Regulation of Cx43 Gap Junction Intercellular Communication by Bruton's Tyrosine Kinase and Interleukin-2-Inducible T-Cell Kinase.
Regulation of Cx43 Gap Junction Intercellular Communication by Bruton's Tyrosine Kinase and Interleukin-2-Inducible T-Cell Kinase.
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Bruton的酪氨酸激酶和白细胞介素-2诱导的T细胞激酶对CX43 GAP连接间互通的调节。
DOI：
10.3390/biom13040660
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发表时间：
2023-04-08
期刊：
影响因子：
5.5
通讯作者：
中科院分区：
文献类型：
--
作者：
T and B cell receptor signaling involves the activation of Akt, MAPKs, and PKC as well as an increase in intracellular Ca2+ and calmodulin activation. While these coordinate the rapid turnover of gap junctions, also implicated in this process is Src, which is not activated as part of T and B cell receptor signaling. An in vitro kinase screen identified that Bruton’s tyrosine kinase (BTK) and interleukin-2-inducible T-cell kinase (ITK) phosphorylate Cx43. Mass spectroscopy revealed that BTK and ITK phosphorylate Cx43 residues Y247, Y265, and Y313, which are identical to the residues phosphorylated by Src. Overexpression of BTK or ITK in the HEK-293T cells led to increased Cx43 tyrosine phosphorylation as well as decreased gap junction intercellular communication (GJIC) and Cx43 membrane localization. In the lymphocytes, activation of the B cell receptor (Daudi cells) or T cell receptor (Jurkat cells) increased the BTK and ITK activity, respectively. While this led to increased tyrosine phosphorylation of Cx43 and decreased GJIC, the cellular localization of Cx43 changed little. We have previously identified that Pyk2 and Tyk2 also phosphorylate Cx43 at residues Y247, Y265, and Y313 with a similar cellular fate to that of Src. With phosphorylation critical to Cx43 assembly and turnover, and kinase expression varying between different cell types, there would be a need for different kinases to achieve the same regulation of Cx43. The work presented herein suggests that in the immune system, ITK and BTK have the capacity for the tyrosine phosphorylation of Cx43 to alter the gap junction function in a similar manner as Pyk2, Tyk2, and Src.
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影响因子：
3.3
作者：
Fong JT;Kells RM;Falk MM
通讯作者：
Falk MM
DOI：
10.1016/j.bbamem.2017.05.018
发表时间：
2018-01
期刊：
Biochimica et biophysica acta. Biomembranes
影响因子：
--
作者：
Epifantseva I;Shaw RM
通讯作者：
Shaw RM
影响因子：
4
作者：
Gilleron, Jerome;Fiorini, Celine;Pointis, Georges
通讯作者：
Pointis, Georges
影响因子：
2.4
作者：
Falk L;Dang-Lawson M;Vega JL;Pournia F;Choi K;Jang C;Naus CC;Matsuuchi L
通讯作者：
Matsuuchi L
影响因子：
30.5
作者：
Chaturvedi, Akanksha;Martz, Rebecca;Pierce, Susan K.
通讯作者：
Pierce, Susan K.