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J Exp Med. 1974 Dec 1;140(6):1522-33. doi: 10.1084/jem.140.6.1522.
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Fibroblast surface antigen (SF): the external glycoprotein lost in proteolytic stimulation and maligant transfromation.成纤维细胞表面抗原(SF):在蛋白水解刺激和恶性转化过程中丢失的细胞外糖蛋白。
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Fibroblast surface antigen (SF): molecular properties, distribution in vitro and in vivo, and altered expression in transformed cells.成纤维细胞表面抗原(SF):分子特性、体内外分布以及在转化细胞中的表达改变
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Chemical coupling of proteins to agarose.蛋白质与琼脂糖的化学偶联。
Nature. 1967 Sep 30;215(5109):1491-2. doi: 10.1038/2151491a0.
2
A scanning electron microscope study of cell surface and cell contacts of "spontaneouslyk" transformed cells in vitro.体外“自发”转化细胞的细胞表面和细胞接触的扫描电子显微镜研究。
Eur J Cancer (1965). 1970 Jun;6(3):235-9. doi: 10.1016/0014-2964(70)90026-5.
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Release from density dependent growth inhibition by proteolytic enzymes.通过蛋白水解酶从密度依赖性生长抑制中释放出来。
Nature. 1970 Aug 22;227(5260):843-5. doi: 10.1038/227843a0.
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Surface extensions on BHK cells grown in monolayers and agar supension.单层培养和琼脂悬浮培养的BHK细胞上的表面延伸物。
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Lumenal plasma membrane of the urinary bladder. I. Three-dimensional reconstruction from freeze-etch images.膀胱的管腔质膜。I. 基于冷冻蚀刻图像的三维重建。
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Mobility and the restriction of mobility of plasma membrane lectin-binding components.质膜凝集素结合成分的流动性及流动性限制
Science. 1974 Jun 21;184(4143):1294-6. doi: 10.1126/science.184.4143.1294.
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Stimulation of density-inhibited cell cultures by insulin.胰岛素对密度抑制细胞培养物的刺激作用。
J Cell Physiol. 1973 Jun;81(3):355-64. doi: 10.1002/jcp.1040810308.
8
Early contacts between normal fibroblasts and mouse sarcoma cells. An ultrastructural study.正常成纤维细胞与小鼠肉瘤细胞的早期接触。一项超微结构研究。
Exp Cell Res. 1973 Apr;78(2):479-81. doi: 10.1016/0014-4827(73)90098-0.
9
Neuraminidase stimulates division and sugar uptake in density-inhibited cell cultures.神经氨酸酶可刺激密度抑制细胞培养物中的细胞分裂和糖分摄取。
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10
Disappearance of a major cell-type specific surface glycoprotein antigen (SF) after transformation of fibroblasts by Rous sarcoma virus.劳氏肉瘤病毒使成纤维细胞转化后,一种主要的细胞类型特异性表面糖蛋白抗原(SF)消失。
Int J Cancer. 1974 May 15;13(5):579-86. doi: 10.1002/ijc.2910130502.

成纤维细胞表面抗原的分布:与正常细胞的纤维状结构相关以及病毒转化后消失。

Distribution of fibroblast surface antigen: association with fibrillar structures of normal cells and loss upon viral transformation.

作者信息

Wartiovaara J, Linder E, Ruoslahti E, Vaheri A

出版信息

J Exp Med. 1974 Dec 1;140(6):1522-33. doi: 10.1084/jem.140.6.1522.

DOI:10.1084/jem.140.6.1522
PMID:4372293
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2139749/
Abstract

The localization of a cell type-specific, soluble fibroblast surface antigen (SFA) was studied by immunofluorescence and by scanning electron microscopy of the same cells. The antigen had an uneven distribution forming streaks on chick embryo fibroblasts. It was localized to membrane processes and ridges, with a diameter of 50-200 nm. The processes extended from the periphery of the cells to the substratum or to other cells. Trypsin treatment completely removed detectable amounts of SFA. The antigen was detectable within 1 h after trypsin-treated cells were reseeded. The reappearance of SFA correlated with the restoration of membrane processes. Fibroblasts transformed by Rous sarcoma virus (RSV) showed loss of all or most SFA. When normal cells were transformed without subcultivation and trypsinization a fibrillar extracellular network of SFA remained under the transformed fibroblasts while the cells themselves were negative in immunofluorescence. When fibroblasts infected by RSV mutants were transferred to nonpermissive temperature for transformation new SFA was detected within 2 h. These data lead us to propose that loss of stabilizing and anchoring effect of SFA molecules in fibrillar cell surface structures may be critical in altered growth control and malignant transformation.

摘要

通过免疫荧光以及对相同细胞进行扫描电子显微镜观察,研究了一种细胞类型特异性的可溶性成纤维细胞表面抗原(SFA)的定位。该抗原分布不均,在鸡胚成纤维细胞上形成条纹。它定位于直径为50 - 200 nm的膜突起和嵴上。这些突起从细胞周边延伸至基质或其他细胞。胰蛋白酶处理可完全去除可检测到的SFA量。在胰蛋白酶处理过的细胞重新接种后1小时内可检测到该抗原。SFA的重新出现与膜突起的恢复相关。经劳氏肉瘤病毒(RSV)转化的成纤维细胞显示全部或大部分SFA缺失。当正常细胞未经传代培养和胰蛋白酶处理而发生转化时,在转化的成纤维细胞下方会残留一个由SFA构成的纤维状细胞外网络,而细胞本身在免疫荧光检测中呈阴性。当感染RSV突变体的成纤维细胞转移至非允许温度进行转化时,在2小时内可检测到新的SFA。这些数据使我们提出,SFA分子在纤维状细胞表面结构中稳定和锚定作用的丧失可能在生长控制改变和恶性转化中起关键作用。