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半乳糖脑苷脂介导培养的胶质瘤细胞中的Ca2+信号传导。

Galactocerebroside mediates Ca2+ signaling in cultured glioma cells.

作者信息

Joshi P G, Mishra S

机构信息

Department of Biophysics, National Institute of Mental Health and Neuro Sciences, Bangalore, India.

出版信息

Brain Res. 1992 Nov 27;597(1):108-13. doi: 10.1016/0006-8993(92)91511-c.

Abstract

Expression of galactocerebroside (GalC) was detected in human glioma cell line (U-87 MG). Exposure of cells to antibody against GalC and fluoresceinated second antibody showed intense fluorescence on the plasma membrane. Possible involvement of GalC in receptor-mediated transmembrane signaling was explored in this cell line. Antibodies raised against GalC were used as ligands. Binding of anti-GalC to these cells caused a transient increase in intracellular free calcium ([Ca2+]i). The response was observed both in the presence and absence of extracellular calcium demonstrating that the rise in [Ca2+]i induced by anti-GalC was due to an influx of Ca2+ through plasma membrane as well as the release of Ca2+ from intracellular pools. Ca2+ influx was blocked by verapamil, indicating that influx is mediated by voltage-sensitive channels. Our results suggest that GalC can play a role in transmembrane signaling by modulation of voltage-sensitive Ca2+ channels.

摘要

在人胶质瘤细胞系(U-87 MG)中检测到半乳糖脑苷脂(GalC)的表达。将细胞暴露于抗GalC抗体和荧光素标记的二抗后,在质膜上显示出强烈的荧光。在该细胞系中探讨了GalC可能参与受体介导的跨膜信号传导。针对GalC产生的抗体用作配体。抗GalC与这些细胞的结合导致细胞内游离钙([Ca2+]i)短暂增加。在有和没有细胞外钙的情况下均观察到该反应,这表明抗GalC诱导的[Ca2+]i升高是由于Ca2+通过质膜内流以及从细胞内钙库释放所致。维拉帕米阻断了Ca2+内流,表明内流是由电压敏感通道介导的。我们的结果表明,GalC可通过调节电压敏感的Ca2+通道在跨膜信号传导中发挥作用。

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