Phosphorylation of connexin43 induced by Src: regulation of gap junctional communication between transformed cells.
Phosphorylation of connexin43 induced by Src: regulation of gap junctional communication between transformed cells.
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DOI：
10.1016/j.yexcr.2007.09.010
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发表时间：
2007-12
影响因子：
3.7
通讯作者：
Madhuri Pahujaa;M. Anikin;G. Goldberg
中科院分区：
文献类型：
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作者：
Madhuri Pahujaa;M. Anikin;G. Goldberg
Cx43是一种广泛表达的缝隙连接蛋白，介导多种细胞类型之间的通讯。一般说来，肿瘤细胞表现出的细胞间通讯比它们未转化的前体细胞少。Src酪氨酸激酶与多种癌症的进展有关。SRC可以磷酸化Cx43，这一事件与抑制缝隙连接通讯有关。然而，Src激活了多个信号通路，这些信号通路也可以影响细胞间的通讯。例如，包括PKC和MAPK在内的丝氨酸激酶是Src的下游效应者，也可以磷酸化Cx43并干扰缝隙连接通讯。此外，Src还可以影响其他可能影响细胞间通讯的蛋白质的表达。事实上，src对缝隙连接的破坏似乎很复杂。已明确的是，Src可以通过多种机制影响Cx43活性。在这里，我们回顾了Src如何协调调控由Cx43介导的细胞间通信的事件。
Cx43 is a widely expressed gap junction protein that mediates communication between many cell types. In general, tumor cells display less intercellular communication than their nontransformed precursors. The Src tyrosine kinase has been implicated in progression of a wide variety of cancers. Src can phosphorylate Cx43, and this event is associated with the suppression of gap junction communication. However, Src activates multiple signaling pathways that can also affect intercellular communication. For example, serine kinases including PKC and MAPK are downstream effectors of Src that can also phosphorylate Cx43 and disrupt gap junctional communication. In addition, Src can affect the expression of other proteins that may affect intercellular communication. Indeed, disruption of gap junctions by Src appears to be complex. It has become clear that Src can affect Cx43 activity by multiple mechanisms. Here, we review how Src may orchestrate events that regulate intercellular communication mediated by Cx43.