Cell Stress & Chaperones最新文献

Corrigendum to “The mechanism and therapeutic strategies in doxorubicin induced cardiotoxicity: Role of programmed cell death” [Cell Stress Chaperones. 2024;29:666-680] 多柔比星诱发心脏毒性的机制和治疗策略：细胞应激合子的作用》[Cell Stress Chaperones.］

IF 3.3 3区生物学

Cell Stress & Chaperones Pub Date : 2024-10-24 DOI: 10.1016/j.cstres.2024.10.005

Yanzhao Li , Jing Yan , Pingzhen Yang

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The heat shock factor code: Specifying a diversity of transcriptional regulatory programs broadly promoting stress resilience 热休克因子代码：明确转录调控程序的多样性，广泛促进应激恢复能力。

IF 3.3 3区生物学

Cell Stress & Chaperones Pub Date : 2024-10-23 DOI: 10.1016/j.cstres.2024.10.006

Milad J. Alasady , Marc L. Mendillo

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IF 3.3 3区生物学

Cell Stress & Chaperones Pub Date : 2024-10-18 DOI: 10.1016/j.cstres.2024.10.004

Brenda A. Schilke , Thomas Ziegelhoffer , Przemyslaw Domanski , Jaroslaw Marszalek , Bartlomiej Tomiczek , Elizabeth A. Craig

{"title":"Functional similarities and differences among subunits of the nascent polypeptide-associated complex (NAC) of Saccharomyces cerevisiae","authors":"Brenda A. Schilke , Thomas Ziegelhoffer , Przemyslaw Domanski , Jaroslaw Marszalek , Bartlomiej Tomiczek , Elizabeth A. Craig","doi":"10.1016/j.cstres.2024.10.004","DOIUrl":"10.1016/j.cstres.2024.10.004","url":null,"abstract":"<div><div>Protein factors bind ribosomes near the tunnel exit, facilitating protein trafficking and folding. In eukaryotes, the heterodimeric nascent polypeptide-associated complex (NAC) is the most abundant—equimolar to ribosomes. <em>Saccharomyces cerevisiae</em> has a minor β-type subunit (Nacβ2) in addition to abundant Nacβ1, and therefore two NAC heterodimers, α/β1 and α/β12. The additional beta NAC gene arose at the time of the whole genome duplication that occurred in the <em>S. cerevisiae</em> lineage. Nacβ2 has been implicated in regulating the fate of messenger RNA encoding ribosomal protein Rpl4 during translation <em>via</em> its interaction with the Caf130 subunit of the regulatory CCR4-Not complex. We found that Nacβ2 residues just C-terminal to the globular domain are required for its interaction with Caf130 and its negative effect on the growth of cells lacking Acl4, the specialized chaperone for Rpl4. Substitution of these Nacβ2 residues at homologous positions in Nacβ1 results in a chimeric protein that interacts with Caf130 and slows the growth of ∆<em>acl4</em> cells lacking Nacβ2. Furthermore, alteration of residues in the N-terminus of Nacβ2 or chimeric Nacβ1 previously shown to affect ribosome binding overcomes the growth defect of ∆<em>acl4</em>. Our results are consistent with a model in which Nacβ2’s ribosome association <em>per se</em> or its precise positioning is necessary for productive recruitment of CCR4-Not <em>via</em> its interaction with the Caf130 subunit to drive Rpl4 messenger RNA degradation.</div></div>","PeriodicalId":9684,"journal":{"name":"Cell Stress & Chaperones","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142459007","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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In memoriam James S. Clegg (1933–2024) 纪念詹姆斯-克莱格（James S. Clegg，1933-2024 年）。

IF 3.3 3区生物学

Cell Stress & Chaperones Pub Date : 2024-10-11 DOI: 10.1016/j.cstres.2024.10.003

Lawrence E. Hightower

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Flow cytometry FRET reveals post-translational modifications drive Protein Phosphatase-5 conformational changes in mammalian cells 流式细胞仪 FRET 揭示翻译后修饰驱动蛋白磷酸酶-5 在哺乳动物细胞中的构象变化

IF 3.3 3区生物学

Cell Stress & Chaperones Pub Date : 2024-10-10 DOI: 10.1016/j.cstres.2024.10.002

Rebecca A. Sager , Sarah J. Backe , Jennifer Heritz , Mark R. Woodford , Dimitra Bourboulia , Mehdi Mollapour

{"title":"Flow cytometry FRET reveals post-translational modifications drive Protein Phosphatase-5 conformational changes in mammalian cells","authors":"Rebecca A. Sager , Sarah J. Backe , Jennifer Heritz , Mark R. Woodford , Dimitra Bourboulia , Mehdi Mollapour","doi":"10.1016/j.cstres.2024.10.002","DOIUrl":"10.1016/j.cstres.2024.10.002","url":null,"abstract":"<div><div>The serine/threonine Protein Phosphatase-5 (PP5) plays an essential role in regulating hormone and stress-induced signaling networks as well as extrinsic apoptotic pathways in cells. Unlike other Protein Phosphatases, PP5 possesses both regulatory and catalytic domains, and its function is further modulated through post-translational modifications (PTMs). PP5 contains a tetratricopeptide repeat (TPR) domain, which usually inhibits its phosphatase activity by blocking the active site (closed conformation). Certain activators bind to the PP5–TPR domain, alleviating this inhibition and allowing the catalytic domain to adopt an active (open) conformation. While this mechanism has been proposed based on structural and biophysical studies, PP5 conformational changes and activity have yet to be observed in cells. Here, we designed and developed a flow cytometry-based fluorescence resonance energy transfer (FC-FRET) method, enabling real-time observation of PP5 autoinhibition and activation within live mammalian cells. By quantifying FRET efficiency using sensitized emission, we established a standardized and adaptable data acquisition workflow. Our findings revealed that, in a cellular context, PP5 exists in multiple conformational states, none of which alone fully predicts its activity. Additionally, we have demonstrated that PTMs such as phosphorylation and SUMOylation impact PP5 conformational changes, representing a significant advancement in our understanding of its regulatory mechanisms.</div></div>","PeriodicalId":9684,"journal":{"name":"Cell Stress & Chaperones","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142459006","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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Ebeiedinone and peimisine inhibit cigarette smoke extract-induced oxidative stress injury and apoptosis in BEAS-2B cells 依贝地农和peimisine可抑制香烟烟雾提取物诱导的BEAS-2B细胞氧化应激损伤和凋亡。

IF 3.3 3区生物学

Cell Stress & Chaperones Pub Date : 2024-10-04 DOI: 10.1016/j.cstres.2024.10.001

Chuanlan Liu , Xiaomu Zhu , Erbu Aga , Wai Ming Tse , Kathy Wai Gaun Tse , Yanyong Liu , Bengui Ye

{"title":"Ebeiedinone and peimisine inhibit cigarette smoke extract-induced oxidative stress injury and apoptosis in BEAS-2B cells","authors":"Chuanlan Liu , Xiaomu Zhu , Erbu Aga , Wai Ming Tse , Kathy Wai Gaun Tse , Yanyong Liu , Bengui Ye","doi":"10.1016/j.cstres.2024.10.001","DOIUrl":"10.1016/j.cstres.2024.10.001","url":null,"abstract":"<div><div>Ebeiedinone and peimisine are the major active ingredients of Fritillariae Cirrhosae Bulbus. In this study, we looked at how these two forms of isosteroidal alkaloids protect human bronchial epithelial BEAS-2B cells from oxidative stress and apoptosis caused by cigarette smoke extract (CSE). First, the cytotoxicity was determined using the CCK8 assay, and an oxidative stress model was established. Then the antioxidative stress activity and mechanism were investigated by ELISA, flow cytometry, and Western blotting. By the CCK-8 assay, exposure to CSE (20%, 40%, and 100%) reduced the viability of BEAB-2S cells. The flow cytometry findings indicated that CSE-induced production of ROS (0.5% to maximum) and treatments with 10 μM ebeiedinone and 20 μM peimisine attenuated the production of ROS. The western blot assay results indicate that ebeiedinone and peimisine reduce CSE-induced oxidative stress, DNA damage, apoptosis, and autophagy dysregulation by inhibiting ROS, upregulating SOD and GSH/GSSG, and downregulating MDA, 4-HNE, and 8-OHdG through the NRF2/KEAP1 and JNK/MAPK-dependent pathways, thereby delaying the pathological progression of COPD caused by CS.Our data suggest that CSE causes oxidative stress, DNA damage, and apoptosis in BEAS-2B cells, as well as the progression of COPD. Ebeiedinone and peimisine fight CS-induced COPD by suppressing autophagy deregulation and apoptosis.</div></div>","PeriodicalId":9684,"journal":{"name":"Cell Stress & Chaperones","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142380110","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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Editorial Board Members/Copyright 编委会成员/版权

IF 3.3 3区生物学

Cell Stress & Chaperones Pub Date : 2024-10-01 DOI: 10.1016/S1355-8145(24)00122-6

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Cover and caption 封面和标题

IF 3.3 3区生物学

Cell Stress & Chaperones Pub Date : 2024-10-01 DOI: 10.1016/S1355-8145(24)00121-4

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The mechanism and therapeutic strategies in doxorubicin-induced cardiotoxicity: Role of programmed cell death 多柔比星诱发心脏毒性的机制和治疗策略：程序性细胞死亡的作用

IF 3.3 3区生物学

Cell Stress & Chaperones Pub Date : 2024-10-01 DOI: 10.1016/j.cstres.2024.09.001

Yanzhao Li , Jing Yan , Pingzhen Yang

{"title":"The mechanism and therapeutic strategies in doxorubicin-induced cardiotoxicity: Role of programmed cell death","authors":"Yanzhao Li , Jing Yan , Pingzhen Yang","doi":"10.1016/j.cstres.2024.09.001","DOIUrl":"10.1016/j.cstres.2024.09.001","url":null,"abstract":"<div><div>Doxorubicin (DOX) is the most commonly used anthracycline anticancer agent, while its clinical utility is limited by harmful side effects like cardiotoxicity. Numerous studies have elucidated that programmed cell death plays a significant role in DOX-induced cardiotoxicity (DIC). This review summarizes several kinds of programmed cell death, including apoptosis, pyroptosis, necroptosis, autophagy, and ferroptosis. Furthermore, oxidative stress, inflammation, and mitochondrial dysfunction are also important factors in the molecular mechanisms of DIC. Besides, a comprehensive understanding of specific signal pathways of DIC can be helpful to its treatment. Therefore, the related signal pathways are elucidated in this review, including sirtuin deacetylase (silent information regulator 2 [Sir2]) 1 (SIRT1)/nuclear factor erythroid 2-related factor 2, SIRT1/Klotho, SIRT1/Recombinant Sestrin 2, adenosine monophosphate-activated protein kinase, AKT, and peroxisome proliferator-activated receptor. Heat shock proteins function as chaperones, which play an important role in various stressful situations, especially in the heart. Thus, some of heat shock proteins involved in DIC are also included. Hence, the last part of this review focuses on the therapeutic research based on the mechanisms above.</div></div>","PeriodicalId":9684,"journal":{"name":"Cell Stress & Chaperones","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142342430","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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HSPA12A stimulates “Smurf1-Hif1α-aerobic glycolysis” axis to promote proliferation of renal tubular epithelial cells after hypoxia/reoxygenation injury 缺氧/复氧损伤后，HSPA12A刺激 "Smurf1-Hif1α-有氧糖酵解 "轴，促进肾小管上皮细胞增殖。

IF 3.3 3区生物学

Cell Stress & Chaperones Pub Date : 2024-10-01 DOI: 10.1016/j.cstres.2024.09.002

Xinxu Min , Yunfan Li , Xiaojin Zhang , Shijiang Liu , Ziyang Chen , Qian Mao , Qiuyue Kong , Zhaohe Wang , Li Liu , Zhengnian Ding

{"title":"HSPA12A stimulates “Smurf1-Hif1α-aerobic glycolysis” axis to promote proliferation of renal tubular epithelial cells after hypoxia/reoxygenation injury","authors":"Xinxu Min , Yunfan Li , Xiaojin Zhang , Shijiang Liu , Ziyang Chen , Qian Mao , Qiuyue Kong , Zhaohe Wang , Li Liu , Zhengnian Ding","doi":"10.1016/j.cstres.2024.09.002","DOIUrl":"10.1016/j.cstres.2024.09.002","url":null,"abstract":"<div><div>Proliferation of renal tubular epithelial cells (TECs) is critical for the recovery after kidney ischemia/reperfusion (KI/R). However, there is still a lack of ideal therapies for promoting TEC proliferation. Heat shock protein A12A (HSPA12A) shows abundant expression in kidney in our previous studies. To investigate the role of HSPA12A in TEC proliferation after KI/R, an <em>in vitro</em> KI/R model was simulated by hypoxia (12 h) and reoxygenation (12 h) in human kidney tubular epithelial HK-2 cells. We found that, when hypoxia/reoxygenation (H/R) triggered HK-2 cell injury, HSPA12A expression was downregulated, and extracellular lactate, the readout of glycolysis, was also decreased. Loss and gain of functional studies showed that HSPA12A did not change cell viability after hypoxia but increased cell proliferation as well as glycolytic flux of HK-2 cells after H/R. When blocking glycolysis by 2-deoxy-D-glucose or oxamate, the HSPA12A promoted HK-2 cell proliferation was also abolished. Further analysis revealed that HSPA12A overexpression increased hypoxia-inducible factor 1α (Hif1α) protein expression and nuclear localization in HK-2 cells in response to H/R, whereas HSPA12A knockdown showed the opposite effects. Notably, pharmacological inhibition of Hif1α with YC-1 reversed the HSPA12A-induced increases of both glycolytic flux and proliferation of H/R HK-2 cells. Moreover, the HSPA12A increased Hif1α protein expression was not <em>via</em> upregulating its transcription but through increasing its protein stability in a Smurf1-dependent manner. The findings indicate that HSPA12A might serve as a promising target for TEC proliferation to help recovery after KI/R.</div></div>","PeriodicalId":9684,"journal":{"name":"Cell Stress & Chaperones","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142342429","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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