BAG5

Last update 08 May 2025

Basic Info

Synonyms

BAG cochaperone 5, BAG family molecular chaperone regulator 5, BAG-5

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Introduction

Co-chaperone for HSP/HSP70 proteins. It functions as a nucleotide-exchange factor promoting the release of ADP from HSP70, thereby activating HSP70-mediated protein refolding (PubMed:20223214). Has an essential role in maintaining proteostasis at junctional membrane complexes (JMC), where it may function as a scaffold between the HSPA8 chaperone and JMC proteins enabling correct, HSPA8-dependent JMC protein folding (By similarity). Inhibits both auto-ubiquitination of PRKN and ubiquitination of target proteins by PRKN (By similarity).

100 Clinical Results associated with BAG5

100 Translational Medicine associated with BAG5

0 Patents (Medical) associated with BAG5

Literatures (Medical) associated with BAG5

05 Nov 2024·Toxicology Research

Sevoflurane attenuates hypoxia/reoxygenation-induced cardiomyocyte injury by regulating miR-4454

Article

Author: Huang, Mingshan ; Zhai, Shuang ; Guo, Aili ; Du, Meiqing ; Mou, Changliang ; Zhang, Gaofeng ; Chen, Jianxing

AbstractBackground: Sevoflurane (Sevo) prevents hypoxia/reoxygenation (H/R)-induced cardiomyocytes injury. The expression of miR-4,454 was increased in individuals experiencing an acute myocardial infarction. Objective: The purpose of current investigation was to delved into whether the effects of Sevo on cardiomyocytes are mediated through regulation of miR-4,454 expression. Method: In this study, the expression levels of miR-4,454 and BAG5 were detected by real-time quantitative polymerase chain reaction (RT-qPCR). Cell viability was detected by cell counting kit-8 (CCK-8). The levels of creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH) and cardiac troponin I (cTnI) were detected by enzyme-linked immunosorbent assay (ELISA). Reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD) and catalase (CAT) were detected using various commercially available kits to assess the level of oxidative stress in the cells. The luciferase reporter gene assay was used to verify the interaction of miR-4,454 with downstream target genes. Results: There was a notable upregulation of miR-4,454 expression in H/R-induced cardiomyocyte models. This was accompanied by a decrease in the viability of myocardial cells induced by H/R and an intensification of the extent of myocardial injury and oxidative stress. However, the detrimental effects were mitigated by the administration of Sevo. miR-4,454 had a target site for binding to BAG5, and its expression was negatively modulated by miR-4,454. An increase in the expression of BAG5 was shown to directly offset the exacerbation of cardiomyocyte damage induced by the overexpression of miR-4,454. Conclusion: Sevo may attenuate H/R-induced cardiomyocyte injury by regulating miR-4454.

28 Jul 2024·Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences

Beta-amyloid protein regulates miR-15a and activates Bag5 to influence neuronal apoptosis in Alzheimer's disease.

Article

Author: Pan, Qiong ; Guo, Ke ; Hu, Xinyu

OBJECTIVESThe prevalence of Alzheimer's disease (AD) is increasing globally, however its pathogenesis is still unclear. The evidence showed that the progression of AD was closely related to the apoptosis of nerve cells. This study amis to explore the role and specific mechanism of miR-15a and Bag5 in the apoptosis of nerve cells induced by beta-amyloid protein (Aβ) in AD.METHODSThe AD rat model was constructed by injecting Aβ42 into SD rat brain and the AD cell model was constructed by treating SH-SY5Y cells with Aβ42. The learning and memory ability of rats was detected by Morris Water Maze. Hematoxylin and eosin (HE) staining was used to detect the pathological changes of brain tissues. Nissl staining was used to detect the changes of cell morphology and number in brain tissues. The upstream miRNA that interacted with Bag5 were screened by bioinformatics analysis. Methyl thiazolyl tetrazolium (MTT) assay was used to detect cell proliferation. Flow cytometry was used to detect the apoptosis rate of cells. Real-time reverse transcription PCR (real-time RT-PCR) was used to detect the mRNA levels of miR-15a and Bag5. Western blotting was used to detect the protein expression levels of Bag5, Bax and Caspase-3. MiR-15a knockdown or overexpression vectors or Bag5 knockdown vectors were transfected into AD rat model and AD cell models, respectively. Luciferase reporter assay was used to verify the binding relationship between miR-15a and Bag5.RESULTSMorris Water Maze, HE staining and Nissl staining showed that the rat model of AD was established successfully, and Aβ could induce neuronal apoptosis and inhibit the expression of miR-15a in AD rats. Compared with normal cells, Aβ treatment significantly increased apoptosis rate and Bag5 expression, and weakened cell proliferation and miR-15a (all P<0.01). Overexpression of miR-15a further enhanced the effect of Aβ on cell proliferation and apoptosis, while knockdown of miR-15a expression had the opposite effect (all P<0.01). Luciferase reporter assay confirmed that there was a negative targeting relationship between miR-15a and Bag5. Compared with Bag5 knockdown alone, the co-transfection of miR-15a inhibitor and si-Bag5 significantly increased the cell proliferation ability and mRNA and protein levels of Bag5, and significantly reduced the cell apoptosis rate and the expression of Bax and Caspase-3, animal studies have also shown consistent results (all P<0.01).CONCLUSIONSAβ can inhibit the expression of miR-15a, thereby inducing the expression of Bag5 and activating the protective mechanism of Bag5 against Aβ induced apoptosis.

01 Mar 2024·Plant Physiology and Biochemistry

Arabidopsis BECLIN1-induced autophagy mediates reprogramming in tapetal programmed cell death by altering the gross cellular homeostasis

Article

Author: Singh, Ram Rakshpal ; Kumar, Verandra ; Verma, Rishi Kumar ; Sawant, Samir V ; Goel, Ridhi ; Singh, Surendra Pratap

In flowering plants, the tapetum degeneration in post-meiotic anther occurs through developmental programmed cell death (dPCD), which is one of the most critical and sensitive steps for the proper development of male gametophytes and fertility. Yet the pathways of dPCD, its regulation, and its interaction with autophagy remain elusive. Here, we report that high-level expression of Arabidopsis autophagy-related gene BECLIN1 (BECN1 or AtATG6) in the tobacco tapetum prior to their dPCD resulted in developmental defects. BECN1 induces severe autophagy and multiple cytoplasm-to-vacuole pathways, which alters tapetal cell reactive oxygen species (ROS)-homeostasis that represses the tapetal dPCD. The transcriptome analysis reveals that BECN1- expression caused major changes in the pathway, resulting in altered cellular homeostasis in the tapetal cell. Moreover, BECN1-mediated autophagy reprograms the execution of tapetal PCD by altering the expression of the key developmental PCD marker genes: SCPL48, CEP1, DMP4, BFN1, MC9, EXI1, and Bcl-2 member BAG5, and BAG6. This study demonstrates that BECN1-mediated autophagy is inhibitory to the dPCD of the tapetum, but the severity of autophagy leads to autophagic death in the later stages. The delayed and altered mode of tapetal degeneration resulted in male sterility.

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