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首页> 外文期刊>Journal of Cellular Physiology >Role of human LZIP in differential activation of the NF-kappaB pathway that is induced by CCR1-dependent chemokines.
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Role of human LZIP in differential activation of the NF-kappaB pathway that is induced by CCR1-dependent chemokines.

机译:人类LZIP微分激活的作用NF-kappaB通路引起的CCR1-dependent趋化因子。

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Human leucine zipper protein (LZIP) associates with CC chemokine receptor 1 (CCR1) and this protein-protein interaction should play an important role in leukocyte cell mobility. LZIP is known to regulate leukotactin-1 (Lkn-1)-dependent cell migration without affecting the chemotactic activities of other CC chemokines that bind to CCR1. Since Lkn-1 is engaged in the transcriptional activation of nuclear factor kappaB (NF-kappaB) and subsequent activation of the chemoattractant ability of leukocytes, we investigated the regulatory role of LZIP in the NF-kappaB pathway that is induced by CCR1-dependent chemokines. LZIP increased NF-kappaB-dependent luciferase activity in response to Lkn-1 in HOS/CCR1 cells and THP-1 cells. However, the NF-kappaB-dependent luciferase activities induced by other CCR1-dependent chemokines were not affected by LZIP overexpression. LZIP also increased Lkn-1-induced chemotactic activity through activation of the NF-kappaB pathway, whereas LZIP did not affect either the transactivation of NF-kappaB or the chemotactic activities induced by other CCR1-dependent chemokines. Western blot analysis showed that LZIP increased the degradation of IkappaBalpha induced by Lkn-1 but not by other CCR1-dependent chemokines. Results from electrophoretic mobility shift assay (EMSA) showed that LZIP enhanced the Lkn-1-induced DNA-binding activity of NF-kappaB. These data indicate that LZIP functions as a positive regulator in the NF-kappaB activation pathway that is triggered by Lkn-1 without affecting the transcriptional activation of NF-kappaB induced by other CCR1-dependent chemokines.
机译:人类亮氨酸拉链蛋白(LZIP)同事与CC趋化因子受体1 (CCR1)和这个蛋白质相互作用应该发挥重要作用,在细胞的白细胞迁移。众所周知,调节leukotactin-1吗(Lkn-1)端依赖细胞迁移影响其他的CC趋化现象的活动绑定到CCR1趋化因子。参与的转录激活核因子kappaB (NF-kappaB)和随后的激活的化学引诱物的能力白细胞,我们调查了监管职责的LZIP NF-kappaB诱导的途径CCR1-dependent趋化因子。NF-kappaB-dependent荧光素酶的活动应对Lkn-1居屋/ CCR1细胞和THP-1细胞。荧光素酶引起的其他活动CCR1-dependent趋化因子没有影响LZIP超表达。Lkn-1-induced趋化现象的活动通过NF-kappaB通路的激活,而LZIP没有影响的transactivationNF-kappaB或诱导趋化现象的活动由其他CCR1-dependent趋化因子。分析表明,LZIP增加了退化引起的IkappaBalpha Lkn-1但是而不是其他CCR1-dependent趋化因子。从电泳迁移率改变分析(EMSA)表明LZIP Lkn-1-induced增强NF-kappaB dna结合活性。表明LZIP函数作为一个积极的监管机构在NF-kappaB激活途径所引发的Lkn-1没有影响NF-kappaB诱导的转录激活由其他CCR1-dependent趋化因子。

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