Advances in biological regulation最新文献_第8页

Key to photograph of participants 参加者照片的钥匙

Advances in biological regulation Pub Date : 2023-01-01 DOI: 10.1016/j.jbior.2022.100952

引用次数: 0

Phospholipase D and cancer metastasis: A focus on exosomes 磷脂酶D与肿瘤转移:以外泌体为中心

Advances in biological regulation Pub Date : 2023-01-01 DOI: 10.1016/j.jbior.2022.100924

Alexander Wolf, Emeline Tanguy, Qili Wang, Stéphane Gasman, Nicolas Vitale

{"title":"Phospholipase D and cancer metastasis: A focus on exosomes","authors":"Alexander Wolf, Emeline Tanguy, Qili Wang, Stéphane Gasman, Nicolas Vitale","doi":"10.1016/j.jbior.2022.100924","DOIUrl":"10.1016/j.jbior.2022.100924","url":null,"abstract":"<div><p>In mammals, phospholipase D (PLD) enzymes involve 6 isoforms, of which only three have established lipase activity to produce the signaling lipid phosphatidic acid (PA). This phospholipase activity has been postulated to contribute to cancer progression for over three decades now, but the exact mechanisms involved have yet to be uncovered. Indeed, using various models, an altered PLD activity has been proposed altogether to increase cell survival rate, promote angiogenesis, boost rapamycin resistance, and favor metastasis. Although for some part, the molecular pathways by which this increase in PA is pro-oncogenic are partially known, the pleiotropic functions of PA make it quite difficult to distinguish which among these simple signaling pathways is responsible for each of these PLD facets. In this review, we will describe an additional potential contribution of PA generated by PLD1 and PLD2 in the biogenesis, secretion, and uptake of exosomes. Those extracellular vesicles are now viewed as membrane vehicles that carry informative molecules able to modify the fate of receiving cells at distance from the original tumor to favor homing of metastasis. The perspectives for a better understanding of these complex role of PLDs will be discussed.</p></div>","PeriodicalId":7214,"journal":{"name":"Advances in biological regulation","volume":"87 ","pages":"Article 100924"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9173474","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Advances in MDS/AML and inositide signalling MDS/AML和肌苷信号传导的研究进展

Advances in biological regulation Pub Date : 2023-01-01 DOI: 10.1016/j.jbior.2023.100955

Alessia De Stefano , Maria Vittoria Marvi , Antonietta Fazio , James A. McCubrey , Pann-Ghill Suh , Stefano Ratti , Giulia Ramazzotti , Lucia Manzoli , Lucio Cocco , Matilde Y. Follo

引用次数: 1

Silencing effects of mutant RAS signalling on transcriptomes 突变体RAS信号对转录组的沉默作用

Advances in biological regulation Pub Date : 2023-01-01 DOI: 10.1016/j.jbior.2022.100936

Christine Sers , Reinhold Schäfer

{"title":"Silencing effects of mutant RAS signalling on transcriptomes","authors":"Christine Sers , Reinhold Schäfer","doi":"10.1016/j.jbior.2022.100936","DOIUrl":"10.1016/j.jbior.2022.100936","url":null,"abstract":"<div><p>Mutated genes of the RAS family encoding small GTP-binding proteins drive numerous cancers, including pancreatic, colon and lung tumors. Besides the numerous effects of mutant RAS gene expression on aberrant proliferation, transformed phenotypes, metabolism, and therapy resistance, the most striking consequences of chronic RAS activation are changes of the genetic program. By performing systematic gene expression studies in cellular models that allow comparisons of pre-neoplastic with RAS-transformed cells, we and others have estimated that 7 percent or more of all transcripts are altered in conjunction with the expression of the oncogene. In this context, the number of up-regulated transcripts approximates that of down-regulated transcripts. While up-regulated transcription factors such as MYC, FOSL1, and HMGA2 have been identified and characterized as RAS-responsive drivers of the altered transcriptome, the suppressed factors have been less well studied as potential regulators of the genetic program and transformed phenotype in the breadth of their occurrence. We therefore have collected information on downregulated RAS-responsive factors and discuss their potential role as tumor suppressors that are likely to antagonize active cancer drivers. To better understand the active mechanisms that entail anti-RAS function and those that lead to loss of tumor suppressor activity, we focus on the tumor suppressor HREV107 (alias PLAAT3 [Phospholipase A and acyltransferase 3], PLA2G16 [Phospholipase A2, group XVI] and HRASLS3 [HRAS-like suppressor 3]). Inactivating HREV107 mutations in tumors are extremely rare, hence epigenetic causes modulated by the RAS pathway are likely to lead to down-regulation and loss of function.</p></div>","PeriodicalId":7214,"journal":{"name":"Advances in biological regulation","volume":"87 ","pages":"Article 100936"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9173956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Novel aspects of intra-islet communication: Primary cilia and filopodia 胰岛内通讯的新方面:初级纤毛和丝状足

Advances in biological regulation Pub Date : 2023-01-01 DOI: 10.1016/j.jbior.2022.100919

Noah Moruzzi, Barbara Leibiger, Christopher J. Barker, Ingo B. Leibiger, Per-Olof Berggren

{"title":"Novel aspects of intra-islet communication: Primary cilia and filopodia","authors":"Noah Moruzzi, Barbara Leibiger, Christopher J. Barker, Ingo B. Leibiger, Per-Olof Berggren","doi":"10.1016/j.jbior.2022.100919","DOIUrl":"10.1016/j.jbior.2022.100919","url":null,"abstract":"<div><p>Pancreatic islets are micro-organs composed of a mixture of endocrine and non-endocrine cells, where the former secrete hormones and peptides necessary for metabolic homeostasis. Through vasculature and innervation the cells within the islets are in communication with the rest of the body, while they interact with each other through juxtacrine, paracrine and autocrine signals, resulting in fine-tuned sensing and response to stimuli. In this context, cellular protrusion in islet cells, such as primary cilia and filopodia, have gained attention as potential signaling hubs. During the last decade, several pieces of evidence have shown how the primary cilium is required for islet vascularization, function and homeostasis. These findings have been possible thanks to the development of ciliary/basal body specific knockout models and technological advances in microscopy, which allow longitudinal monitoring of engrafted islets transplanted in the anterior chamber of the eye in living animals. Using this technique in combination with optogenetics, new potential paracrine interactions have been suggested. For example, reshaping and active movement of filopodia-like protrusions of δ-cells were visualized <em>in vivo</em>, suggesting a continuous cell remodeling to increase intercellular contacts. In this review, we discuss these recent discoveries regarding primary cilia and filopodia and their role in islet homeostasis and intercellular islet communication.</p></div>","PeriodicalId":7214,"journal":{"name":"Advances in biological regulation","volume":"87 ","pages":"Article 100919"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9180901","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

Sixty-third international symposium on biological regulation and enzyme activity in normal and neoplastic tissues 第六十三届正常和肿瘤组织的生物调控和酶活性国际研讨会

Advances in biological regulation Pub Date : 2023-01-01 DOI: 10.1016/j.jbior.2022.100949

引用次数: 0

A consensus of evidence: The role of SPI-M-O in the UK COVID-19 response 证据共识:SPI-M-O在英国COVID-19应对中的作用

Advances in biological regulation Pub Date : 2022-12-01 DOI: 10.1016/j.jbior.2022.100918

Graham F. Medley

引用次数: 8

Virus spread on a scale-free network reproduces the Gompertz growth observed in isolated COVID-19 outbreaks 病毒在无标度网络上的传播再现了在孤立的COVID-19爆发中观察到的冈珀茨生长

Advances in biological regulation Pub Date : 2022-12-01 DOI: 10.1016/j.jbior.2022.100915

Francesco Zonta , Michael Levitt

{"title":"Virus spread on a scale-free network reproduces the Gompertz growth observed in isolated COVID-19 outbreaks","authors":"Francesco Zonta , Michael Levitt","doi":"10.1016/j.jbior.2022.100915","DOIUrl":"10.1016/j.jbior.2022.100915","url":null,"abstract":"<div><p>The counts of confirmed cases and deaths in isolated SARS-CoV-2 outbreaks follow the Gompertz growth function for locations of very different sizes. This lack of dependence on region size leads us to hypothesize that virus spread depends on the universal properties of the network of social interactions. We test this hypothesis by simulating the propagation of a virus on networks of different topologies or connectivities. Our main finding is that we can reproduce the Gompertz growth observed for many early outbreaks with a simple virus spread model on a scale-free network, in which nodes with many more neighbors than average are common. Nodes that have very many neighbors are infected early in the outbreak and then spread the infection very rapidly. When these nodes are no longer infectious, the remaining nodes that have most neighbors take over and continue to spread the infection. In this way, the rate of spread is fastest at the very start and slows down immediately. Geometrically we see that the \"surface\" of the epidemic, the number of susceptible nodes in contact with the infected nodes, starts to rapidly decrease very early in the epidemic and as soon as the larger nodes have been infected. In our simulation, the speed and impact of an outbreak depend on three parameters: the average number of contacts each node makes, the probability of being infected by a neighbor, and the probability of recovery. Intelligent interventions to reduce the impact of future outbreaks need to focus on these critical parameters in order to minimize economic and social collateral damage.</p></div>","PeriodicalId":7214,"journal":{"name":"Advances in biological regulation","volume":"86 ","pages":"Article 100915"},"PeriodicalIF":0.0,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9523942/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9575550","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

Establishing COVID-19 trials at scale and pace: Experience from the RECOVERY trial 以规模和速度建立COVID-19试验:来自康复试验的经验

Advances in biological regulation Pub Date : 2022-12-01 DOI: 10.1016/j.jbior.2022.100901

Leon Peto , Peter Horby , Martin Landray

{"title":"Establishing COVID-19 trials at scale and pace: Experience from the RECOVERY trial","authors":"Leon Peto , Peter Horby , Martin Landray","doi":"10.1016/j.jbior.2022.100901","DOIUrl":"10.1016/j.jbior.2022.100901","url":null,"abstract":"<div><p>The Randomised Evaluation of COVID-19 Therapy (RECOVERY) Trial was set up in March 2020 to evaluate treatments for people hospitalised with COVID-19. To maximise recruitment it was designed to fit into routine clinical care throughout the UK, and as a result it has enrolled more patients than any other COVID-19 treatment trial. RECOVERY has shown four drugs to be life-saving – dexamethasone, tocilizumab, baricitinib and casirivimab-imdevimab – and a further six have been shown to be of little or no benefit. In each case, results from RECOVERY were clear enough to rapidly influence global practice. Some of the reasons for this success relate to its particular setting in the UK during the SARS-CoV-2 pandemic, but many are generalisable to other contexts. In particular, its focus on recruiting large numbers of patients to identify or rule out moderate but worthwhile benefits of treatment, and the design decisions that followed from this. Similar large streamlined trials could produce similarly clear answers about the treatment of many other common diseases.</p></div>","PeriodicalId":7214,"journal":{"name":"Advances in biological regulation","volume":"86 ","pages":"Article 100901"},"PeriodicalIF":0.0,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9293394/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9941673","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: 9

Gaining insight into the role of FoxO1 in the progression of disuse-induced skeletal muscle atrophy 深入了解fox01在废用性骨骼肌萎缩进展中的作用

Advances in biological regulation Pub Date : 2022-08-01 DOI: 10.1016/j.jbior.2022.100903

Natalia Vilchinskaya , Erzhena Altaeva , Yulia Lomonosova

{"title":"Gaining insight into the role of FoxO1 in the progression of disuse-induced skeletal muscle atrophy","authors":"Natalia Vilchinskaya , Erzhena Altaeva , Yulia Lomonosova","doi":"10.1016/j.jbior.2022.100903","DOIUrl":"10.1016/j.jbior.2022.100903","url":null,"abstract":"<div><p>Expression of FoxO transcription factors increases during certain forms of atrophy. In a dephosphorylated state, FoxOs participate in ubiquitin-mediated proteasomal degradation through the transcriptional activation of E3-ubiquitin ligases such as MAFbx/atrogin-1 and MuRF1. There is exhaustive research demonstrating that FoxO3a is sufficient to induce MAFbx/atrogin-1 and MuRF-1 expressions. In contrast, the data are conflicting on the requirement of FoxO1 signaling in the activation of the E3-ubiquitin ligases. Moreover, no reports currently exist on the particular role of FoxO1 in the molecular mechanisms involved in the progression of physiological muscle wasting. Here, we have applied the most extensively used rodent model of microgravity/functional unloading to stimulate disuse-induced skeletal muscle atrophy such as rat hindlimb suspension (HS). We showed that inhibition of FoxO1 activity by a selective inhibitor AS1842856 completely reversed an increase in expression of MuRF-1, but not MAFbx/atrogin-1, observed upon HS. Furthermore, we demonstrated that FoxO1 induced upregulation of another E3-ubiquitin-ligase of a MuRF protein family MuRF-2 in skeletal muscle subjected to disuse. Prevention of the MuRF increase upon HS impeded upregulation of transcript expression of a negative regulator of NFATc1 pathway calsarcin-2, which was associated with a partial reversion of MyHC-IId/x and MyHC-IIb mRNA expressions. Importantly, FoxO1 inhibition induced a marked increase in p70S6k phosphorylation, an important stage in the initiation of protein translation, concomitant with the restoration of global protein synthesis in the skeletal muscle of the HS rats. Examination of eIF3f expression and the eEF2k/eEF2 pathway, other factors controlling translation initiation and elongation respectively, did not reveal any impact of FoxO1 on their activity. Lastly, we observed a decrease in transcript levels of Sesn3, but not Sesn1 and Sesn2, upon disuse, which was completely reversed by FoxO1 inhibition. These data demonstrate that FoxO1 signaling contributes to the development of disuse-induced skeletal muscle atrophy, including slow to fast MyHC isoform shift, mostly through upregulation of MuRF-1 and MuRF-2 expression. Furthermore, FoxO1 inhibition is required to recover Sesn3 mRNA expression in atrophic conditions, which likely contributes to the enhanced p70S6k activity and restoration of the protein synthesis rate.</p></div>","PeriodicalId":7214,"journal":{"name":"Advances in biological regulation","volume":"85 ","pages":"Article 100903"},"PeriodicalIF":0.0,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2212492622000434/pdfft?md5=032267105d296d0306025777dea3e5e1&pid=1-s2.0-S2212492622000434-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10376354","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: 6