补偿作用。
Biomaterials. 2019 Oct;218:119337. doi: 10.1016/j.biomaterials.2019.119337. Epub 2019 Jul 9.
3
Integrins and epithelial cell polarity.整合素与上皮细胞极性。
J Cell Sci. 2014 Aug 1;127(Pt 15):3217-25. doi: 10.1242/jcs.146142. Epub 2014 Jul 2.
4
Loss of LARGE2 disrupts functional glycosylation of α-dystroglycan in prostate cancer.LARGE2 的缺失破坏了前列腺癌中 α- dystroglycan 的功能糖基化。
J Biol Chem. 2013 Jan 25;288(4):2132-42. doi: 10.1074/jbc.M112.432807. Epub 2012 Dec 6.
5
Slow disease progression in a C57BL/6 pten-deficient mouse model of prostate cancer.前列腺癌 C57BL/6 ptendeficient 小鼠模型中疾病进展缓慢。
Am J Pathol. 2011 Jul;179(1):502-12. doi: 10.1016/j.ajpath.2011.03.014. Epub 2011 May 7.
6
Dystroglycan controls signaling of multiple hormones through modulation of STAT5 activity.肌营养不良聚糖通过调节 STAT5 活性来控制多种激素的信号转导。
J Cell Sci. 2010 Nov 1;123(Pt 21):3683-92. doi: 10.1242/jcs.070680. Epub 2010 Oct 12.

本文引用的文献

1
A luminal epithelial stem cell that is a cell of origin for prostate cancer.一种作为前列腺癌起源细胞的管腔上皮干细胞。
Nature. 2009 Sep 24;461(7263):495-500. doi: 10.1038/nature08361. Epub 2009 Sep 9.
2
Dystroglycan and perlecan provide a basal cue required for epithelial polarity during energetic stress.在能量应激期间,肌营养不良聚糖和基底膜聚糖为上皮极性提供了所需的基础信号。
Dev Cell. 2009 Jan;16(1):83-92. doi: 10.1016/j.devcel.2008.11.006.
3
Brain and eye malformations resembling Walker-Warburg syndrome are recapitulated in mice by dystroglycan deletion in the epiblast.通过在小鼠上胚层中缺失肌营养不良聚糖,可重现出类似于沃克-沃尔堡综合征的脑和眼畸形。
J Neurosci. 2008 Oct 15;28(42):10567-75. doi: 10.1523/JNEUROSCI.2457-08.2008.
4
Laminin alpha 5 influences the architecture of the mouse small intestine mucosa.层粘连蛋白α5影响小鼠小肠黏膜的结构。
J Cell Sci. 2008 Aug 1;121(Pt 15):2493-502. doi: 10.1242/jcs.025528. Epub 2008 Jul 15.
5
Dystroglycan expression is reduced during prostate tumorigenesis and is regulated by androgens in prostate cancer cells.在前列腺肿瘤发生过程中,肌营养不良聚糖表达降低,且在前列腺癌细胞中受雄激素调控。
J Cell Physiol. 2007 Nov;213(2):528-39. doi: 10.1002/jcp.21130.
6
Dystroglycan loss disrupts polarity and beta-casein induction in mammary epithelial cells by perturbing laminin anchoring.肌营养不良聚糖缺失通过扰乱层粘连蛋白锚定,破坏乳腺上皮细胞的极性并抑制β-酪蛋白的诱导。
J Cell Sci. 2006 Oct 1;119(Pt 19):4047-58. doi: 10.1242/jcs.03103. Epub 2006 Sep 12.
7
Perlecan and Dystroglycan act at the basal side of the Drosophila follicular epithelium to maintain epithelial organization.基底膜聚糖和肌营养不良聚糖在果蝇卵泡上皮细胞的基底侧发挥作用,以维持上皮组织的结构。
Development. 2006 Oct;133(19):3805-15. doi: 10.1242/dev.02549. Epub 2006 Aug 30.
8
Proximal prostatic stem cells are programmed to regenerate a proximal-distal ductal axis.前列腺近端干细胞被编程以再生近端-远端导管轴。
Stem Cells. 2006 Aug;24(8):1859-68. doi: 10.1634/stemcells.2005-0585. Epub 2006 Apr 27.
9
C. elegans dystroglycan DGN-1 functions in epithelia and neurons, but not muscle, and independently of dystrophin.秀丽隐杆线虫的肌营养不良聚糖DGN-1在上皮细胞和神经元中发挥作用,但在肌肉中不发挥作用,且其作用独立于肌营养不良蛋白。
Development. 2006 May;133(10):1911-21. doi: 10.1242/dev.02363. Epub 2006 Apr 12.
10
Disruption of perlecan binding and matrix assembly by post-translational or genetic disruption of dystroglycan function.通过翻译后修饰或基因手段破坏肌营养不良蛋白聚糖功能,导致基底膜聚糖结合及基质组装受损。
FEBS Lett. 2005 Aug 29;579(21):4792-6. doi: 10.1016/j.febslet.2005.07.059.

肌营养不良蛋白聚糖对于维持小鼠前列腺管腔上皮基底膜或细胞极性不是必需的。

Dystroglycan is not required for maintenance of the luminal epithelial basement membrane or cell polarity in the mouse prostate.

机构信息

Department of Molecular Physiology and Biophysics, Roy J. and Lucille A. Carver College of Medicine, Holden Comprehensive Cancer Center, The University of Iowa, Iowa City, Iowa, USA.

出版信息

Prostate. 2010 May 15;70(7):777-87. doi: 10.1002/pros.21110.

DOI:10.1002/pros.21110
PMID:20054819
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2857647/
Abstract

BACKGROUND

Dystroglycan is a cell-surface receptor for extracellular matrix proteins including laminins and perlecan. Prior studies have shown its involvement in assembly and/or maintenance of basement membrane structures, cell polarity and tissue morphogenesis; and its expression is often reduced in prostate and other cancers. However, the role of dystroglycan in normal epithelial tissues such as the prostate is unclear.

METHODS

To investigate this, we disrupted dystroglycan expression in the prostate via a conditional gene targeting strategy utilizing Cre recombinase expressed in luminal prostate epithelial cells.

RESULTS

Contrary to expectations, deletion of dystroglycan in luminal epithelial cells resulted in no discernable phenotype as judged by histology, basement membrane ultrastructure, localization of dystroglycan ligands, cell polarity or regenerative capacity of the prostate following castration. Dystroglycan expression remains in keratin-5-positive basal cells located in the proximal ducts where dystroglycan expression is elevated in regenerating prostates.

CONCLUSIONS

Our results show that dystroglycan in luminal epithelial cells is not required for the maintenance of basement membranes, cell polarity or prostate regeneration. However, it is possible that persistent dystroglycan expression in the basal cell compartment may support these or other functions.

摘要

背景

层粘连蛋白和 Perlecan 等细胞外基质蛋白的细胞表面受体是 dystroglycan。先前的研究表明它参与了基底膜结构、细胞极性和组织形态发生的组装和/或维持;其表达在前列腺癌和其他癌症中常常降低。然而,dystroglycan 在前列腺等正常上皮组织中的作用尚不清楚。

方法

为了研究这一点,我们利用在腔上皮细胞中表达的 Cre 重组酶,通过条件性基因靶向策略破坏前列腺中的 dystroglycan 表达。

结果

出乎意料的是,腔上皮细胞中 dystroglycan 的缺失并没有导致组织学、基底膜超微结构、dystroglycan 配体的定位、细胞极性或去势后前列腺的再生能力的可察觉表型。dystroglycan 的表达仍然存在于位于近端导管中的角蛋白 5 阳性基底细胞中,在再生的前列腺中,dystroglycan 的表达升高。

结论

我们的结果表明,腔上皮细胞中的 dystroglycan 对于维持基底膜、细胞极性或前列腺再生不是必需的。然而,基底细胞隔室中持续的 dystroglycan 表达可能支持这些或其他功能。