Dephosphorylation of the Cadherin-associated p100/p120 Proteins in Response to Activation of Protein Kinase C in Epithelial Cells*
Dephosphorylation of the Cadherin-associated p100/p120 Proteins in Response to Activation of Protein Kinase C in Epithelial Cells*
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上皮细胞中蛋白激酶 C 激活导致钙粘蛋白相关 p100/p120 蛋白去磷酸化*
DOI：
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发表时间：
1997
影响因子：
4.8
通讯作者：
J. Staddon
中科院分区：
文献类型：
--
作者：
M. Ratcliffe;L. Rubin;J. Staddon
蛋白激酶C信号通路与细胞间连接的破坏有关，但机制尚不清楚。p100和p120是犰狳蛋白家族的成员，定位于细胞粘附连接。在菌株I Madin-Darby犬肾细胞中，蛋白激酶C的激活导致紧密连接的破坏和细胞单层通透性的增加。我们发现这种通透性增加伴随着丝氨酸和苏氨酸残基上p100/p120的去磷酸化。这些蛋白的去磷酸化也可以由激酶抑制剂staurosporine、KT5926和Gö 6976诱导。用磷酸酶抑制剂处理细胞诱导p100和p120过度磷酸化。因此，p100和p120参与了丝氨酸/苏氨酸磷酸化和去磷酸化的可调节循环。蛋白激酶C必须直接或间接地通过扰乱磷酸化循环、抑制p100/p120激酶和/或激活磷酸酶来起作用。这些数据清楚地表明p100和p120是一种新的蛋白激酶C信号通路的靶点。这些蛋白的去磷酸化先于上皮细胞单层通透性增加，这是对磷酯的反应，提高了该途径在细胞间连接调节中发挥作用的可能性。
Protein kinase C signaling pathways have been implicated in the disruption of intercellular junctions, but mechanisms are not clear. p100 and p120 are members of the Armadillo family of proteins and are localized to cellular adherens junctions. In strain I Madin-Darby canine kidney cells, protein kinase C activation leads to disruption of tight junctions and an increase in permeability of cell monolayers. We show that this permeability increase is accompanied by dephosphorylation of p100/p120 on serine and threonine residues. The dephosphorylation of these proteins can also be induced by the kinase inhibitors staurosporine, KT5926, and Gö 6976. Treatment of cells with phosphatase inhibitors induced hyperphosphorylation of p100 and p120. Thus, p100 and p120 participate in a regulatable cycle of serine/threonine phosphorylation and dephosphorylation. Protein kinase C must act, directly or indirectly, by perturbing this phosphorylation cycle, by inhibition of a p100/p120 kinase and/or activation of a phosphatase. These data clearly show that p100 and p120 are targets of a novel protein kinase C signaling pathway. Dephosphorylation of these proteins precedes the permeability increase across epithelial cell monolayers seen in response to phorbol esters, raising the possibility that this pathway may play a role in the modulation of intercellular junctions.
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PDGF、CSF-1 和 EGF 诱导 p120（一种 pp60src 转化相关底物）的酪氨酸磷酸化。
影响因子：
8
作者：
Downing,JR;Reynolds,AB
通讯作者：
Reynolds,AB
铃蟾肽、加压素和内皮素可快速刺激 Swiss 3T3 细胞中粘着斑相关蛋白桩蛋白的酪氨酸磷酸化。
DOI：
--
发表时间：
1993
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Zachary,I;Sinnett-Smith,J;Turner,CE;Rozengurt,E
通讯作者：
Rozengurt,E
表皮生长因子与佛波酯对肾上皮 (LLC-PK1) 紧密连接通透性和细胞分裂的影响。
影响因子：
3.7
作者：
Soler,AP;Laughlin,KV;Mullin,JM
通讯作者：
Mullin,JM
影响因子：
4
作者：
Karin M. McCarthy;I. Skare;Michael C. Stankewich;M. Furuse;S. Tsukita;R. Rogers;R. Lynch;E. Schneeb
通讯作者：
Karin M. McCarthy;I. Skare;Michael C. Stankewich;M. Furuse;S. Tsukita;R. Rogers;R. Lynch;E. Schneeb
影响因子：
10.5
作者：
RIGGLEMAN, B;WIESCHAUS, E;SCHEDL, P
通讯作者：
SCHEDL, P