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连接蛋白/间隙连接蛋白通道在传染病中的作用。

Role of connexin/pannexin containing channels in infectious diseases.

机构信息

Public Health Research Institute (PHRI), Rutgers New Jersey Medical School, Rutgers The State University of New Jersey, Newark, NJ, USA; Department of Microbiology and Molecular Genetics, Rutgers New Jersey Medical School, Rutgers The State University of New Jersey, Newark, NJ, USA.

出版信息

FEBS Lett. 2014 Apr 17;588(8):1389-95. doi: 10.1016/j.febslet.2014.01.030. Epub 2014 Jan 28.

DOI:10.1016/j.febslet.2014.01.030
PMID:24486013
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4229019/
Abstract

In recent years it has become evident that gap junctions and hemichannels, in concert with extracellular ATP and purinergic receptors, play key roles in several physiological processes and pathological conditions. However, only recently has their importance in infectious diseases been explored, likely because early reports indicated that connexin containing channels were completely inactivated under inflammatory conditions, and therefore no further research was performed. However, recent evidence indicates that several infectious agents take advantage of these communication systems to enhance inflammation and apoptosis, as well as to participate in the infectious cycle of several pathogens. In the current review, we will discuss the role of these channels/receptors in the pathogenesis of several infectious diseases and the possibilities of generating novel therapeutic approaches to reduce or prevent these diseases.

摘要

近年来,缝隙连接和半通道与细胞外 ATP 和嘌呤能受体一起,在几种生理过程和病理状况中发挥着关键作用,这一点已经变得很明显。然而,直到最近,它们在传染病中的重要性才被探索出来,这可能是因为早期的报告表明,连接蛋白通道在炎症条件下完全失活,因此没有进一步的研究。然而,最近的证据表明,几种感染因子利用这些通讯系统来增强炎症和细胞凋亡,并参与几种病原体的感染周期。在当前的综述中,我们将讨论这些通道/受体在几种传染病发病机制中的作用,以及产生新的治疗方法来减少或预防这些疾病的可能性。

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本文引用的文献

1
HIV increases the release of dickkopf-1 protein from human astrocytes by a Cx43 hemichannel-dependent mechanism.HIV 通过 Cx43 半通道依赖性机制增加人星形胶质细胞中 dickkopf-1 蛋白的释放。
J Neurochem. 2014 Mar;128(5):752-63. doi: 10.1111/jnc.12492. Epub 2013 Nov 13.
2
Cytochrome C dysregulation induced by HIV infection of astrocytes results in bystander apoptosis of uninfected astrocytes by an IP3 and calcium-dependent mechanism.HIV 感染星形胶质细胞导致细胞色素 C 失调,通过 IP3 和钙依赖性机制诱导未感染星形胶质细胞的旁观者凋亡。
J Neurochem. 2013 Dec;127(5):644-51. doi: 10.1111/jnc.12443. Epub 2013 Oct 20.
3
Human cytomegalovirus immediate early proteins promote degradation of connexin 43 and disrupt gap junction communication: implications for a role in gliomagenesis.人巨细胞病毒即刻早期蛋白促进连接蛋白 43 的降解并破坏缝隙连接通讯:在神经胶质瘤发生中的作用。
Carcinogenesis. 2014 Jan;35(1):145-54. doi: 10.1093/carcin/bgt292. Epub 2013 Aug 25.
4
Hirsutella sinensis mycelium suppresses interleukin-1β and interleukin-18 secretion by inhibiting both canonical and non-canonical inflammasomes.中华毛囊被孢霉菌丝通过抑制经典和非经典炎性小体来抑制白细胞介素-1β和白细胞介素-18 的分泌。
Sci Rep. 2013;3:1374. doi: 10.1038/srep01374.
5
Pannexin1 hemichannels are critical for HIV infection of human primary CD4+ T lymphocytes.Pannexin1 半通道对于 HIV 感染人源原代 CD4+T 淋巴细胞至关重要。
J Leukoc Biol. 2013 Sep;94(3):399-407. doi: 10.1189/jlb.0512249. Epub 2013 Mar 1.
6
ATP release and purinergic signaling: a common pathway for particle-mediated inflammasome activation.三磷酸腺苷释放和嘌呤能信号转导:颗粒介导的炎症小体激活的共同途径。
Cell Death Dis. 2012 Oct 11;3(10):e403. doi: 10.1038/cddis.2012.144.
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IL-18 associates to microvesicles shed from human macrophages by a LPS/TLR-4 independent mechanism in response to P2X receptor stimulation.白细胞介素 18 通过一种 LPS/TLR-4 非依赖机制与源自人巨噬细胞的微泡结合,这种机制是对嘌呤能 P2X 受体刺激的反应。
Eur J Immunol. 2012 Dec;42(12):3334-45. doi: 10.1002/eji.201142268. Epub 2012 Oct 26.
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Association between C1019T polymorphism in the connexin 37 gene and Helicobacter pylori infection in patients with gastric cancer.胃癌患者中连接蛋白37基因C1019T多态性与幽门螺杆菌感染的相关性
Asian Pac J Cancer Prev. 2012;13(5):2363-7. doi: 10.7314/apjcp.2012.13.5.2363.
9
Paracrine signaling through plasma membrane hemichannels.通过质膜半通道的旁分泌信号传导。
Biochim Biophys Acta. 2013 Jan;1828(1):35-50. doi: 10.1016/j.bbamem.2012.07.002. Epub 2012 Jul 13.
10
Multifaceted roles of purinergic receptors in viral infection.嘌呤能受体在病毒感染中的多方面作用。
Microbes Infect. 2012 Nov;14(14):1278-83. doi: 10.1016/j.micinf.2012.05.010. Epub 2012 Jun 7.