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首页> 外文期刊>Cellular Signalling >The role of the C-terminal tail in protease-activated receptor-2-mediated Ca2+ signalling, proline-rich tyrosine kinase-2 activation, and mitogen-activated protein kinase activity
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The role of the C-terminal tail in protease-activated receptor-2-mediated Ca2+ signalling, proline-rich tyrosine kinase-2 activation, and mitogen-activated protein kinase activity

机译：C末端尾巴在蛋白酶激活的受体2介导的Ca2 +信号传导，脯氨酸丰富的酪氨酸激酶2激活和有丝分裂原激活的蛋白激酶活性中的作用

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C-terminal truncation mutants were made to investigate the role of the C-terminus in coupling proteinase-activated receptor-2 (PAR-2) to various signalling pathways. Membrane expression of the delta15, delta34, delta43, and delta34-43 mutants was similar; however, expression of deltatail was lost, as was agonist-mediated internalisation of deltatail, delta43, and delta34-43. Additionally, trypsin and SLIGKV-stimulated [H-3]IP accumulation was abrogated in cells transiently expressing delta43 or delta34-43 truncations, but remained unaffected in cells expressing delta34 or delta15. PAR-2 agonist-stimulated intracellular Ca2+ mobilisation and PYK-2 activity were also abolished by deltatail, delta43, and delta34-43 mutants. However, trypsin-stimulated stress-activated protein kinases (SAPKs) or extracellular signal-regulated kinase (ERK) activities were unaffected by the delta34-43 mutation, although activity was abrogated following delta43 or deltatail truncations, suggesting that Ca2+ mobilisation, PYK-2, or receptor internalisation are not required for activation of SAPKs or ERK. These studies identify a novel sequence within the PAR-2 C-terminus essential for InsP(3) generation and PYK-2 activity but not mitogen-activated protein kinase (MAPK) activation. (C) 2003 Elsevier Inc. All rights reserved. [References: 38]
机译：制作了C端截短突变体，以研究C末端在将蛋白酶激活的受体2（PAR-2）偶联到各种信号传导途径中的作用。 delta15，delta34，delta43和delta34-43突变体的膜表达相似。然而，deltatail的表达丢失，激动剂介导的deltatail，delta43和delta34-43的内部化也丢失了。此外，胰蛋白酶和SLIGKV刺激的[H-3] IP积累在瞬时表达Δ43或Δ34-43截短的细胞中被消除，但在表达Δ34或Δ15的细胞中不受影响。 deltatail，delta43和delta34-43突变体也废除了PAR-2激动剂刺激的细胞内Ca2 +动员和PYK-2活性。然而，尽管delta43或deltatail截短后活性被取消，但胰蛋白酶刺激的应激激活蛋白激酶（SAPKs）或细胞外信号调节激酶（ERK）的活性不受delta34-43突变的影响，这表明Ca2 +动员了PYK-2。 SAPKs或ERK激活不需要受体内在化。这些研究确定InsP（3）生成和PYK-2活性而不是有丝分裂原激活的蛋白激酶（MAPK）激活所必需的PAR-2 C末端内的新序列。 （C）2003 Elsevier Inc.保留所有权利。 [参考：38]

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