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本文引用的文献

1
Tenascin-W: an extracellular matrix protein associated with osteogenesis and cancer.Tenascin-W:一种与成骨和癌症相关的细胞外基质蛋白。
Int J Biochem Cell Biol. 2010 Sep;42(9):1412-5. doi: 10.1016/j.biocel.2010.06.004. Epub 2010 Jun 9.
2
14-3-3Tau regulates Beclin 1 and is required for autophagy.14-3-3Tau 调控 Beclin 1 并对自噬起作用。
PLoS One. 2010 Apr 29;5(4):e10409. doi: 10.1371/journal.pone.0010409.
3
Improved reversal learning and working memory and enhanced reactivity to novelty in mice with enhanced GABAergic innervation in the dentate gyrus.增强齿状回 GABA 能传入的小鼠表现出更好的反转学习和工作记忆能力,以及对新奇事物更强的反应性。
Cereb Cortex. 2010 Nov;20(11):2712-27. doi: 10.1093/cercor/bhq017. Epub 2010 Mar 1.
4
Transcriptional regulation of the endogenous danger signal tenascin-C: a novel autocrine loop in inflammation.内源性危险信号 tenascin-C 的转录调控:炎症中的新型自分泌环。
J Immunol. 2010 Mar 1;184(5):2655-62. doi: 10.4049/jimmunol.0903359. Epub 2010 Jan 27.
5
Tenascin-C may aggravate left ventricular remodeling and function after myocardial infarction in mice.纤连蛋白-C 可能会加重心肌梗死后小鼠的左心室重构和功能障碍。
Am J Physiol Heart Circ Physiol. 2010 Mar;298(3):H1072-8. doi: 10.1152/ajpheart.00255.2009. Epub 2010 Jan 15.
6
Tenascin-W is a specific marker of glioma-associated blood vessels and stimulates angiogenesis in vitro.Tenascin-W 是神经胶质瘤相关血管的特异性标志物,并能在体外刺激血管生成。
FASEB J. 2010 Mar;24(3):778-87. doi: 10.1096/fj.09-140491. Epub 2009 Nov 2.
7
Matrix metalloproteinase-19 deficiency promotes tenascin-C accumulation and allergen-induced airway inflammation.基质金属蛋白酶-19 缺乏促进 tenascin-C 积累和变应原诱导的气道炎症。
Am J Respir Cell Mol Biol. 2010 Sep;43(3):286-95. doi: 10.1165/rcmb.2008-0426OC. Epub 2009 Oct 20.
8
The role of tenascin-C in tissue injury and tumorigenesis.细胞外基质蛋白 tenascin-C 在组织损伤和肿瘤发生中的作用。
J Cell Commun Signal. 2009 Dec;3(3-4):287-310. doi: 10.1007/s12079-009-0075-1. Epub 2009 Oct 17.
9
Tenascin-X induces cell detachment through p38 mitogen-activated protein kinase activation.Tenascin-X 通过激活 p38 丝裂原活化蛋白激酶诱导细胞脱落。
Biol Pharm Bull. 2009 Oct;32(10):1795-9. doi: 10.1248/bpb.32.1795.
10
Accelerated closure of skin wounds in mice deficient in the homeobox gene Msx2.缺乏同源框基因Msx2的小鼠皮肤伤口愈合加速。
Wound Repair Regen. 2009 Sep-Oct;17(5):639-48. doi: 10.1111/j.1524-475X.2009.00535.x.

细胞外基质蛋白 tenascins 及其在黏附调控中的重要性。

Tenascins and the importance of adhesion modulation.

机构信息

Friedrich Miescher Institute for Biomedical Research, Novartis Research Foundation, Basel, Switzerland.

出版信息

Cold Spring Harb Perspect Biol. 2011 May 1;3(5):a004960. doi: 10.1101/cshperspect.a004960.

DOI:10.1101/cshperspect.a004960
PMID:21441591
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3101840/
Abstract

Tenascins are a family of extracellular matrix proteins that evolved in early chordates. There are four family members: tenascin-X, tenascin-R, tenascin-W, and tenascin-C. Tenascin-X associates with type I collagen, and its absence can cause Ehlers-Danlos Syndrome. In contrast, tenascin-R is concentrated in perineuronal nets. The expression of tenascin-C and tenascin-W is developmentally regulated, and both are expressed during disease (e.g., both are associated with cancer stroma and tumor blood vessels). In addition, tenascin-C is highly induced by infections and inflammation. Accordingly, the tenascin-C knockout mouse has a reduced inflammatory response. All tenascins have the potential to modify cell adhesion either directly or through interaction with fibronectin, and cell-tenascin interactions typically lead to increased cell motility. In the case of tenascin-C, there is a correlation between elevated expression and increased metastasis in several types of tumors.

摘要

纤连蛋白是一类在早期脊索动物中进化而来的细胞外基质蛋白。有四个家族成员: tenascin-X、tenascin-R、tenascin-W 和 tenascin-C。tenascin-X 与 I 型胶原结合,其缺失可导致埃勒斯-当洛斯综合征。相比之下,tenascin-R 集中在神经周围网中。tenascin-C 和 tenascin-W 的表达受发育调控,并且在疾病期间表达(例如,两者都与癌症基质和肿瘤血管相关)。此外,tenascin-C 可被感染和炎症高度诱导。相应地,tenascin-C 敲除小鼠的炎症反应减少。所有纤连蛋白都有可能通过与纤维连接蛋白的直接或间接相互作用来改变细胞黏附,并且细胞纤连蛋白相互作用通常导致细胞迁移增加。在 tenascin-C 的情况下,在几种类型的肿瘤中,高表达与转移增加之间存在相关性。