Cell Stress最新文献_第5页

Macroautophagy and normal aging of the nervous system: Lessons from animal models. 巨噬和神经系统的正常衰老:来自动物模型的教训。

IF 6.4

Cell Stress Pub Date : 2021-10-06 eCollection Date: 2021-10-01 DOI: 10.15698/cst2021.10.257

Emmanouela Kallergi, Vassiliki Nikoletopoulou

引用次数: 5

Host upregulation of lipid droplets drives antiviral responses. 宿主脂滴的上调驱动抗病毒反应。

IF 6.4

Cell Stress Pub Date : 2021-08-25 eCollection Date: 2021-09-01 DOI: 10.15698/cst2021.09.256

Ebony A Monson, Karla J Helbig

{"title":"Host upregulation of lipid droplets drives antiviral responses.","authors":"Ebony A Monson, Karla J Helbig","doi":"10.15698/cst2021.09.256","DOIUrl":"https://doi.org/10.15698/cst2021.09.256","url":null,"abstract":"When a host cell is infected by a virus, it activates the innate immune response, setting off a cascade of signalling events leading to the production of an antiviral response. This immune response is typically robust and in general works well to clear viral infections, however, viruses have evolved evasion strategies to combat this, and therefore, a better understanding of how this response works in more detail is needed for the development of novel and effective therapeutics. Lipid droplets (LDs) are intracellular organelles and have historically been thought of simply as cellular energy sources, however, have more recently been recognised as critical organelles in signalling events. Importantly, many viruses are known to take over host cellular production of LDs, and it has traditionally been assumed the sole purpose of this is to supply energy for viral life cycle events. However, our recent work positions LDs as important organelles during the first few hours of an antiviral response, showing that they underpin the production of important antiviral cytokines following viral infection. Following infection of cells with either RNA viruses (Zika, Dengue, Influenza A) or a DNA (Herpes Simplex Virus-1) virus, LDs were rapidly upregulated, and this response was also replicated following stimulation with viral mimic agonists. This upregulation of LDs following infection was transient, and interestingly, did not follow the well described homeostatic mechanism of LD upregulation, instead being controlled by EGFR. The cell's ability to mount an effective immune response was greatly diminished when inhibiting EGFR, thus inhibiting LD upregulation during infection, also leading to an increase in viral replication. In this microreview, we extrapolate our recent findings and discuss LDs as an important organelle in the innate immune response.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"5 9","pages":"143-145"},"PeriodicalIF":6.4,"publicationDate":"2021-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8404386/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39420927","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 4

Atg8ylation as a general membrane stress and remodeling response. Atg8ylation 是一种普遍的膜应激和重塑反应。

IF 6.4

Cell Stress Pub Date : 2021-08-12 eCollection Date: 2021-09-01 DOI: 10.15698/cst2021.09.255

Suresh Kumar, Jingyue Jia, Vojo Deretic

引用次数: 0

PDLIM1: Structure, function and implication in cancer. PDLIM1:结构、功能及其在癌症中的意义。

IF 6.4

Cell Stress Pub Date : 2021-07-26 eCollection Date: 2021-08-01 DOI: 10.15698/cst2021.08.254

Jian-Kang Zhou, Xin Fan, Jian Cheng, Wenrong Liu, Yong Peng

引用次数: 9

Towards a better understanding of the neuro-developmental role of autophagy in sickness and in health. 更好地理解自噬在疾病和健康中对神经发育的作用。

IF 4.1

Cell Stress Pub Date : 2021-06-29 eCollection Date: 2021-07-01 DOI: 10.15698/cst2021.07.253

Juan Zapata-Muñoz, Beatriz Villarejo-Zori, Pablo Largo-Barrientos, Patricia Boya

引用次数: 0

Elevated plasma levels of the appetite-stimulator ACBP/DBI in fasting and obese subjects. 空腹和肥胖受试者中食欲刺激剂ACBP/DBI血浆水平升高。

IF 6.4

Cell Stress Pub Date : 2021-06-28 eCollection Date: 2021-07-01 DOI: 10.15698/cst2021.07.252

Sijing Li, Adrien Joseph, Isabelle Martins, Guido Kroemer

{"title":"Elevated plasma levels of the appetite-stimulator ACBP/DBI in fasting and obese subjects.","authors":"Sijing Li, Adrien Joseph, Isabelle Martins, Guido Kroemer","doi":"10.15698/cst2021.07.252","DOIUrl":"https://doi.org/10.15698/cst2021.07.252","url":null,"abstract":"Eukaryotic cells release the phylogenetically ancient protein acyl coenzyme A binding protein (ACBP, which in humans is encoded by the gene DBI, diazepam binding inhibitor) upon nutrient deprivation. Accordingly, mice that are starved for one to two days and humans that undergo voluntary fasting for one to three weeks manifest an increase in the plasma concentration of ACBP/DBI. Paradoxically, ACBP/DBI levels also increase in obese mice and humans. Since ACBP/DBI stimulates appetite, this latter finding may explain why obesity constitutes a self-perpetuating state. Here, we present a theoretical framework to embed these findings in the mechanisms of weight control, as well as a bioinformatics analysis showing that, irrespective of the human cell or tissue type, one single isoform of ACBP/DBI (ACBP1) is preponderant (~90% of all DBI transcripts, with the sole exception of the testis, where it is ~70%). Based on our knowledge, we conclude that ACBP1 is subjected to a biphasic transcriptional and post-transcriptional regulation, explaining why obesity and fasting both are associated with increased circulating ACBP1 protein levels.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"5 7","pages":"89-98"},"PeriodicalIF":6.4,"publicationDate":"2021-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8283301/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39221485","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

Ribosome traffic jam in neurodegeneration: decoding hurdles in Huntington disease. 神经退行性疾病中的核糖体阻塞:亨廷顿病的解码障碍。

IF 6.4

Cell Stress Pub Date : 2021-05-03 DOI: 10.15698/cst2021.06.251

Srinivasa Subramaniam

{"title":"Ribosome traffic jam in neurodegeneration: decoding hurdles in Huntington disease.","authors":"Srinivasa Subramaniam","doi":"10.15698/cst2021.06.251","DOIUrl":"https://doi.org/10.15698/cst2021.06.251","url":null,"abstract":"A ribosome typically moves at a particular rate on a given mRNA transcript to decode the nucleic acid information required to synthesize proteins. The speed and directionality of the ribosome movements during mRNA translation are determined by the mRNA sequence and structure and by various decoding factors. However, the molecular mechanisms of this remarkable movement during protein synthesis, or its relevance in brain disorders, remain unknown. Recent studies have indicated that defects in protein synthesis occur in various neurodegenerative diseases, but the mechanistic details are unclear. This is a major problem because identifying the factors that determine protein synthesis defects may offer new avenues for developing therapeutic remedies for currently incurable diseases like neurodegenerative disorders. Based on our recent study (Eshraghi et al., Nat Commun 12(1):1461; doi: 10.1038/s41467-021-21637-y), this short commentary will review the mechanistic understanding of Huntingtin (HTT)-mediated ribosome stalling indicating that central defects in protein synthesis in Huntington disease (HD) are orchestrated by jamming of ribosomes on mRNA transcripts.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"5 6","pages":"86-88"},"PeriodicalIF":6.4,"publicationDate":"2021-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8166216/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39092560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

The evolution of the concept of stress and the framework of the stress system. 应力概念的演变和应力系统的框架。

IF 6.4

Cell Stress Pub Date : 2021-04-26 DOI: 10.15698/cst2021.06.250

Siyu Lu, Fang Wei, Guolin Li

{"title":"The evolution of the concept of stress and the framework of the stress system.","authors":"Siyu Lu, Fang Wei, Guolin Li","doi":"10.15698/cst2021.06.250","DOIUrl":"10.15698/cst2021.06.250","url":null,"abstract":"Stress is a central concept in biology and has now been widely used in psychological, physiological, social, and even environmental fields. However, the concept of stress was cross-utilized to refer to different elements of the stress system including stressful stimulus, stressor, stress response, and stress effect. Here, we summarized the evolution of the concept of stress and the framework of the stress system. We find although the concept of stress is developed from Selye's \"general adaptation syndrome\", it has now expanded and evolved significantly. Stress is now defined as a state of homeostasis being challenged, including both system stress and local stress. A specific stressor may potentially bring about specific local stress, while the intensity of stress beyond a threshold may commonly activate the hypothalamic-pituitary-adrenal axis and result in a systematic stress response. The framework of the stress system indicates that stress includes three types: sustress (inadequate stress), eustress (good stress), and distress (bad stress). Both sustress and distress might impair normal physiological functions and even lead to pathological conditions, while eustress might benefit health through hormesis-induced optimization of homeostasis. Therefore, an optimal stress level is essential for building biological shields to guarantee normal life processes.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"5 6","pages":"76-85"},"PeriodicalIF":6.4,"publicationDate":"2021-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8166217/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39092559","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 47

Coping with the calcium overload caused by cell injury: ER to the rescue. 应对细胞损伤引起的钙超载:ER的救星。

IF 6.4

Cell Stress Pub Date : 2021-04-16 DOI: 10.15698/cst2021.05.249

Goutam Chandra, Davi A G Mázala, Jyoti K Jaiswal

{"title":"Coping with the calcium overload caused by cell injury: ER to the rescue.","authors":"Goutam Chandra, Davi A G Mázala, Jyoti K Jaiswal","doi":"10.15698/cst2021.05.249","DOIUrl":"https://doi.org/10.15698/cst2021.05.249","url":null,"abstract":"Cells maintain their cytosolic calcium (Ca2+) in nanomolar range and use controlled increase in Ca2+ for intracellular signaling. With the extracellular Ca2+ in the millimolar range, there is a steep Ca2+ gradient across the plasma membrane (PM). Thus, injury that damages PM, leads to a cytosolic Ca2+ overload, which helps activate PM repair (PMR) response. However, in order to survive, the cells must cope with the Ca2+ overload. In a recent study (Chandra et al. J Cell Biol, doi: 10.1083/jcb.202006035) we have examined how cells cope with injury-induced cytosolic Ca2+ overload. By monitoring Ca2+ dynamics in the cytosol and endoplasmic reticulum (ER), we found that PM injury-triggered increase in cytosolic Ca2+ is taken up by the ER. Pharmacological inhibition of ER Ca2+ uptake interferes with this process and compromises the repair ability of the injured cells. Muscle cells from patients and mouse model for the muscular dystrophy showed that lack of Anoctamin 5 (ANO5)/Transmembrane protein 16E (TMEM16E), an ER-resident putative Ca2+-activated chloride channel (CaCC), are poor at coping with cytosolic Ca2+ overload. Pharmacological inhibition of CaCC and lack of ANO5, both prevent Ca2+ uptake into ER. These studies identify a requirement of Cl- uptake by the ER in sequestering injury-triggered cytosolic Ca2+ increase in the ER. Further, these studies show that ER helps injured cells cope with Ca2+ overload during PMR, lack of which contributes to muscular dystrophy due to mutations in the ANO5 protein.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"5 5","pages":"73-75"},"PeriodicalIF":6.4,"publicationDate":"2021-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8090859/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38979703","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

Cellular mechanisms linking cancers to obesity. 癌症和肥胖之间的细胞机制。

IF 6.4

Cell Stress Pub Date : 2021-04-12 DOI: 10.15698/cst2021.05.248

Xiao-Zheng Liu, Line Pedersen, Nils Halberg

引用次数: 17