Nontransformed cells can normalize gap junctional communication with transformed cells.

Nontransformed cells can normalize gap junctional communication with transformed cells.
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未转化细胞可以使与转化细胞的间隙连接通讯正常化。

DOI:
10.1016/j.bbrc.2005.05.104
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发表时间:
2005
期刊:
Biochemical and biophysical research communications.
影响因子:
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通讯作者:
Goldberg,GaryS
Goldberg,GaryS
中科院分区:
--
文献类型:
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作者:
Valiunas,Virginijus;Bechberger,JohnF;Naus,ChristianCG;Brink,PeterR;Goldberg,GaryS

文献摘要

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我们证明,Src激酶可以增强来自纯合无效Cx43基因敲除小鼠的细胞之间的间隙连接通讯。Src转化细胞之间的总电导几乎是非转化细胞的两倍。此外,转化细胞之间的大多数单通道事件的单位电导比非转化细胞大约35%。分析表明,两个非转化和转化细胞表达至少两个群体的通道,这表明Src增加连接电导上调一个人口和/或通过增加单位电导的另一个人口的通道。有趣的是,由异源对转化和非转化细胞显示的电导类似于非转化细胞。异源对之间的大多数单通道事件转移回较低的电导,表现出非转化细胞。因此,未转化的细胞可以有效地“正常化”相邻肿瘤细胞表达的间隙连接通道的电导。
We demonstrate that the Src kinase can augment gap junctional communication between cells derived from homozygous null Cx43 knockout mice. The total conductance between Src transformed cells was nearly twice that of nontransformed cells. In addition, the unitary conductance of the majority of single channel events between transformed cells was about 35% greater than that of nontransformed cells. Analysis showed that both nontransformed and transformed cells expressed at least two populations of channels, suggesting that Src increased junctional conductance by up-regulating one population and/or by increasing the unitary conductance of another population of channels. Interestingly, the conductance displayed by heterologous pairs of transformed and nontransformed cells resembled that of nontransformed cells. The majority of single channel events between heterologous pairs shifted back to lower conductances that were exhibited by nontransformed cells. Thus, nontransformed cells can effectively “normalize” the conductance of gap junction channels expressed by adjacent tumor cells.