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C-Terminal HSP90 Inhibitors Block the HIF-1 Hypoxic Response by Degrading HIF-1α through the Oxygen-Dependent Degradation Pathway.C 端热休克蛋白 90 抑制剂通过氧依赖降解途径降解缺氧诱导因子-1α(HIF-1α)来阻断 HIF-1 的缺氧反应。
Cell Physiol Biochem. 2019;53(3):480-495. doi: 10.33594/000000152.
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Analysis of serum Hsp90 as a potential biomarker of β cell autoimmunity in type 1 diabetes.分析血清 Hsp90 作为 1 型糖尿病β细胞自身免疫的潜在生物标志物。
PLoS One. 2019 Jan 10;14(1):e0208456. doi: 10.1371/journal.pone.0208456. eCollection 2019.
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Hsp90 and Hsp70 chaperones: Collaborators in protein remodeling.热休克蛋白 90 和 70 伴侣:蛋白质重塑的合作者。
J Biol Chem. 2019 Feb 8;294(6):2109-2120. doi: 10.1074/jbc.REV118.002806. Epub 2018 Nov 6.
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Clinical Significance of Circulating Serum Cellular Heat Shock Protein 90 (HSP90) Level in Patients with Cutaneous Malignant Melanoma.皮肤恶性黑色素瘤患者循环血清细胞热休克蛋白90(HSP90)水平的临床意义
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Heat Shock Protein 90α Is a Potential Serological Biomarker of Acute Rejection after Renal Transplantation.热休克蛋白90α是肾移植术后急性排斥反应的潜在血清生物标志物。
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Mechanisms of Hsp90 regulation.热休克蛋白90(Hsp90)的调控机制。
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Hsp90 inhibition suppresses NF-κB transcriptional activation via Sirt-2 in human lung microvascular endothelial cells.在人肺微血管内皮细胞中,热休克蛋白90(Hsp90)抑制通过沉默调节蛋白2(Sirt-2)抑制核因子κB(NF-κB)的转录激活。
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Heat shock protein 90 associates with Toll-like receptors 7/9 and mediates self-nucleic acid recognition in SLE.热休克蛋白90与Toll样受体7/9相关联,并介导系统性红斑狼疮中的自身核酸识别。
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Functions of heat shock proteins in pathways of the innate and adaptive immune system.热休克蛋白在固有免疫系统和适应性免疫系统途径中的功能。
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The role of heat shock protein 90 in modulating ischemia-reperfusion injury in the kidney.热休克蛋白 90 在调节肾脏缺血再灌注损伤中的作用。
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血清和尿液中慢性肾小球肾炎患者的热休克蛋白 90 和 NFkB 水平。

Heat shock protein 90 and NFkB levels in serum and urine in patients with chronic glomerulonephritis.

机构信息

Tareev Clinic of Internal Diseases, Sechenov First Moscow State Medical University, Rossolimo 11/5, Moscow, Russia, 119435.

出版信息

Cell Stress Chaperones. 2020 May;25(3):495-501. doi: 10.1007/s12192-020-01089-x. Epub 2020 Apr 2.

DOI:10.1007/s12192-020-01089-x
PMID:32240529
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7193002/
Abstract

Heat shock proteins play an important role in immune inflammation and the formation and restoration of proteins. In recent years, the importance of heat shock protein 90 (Hsp90) in the activation of immune inflammation through nuclear factor kB (NFkB) has been discussed. To assess the activation of the Hsp90-NFkB system by measuring serum and urinary levels in patients with chronic glomerulonephritis (CGN). This study included 32 patients with active forms of CGN and 14 patients with Fabry nephropathy. The control group included 10 healthy individuals. Twenty-one out of 32 CGN patients had nephrotic syndrome (NS). Eleven out of 32 CGN patients had proteinuria levels from 1 to 3 g/day without nephrotic syndrome. A total of 17 patients had renal dysfunction (estimated glomerular filtration rate < 60 ml/min/1.73m). Fourteen patients with Fabry nephropathy had proteinuria without nephrotic syndrome. Serum and urine HSP-90 and NFkB p65 levels were determined using an enzyme-linked immunosorbent assay. The levels of HSP-90 and NFkB in the serum of patients with CGN were significantly higher than in healthy individuals and patients with Fabry nephropathy. In patients with Fabry nephropathy, the HSP-90 and NFkB levels in the urine and serum did not significantly differ from those in the control subjects. Serum Hsp90 levels were significantly higher in the CGN patients with NS than in patients without NS, as well as in patients with normal renal function compared with patients with an eGFR < 60 ml/min/1.73 m and patients with tubulo-interstitial fibrosis. Higher levels of HSP-90 and NFkB in serum were observed in patients with nephrotic forms of CGN, including focal segmental glomerulosclerosis, minimal change disease and membranous nephropathy. There were no correlations between the clinical signs of CGN and urinary HSP90/NFkB levels. Activation of the HSP-90-NFkB system, which is directly involved in the development of immune inflammation in CGN, was found in patients with an active course of CGN, especially in those with nephrotic syndrome.

摘要

热休克蛋白在免疫炎症以及蛋白质的形成和修复中发挥着重要作用。近年来,热休克蛋白 90(Hsp90)通过核因子 kB(NFkB)在免疫炎症激活中的重要性已经被讨论。通过测量慢性肾小球肾炎(CGN)患者的血清和尿液水平来评估 Hsp90-NFkB 系统的激活。本研究纳入了 32 名活动期 CGN 患者和 14 名 Fabry 肾病患者。对照组包括 10 名健康个体。32 名 CGN 患者中有 21 名患有肾病综合征(NS)。32 名 CGN 患者中有 11 名蛋白尿水平为 1-3 g/天,无肾病综合征。共有 17 名患者存在肾功能障碍(估计肾小球滤过率<60 ml/min/1.73m)。14 名 Fabry 肾病患者有蛋白尿,无肾病综合征。采用酶联免疫吸附试验测定血清和尿液 HSP-90 和 NFkB p65 水平。CGN 患者血清 HSP-90 和 NFkB 水平明显高于健康个体和 Fabry 肾病患者。在 Fabry 肾病患者中,尿液和血清中的 HSP-90 和 NFkB 水平与对照组无显著差异。CGN 患者中有 NS 的患者血清 Hsp90 水平明显高于无 NS 的患者,以及肾功能正常的患者与 eGFR<60 ml/min/1.73 m 的患者和存在肾小管间质纤维化的患者。在 CGN 患者中,包括局灶节段性肾小球硬化症、微小病变性肾病和膜性肾病在内的肾病综合征患者,血清中 HSP-90 和 NFkB 水平较高。CGN 的临床体征与尿 HSP90/NFkB 水平之间无相关性。在 CGN 活动期患者中发现了 HSP-90-NFkB 系统的激活,这与 CGN 中免疫炎症的发展直接相关,特别是在肾病综合征患者中。