摘要
Janus激酶-3(JAK3)是一种酪氨酸激酶,在多种组织中表达,包括大脑并参与细胞因子受体的信号转导。 JAK3参与细胞存活和增殖,神经保护,凋亡和细胞对缺氧和缺血再灌注的反应等功能。该激酶进一步有助于造血细胞因子受体的信号传导,树突状细胞的活化,成熟和免疫抑制以及细胞体积调节。最近,JAK3已经被证明是横跨质膜的重要的运输过程调节剂。直接或间接JAK3影响转运蛋白的表达,包括各种离子通道,多种细胞载体和Na + / K +泵。更具体地说,JAK3参与各种钾,钠和氯离子通道的调节,各种Na +偶联的细胞载体包括高亲和力的Na +偶联葡萄糖转运蛋白SGLT1,兴奋性氨基酸转运蛋白EAAT1,EAAT2,EAAT3和EAAT4,肽转运蛋白PepT1和PepT2,CreaT1和Na + / K + -ATPase。通过这些转运蛋白,该激酶在各种生理和病理生理过程中起作用。需要进一步的研究来研究JAK3对其他细胞转运蛋白的影响及其潜在的机制。
关键词: JAK3,JAK-STAT,细胞转运,离子通道,膜载体,Na + / K + -ATP酶
Current Medicinal Chemistry
Title:Regulation of Ion Channels, Cellular Carriers and Na(+)/K(+)/ATPase by Janus Kinase 3
Volume: 24 Issue: 21
关键词: JAK3,JAK-STAT,细胞转运,离子通道,膜载体,Na + / K + -ATP酶
摘要: Janus kinase-3 (JAK3), a tyrosine kinase, is expressed in a variety of tissues, including the brain and is involved in the signaling of cytokine receptors. JAK3 participates in numerous functions, such as cell survival and proliferation, neuroprotection, apoptosis and the cellular response to hypoxia and ischemia-reperfusion. This kinase further contributes to the signaling of hematopoietic cell cytokine receptors, activation of dendritic cells, maturation, and immune suppression as well as to cell volume regulation. Recently, JAK3 has been demonstrated to be an important regulator of transport processes across the plasma membrane. Either directly or indirectly JAK3 affects the expression of transport proteins, including various ion channels, a number of cellular carriers and the Na+/K+ pump. More specifically, JAK3 is involved in the regulation of various potassium, sodium, and chloride ion channels, a wide variety of Na+-coupled cellular carriers including the high-affinity Na+ coupled glucose transporter SGLT1, the excitatory amino acid transporters EAAT1, EAAT2, EAAT3 and EAAT4, the peptide transporters PepT1 and PepT2, CreaT1 and theNa+/K+-ATPase. Via these transporters this kinase plays a role in various physiological and pathophysiological processes. Additional research is needed to investigate the effects of JAK3 on other cellular transporters and the underlying mechanisms.
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Cite this article as:
Regulation of Ion Channels, Cellular Carriers and Na(+)/K(+)/ATPase by Janus Kinase 3, Current Medicinal Chemistry 2017; 24 (21) . https://dx.doi.org/10.2174/0929867324666170203122625
DOI https://dx.doi.org/10.2174/0929867324666170203122625 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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