Modulation of gap junction channels and hemichannels by growth factors.
Modulation of gap junction channels and hemichannels by growth factors.
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DOI：
10.1039/c1mb05294b
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发表时间：
2012-03
影响因子：
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通讯作者：
K. Schalper;M. Riquelme;M. C. Brañes;Agustín D. Martínez;J. Vega;V. M. Berthoud;M. Bennett;J. Sáez
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文献类型：
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作者：
K. Schalper;M. Riquelme;M. C. Brañes;Agustín D. Martínez;J. Vega;V. M. Berthoud;M. Bennett;J. Sáez
间隙连接半通道和细胞-细胞通道由于其对细胞外和细胞内信号分子的渗透性而在协调许多细胞过程中起作用。细胞协调的另一种机制是由大量的生长因子提供的，这些生长因子与相对选择性的细胞膜受体相互作用。这些受体可以影响细胞转导途径，包括改变细胞内游离Ca（2+）和自由基的浓度以及激活蛋白激酶或磷酸酶。连接蛋白和基于泛连接蛋白的通道构成了最近描述的生长因子信号转导途径的靶标，但是关于生长因子信号传导对基于泛连接蛋白的通道的影响知之甚少。生长因子对这两种通道类型的影响似乎取决于细胞类型，细胞阶段和连接蛋白和泛连接蛋白亚型表达。FGF-1通过蛋白激酶依赖性机制以相反方向影响半通道和间隙连接通道的功能状态。这些变化在很大程度上是由通道插入或退出细胞膜来解释的，但开放概率的变化也可能是由于通道亚基的磷酸化和氧化还原状态的变化而发生的。通过这些膜通道的细胞-细胞通信的变化的功能后果与疾病以及正常的细胞反应有关。
Gap junction hemichannels and cell-cell channels have roles in coordinating numerous cellular processes, due to their permeability to extra and intracellular signaling molecules. Another mechanism of cellular coordination is provided by a vast array of growth factors that interact with relatively selective cell membrane receptors. These receptors can affect cellular transduction pathways, including alteration of intracellular concentration of free Ca(2+) and free radicals and activation of protein kinases or phosphatases. Connexin and pannexin based channels constitute recently described targets of growth factor signal transduction pathways, but little is known regarding the effects of growth factor signaling on pannexin based channels. The effects of growth factors on these two channel types seem to depend on the cell type, cell stage and connexin and pannexin isoform expressed. The functional state of hemichannels and gap junction channels are affected in opposite directions by FGF-1 via protein kinase-dependent mechanisms. These changes are largely explained by channels insertion in or withdrawal from the cell membrane, but changes in open probability might also occur due to changes in phosphorylation and redox state of channel subunits. The functional consequence of variation in cell-cell communication via these membrane channels is implicated in disease as well as normal cellular responses.