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The anoctamins: Structure and function 营养素结构与功能
IF 4 2区 生物学
Cell calcium Pub Date : 2024-04-15 DOI: 10.1016/j.ceca.2024.102885
Rainer Schreiber, Jiraporn Ousingsawat, Karl Kunzelmann
{"title":"The anoctamins: Structure and function","authors":"Rainer Schreiber,&nbsp;Jiraporn Ousingsawat,&nbsp;Karl Kunzelmann","doi":"10.1016/j.ceca.2024.102885","DOIUrl":"https://doi.org/10.1016/j.ceca.2024.102885","url":null,"abstract":"<div><p>When activated by increase in intracellular Ca<sup>2+</sup>, anoctamins (TMEM16 proteins) operate as phospholipid scramblases and as ion channels. Anoctamin 1 (ANO1) is the Ca<sup>2+</sup>-activated epithelial anion-selective channel that is coexpressed together with the abundant scramblase ANO6 and additional intracellular anoctamins. In salivary and pancreatic glands, ANO1 is tightly packed in the apical membrane and secretes Cl<sup>−</sup>. Epithelia of airways and gut use cystic fibrosis transmembrane conductance regulator (CFTR) as an apical Cl<sup>−</sup> exit pathway while ANO1 supports Cl<sup>−</sup> secretion mainly by facilitating activation of luminal CFTR and basolateral <em>K</em><sup>+</sup> channels. Under healthy conditions ANO1 modulates intracellular Ca<sup>2+</sup> signals by tethering the endoplasmic reticulum, and except of glands its direct secretory contribution as Cl<sup>−</sup> channel might be small, compared to CFTR. In the kidneys ANO1 supports proximal tubular acid secretion and protein reabsorption and probably helps to excrete HCO<sub>3</sub><sup>−</sup>in the collecting duct epithelium. However, under pathological conditions as in polycystic kidney disease, ANO1 is strongly upregulated and may cause enhanced proliferation and cyst growth. Under pathological condition, ANO1 and ANO6 are upregulated and operate as secretory channel/phospholipid scramblases, partly by supporting Ca<sup>2+</sup>-dependent processes. Much less is known about the role of other epithelial anoctamins whose potential functions are discussed in this review.</p></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"120 ","pages":"Article 102885"},"PeriodicalIF":4.0,"publicationDate":"2024-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0143416024000435/pdfft?md5=6adf751f62121e312218f7d0a3c538d0&pid=1-s2.0-S0143416024000435-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140620607","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
pH regulating mechanisms of astrocytes: A critical component in physiology and disease of the brain 星形胶质细胞的 pH 值调节机制:大脑生理和疾病的关键组成部分
IF 4 2区 生物学
Cell calcium Pub Date : 2024-04-08 DOI: 10.1016/j.ceca.2024.102882
Shefeeq M. Theparambil , Gulnaz Begum , Christine R. Rose
{"title":"pH regulating mechanisms of astrocytes: A critical component in physiology and disease of the brain","authors":"Shefeeq M. Theparambil ,&nbsp;Gulnaz Begum ,&nbsp;Christine R. Rose","doi":"10.1016/j.ceca.2024.102882","DOIUrl":"https://doi.org/10.1016/j.ceca.2024.102882","url":null,"abstract":"<div><p>Strict homeostatic control of pH in both intra- and extracellular compartments of the brain is fundamentally important, primarily due to the profound impact of free protons ([<em>H</em><sup>+</sup>]) on neuronal activity and overall brain function. Astrocytes, crucial players in the homeostasis of various ions in the brain, actively regulate their intracellular [<em>H</em><sup>+</sup>] (pH<sub>i</sub>) through multiple membrane transporters and carbonic anhydrases. The activation of astroglial pH<sub>i</sub> regulating mechanisms also leads to corresponding alterations in the acid-base status of the extracellular fluid. Notably, astrocyte pH regulators are modulated by various neuronal signals, suggesting their pivotal role in regulating brain acid-base balance in both health and disease. This review presents the mechanisms involved in pH regulation in astrocytes and discusses their potential impact on extracellular pH under physiological conditions and in brain disorders. Targeting astrocytic pH regulatory mechanisms represents a promising therapeutic approach for modulating brain acid-base balance in diseases, offering a potential critical contribution to neuroprotection.</p></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"120 ","pages":"Article 102882"},"PeriodicalIF":4.0,"publicationDate":"2024-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S014341602400040X/pdfft?md5=03f3d9286d0f6ca600257cdc4408fefb&pid=1-s2.0-S014341602400040X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140555192","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Simultaneous TIRF imaging of subplasmalemmal Ca2+ dynamics and granule fusions in insulin-secreting INS-1 cells reveals coexistent synchronized and asynchronous release 对分泌胰岛素的 INS-1 细胞浆膜下 Ca2+ 动态和颗粒融合进行同步 TIRF 成像,发现同步和非同步释放同时存在
IF 4 2区 生物学
Cell calcium Pub Date : 2024-04-08 DOI: 10.1016/j.ceca.2024.102883
Charlotte Suckert , Carolin Zosel , Michael Schaefer
{"title":"Simultaneous TIRF imaging of subplasmalemmal Ca2+ dynamics and granule fusions in insulin-secreting INS-1 cells reveals coexistent synchronized and asynchronous release","authors":"Charlotte Suckert ,&nbsp;Carolin Zosel ,&nbsp;Michael Schaefer","doi":"10.1016/j.ceca.2024.102883","DOIUrl":"https://doi.org/10.1016/j.ceca.2024.102883","url":null,"abstract":"<div><p>The basal and glucose-induced insulin secretion from pancreatic beta cells is a tightly regulated process that is triggered in a Ca<sup>2+</sup>-dependent fashion and further positively modulated by substances that raise intracellular levels of adenosine 3′,5′-cyclic monophosphate (cAMP) or by certain antidiabetic drugs. In a previous study, we have temporally resolved the subplasmalemmal [Ca<sup>2+</sup>]<sub>i</sub> dynamics in beta cells that are characterized by trains of sharply delimited spikes, reaching peak values up to 5 µM. Applying total internal reflection fluorescence (TIRF) microscopy and synaptopHluorin to visualize fusion events of individual granules, we found that several fusion events can coincide within 50 to 150 ms. To test whether subplasmalemmal [Ca<sup>2+</sup>]<sub>i</sub> microdomains around single or clustered Ca<sup>2+</sup> channels may cause a synchronized release of insulin-containing vesicles, we applied simultaneous dual-color TIRF microscopy and monitored Ca<sup>2+</sup> fluctuations and exocytotic events in INS-1 cells at high frame rates. The results indicate that fusions can be triggered by subplasmalemmal Ca<sup>2+</sup> spiking. This, however, does account for a minority of fusion events. About 90 %-95 % of fusion events either happen between Ca<sup>2+</sup> spikes or incidentally overlap with subplasmalemmal Ca<sup>2+</sup> spikes. We conclude that only a fraction of exocytotic events in glucose-induced and tolbutamide- or forskolin-enhanced insulin release from INS-1 cells is tightly coupled to Ca<sup>2+</sup> microdomains around voltage-gated Ca<sup>2+</sup> channels.</p></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"120 ","pages":"Article 102883"},"PeriodicalIF":4.0,"publicationDate":"2024-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0143416024000411/pdfft?md5=85c9b28c7c9d3d4d9253198eaf4bcd8d&pid=1-s2.0-S0143416024000411-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140621812","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
A novel probe to monitor lysosome-mitochondria contact sites opens up a new path to study neurodegenerative diseases 监测溶酶体-线粒体接触点的新型探针为研究神经退行性疾病开辟了新途径
IF 4 2区 生物学
Cell calcium Pub Date : 2024-04-08 DOI: 10.1016/j.ceca.2024.102887
Mai Makino , Shuhei Nakamura
{"title":"A novel probe to monitor lysosome-mitochondria contact sites opens up a new path to study neurodegenerative diseases","authors":"Mai Makino ,&nbsp;Shuhei Nakamura","doi":"10.1016/j.ceca.2024.102887","DOIUrl":"https://doi.org/10.1016/j.ceca.2024.102887","url":null,"abstract":"","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"120 ","pages":"Article 102887"},"PeriodicalIF":4.0,"publicationDate":"2024-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140536794","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
TRPM7 in neurodevelopment and therapeutic prospects for neurodegenerative disease 神经发育中的 TRPM7 和神经退行性疾病的治疗前景
IF 4 2区 生物学
Cell calcium Pub Date : 2024-04-06 DOI: 10.1016/j.ceca.2024.102886
Zhengwei Luo , Xinyang Zhang , Andrea Fleig , Daniel Romo , Kenneth G. Hull , F. David Horgen , Hong-Shuo Sun , Zhong-Ping Feng
{"title":"TRPM7 in neurodevelopment and therapeutic prospects for neurodegenerative disease","authors":"Zhengwei Luo ,&nbsp;Xinyang Zhang ,&nbsp;Andrea Fleig ,&nbsp;Daniel Romo ,&nbsp;Kenneth G. Hull ,&nbsp;F. David Horgen ,&nbsp;Hong-Shuo Sun ,&nbsp;Zhong-Ping Feng","doi":"10.1016/j.ceca.2024.102886","DOIUrl":"https://doi.org/10.1016/j.ceca.2024.102886","url":null,"abstract":"<div><p>Neurodevelopment, a complex and highly regulated process, plays a foundational role in shaping the structure and function of the nervous system. The transient receptor potential melastatin 7 (TRPM7), a divalent cation channel with an α-kinase domain, mediates a wide range of cellular functions, including proliferation, migration, cell adhesion, and survival, all of which are essential processes in neurodevelopment. The global knockout of either TRPM7 or TRPM7-kinase is embryonically lethal, highlighting the crucial role of TRPM7 in development <em>in vivo</em>. Subsequent research further revealed that TRPM7 is indeed involved in various key processes throughout neurodevelopment, from maintaining pluripotency during embryogenesis to regulating gastrulation, neural tube closure, axonal outgrowth, synaptic density, and learning and memory. Moreover, a discrepancy in TRPM7 expression and/or function has been associated with neuropathological conditions, including ischemic stroke, Alzheimer's disease, and Parkinson's disease. Understanding the mechanisms of proper neurodevelopment may provide us with the knowledge required to develop therapeutic interventions that can overcome the challenges of regeneration in CNS injuries and neurodegenerative diseases. Considering that ion channels are the third-largest class targeted for drug development, TRPM7′s dual roles in development and degeneration emphasize its therapeutic potential. This review provides a comprehensive overview of the current literature on TRPM7 in various aspects of neurodevelopment. It also discusses the links between neurodevelopment and neurodegeneration, and highlights TRPM7 as a potential therapeutic target for neurodegenerative disorders, with a focus on repair and regeneration.</p></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"120 ","pages":"Article 102886"},"PeriodicalIF":4.0,"publicationDate":"2024-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140558195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
PDX1, a transcription factor essential for organ differentiation, regulates SERCA-dependent Ca2+ homeostasis in sensory neurons 器官分化所必需的转录因子 PDX1 可调节感觉神经元中依赖 SERCA 的 Ca2+ 稳态
IF 4 2区 生物学
Cell calcium Pub Date : 2024-04-02 DOI: 10.1016/j.ceca.2024.102884
Jami L. Saloman , Ariel Y. Epouhe , Catherine F. Ruff , Kathryn M. Albers
{"title":"PDX1, a transcription factor essential for organ differentiation, regulates SERCA-dependent Ca2+ homeostasis in sensory neurons","authors":"Jami L. Saloman ,&nbsp;Ariel Y. Epouhe ,&nbsp;Catherine F. Ruff ,&nbsp;Kathryn M. Albers","doi":"10.1016/j.ceca.2024.102884","DOIUrl":"https://doi.org/10.1016/j.ceca.2024.102884","url":null,"abstract":"<div><p>Pancreatic and duodenal homeobox 1 (PDX1) is a transcription factor required for the development and differentiation of the pancreas. Previous studies indicated that PDX1 expression was restricted to the gastrointestinal tract. Using a cre-dependent reporter, we observed PDX1-dependent expression of tdtomato (PDX1-tom) in a subpopulation of sensory nerves. Many of these PDX1-tom afferents expressed the neurofilament 200 protein and projected to the skin. Tdtomato-labeled terminals were associated with hair follicles in the form of longitudinal and circumferential lanceolate endings suggesting a role in tactile and proprioceptive perception. To begin to examine the functional significance of PDX1 in afferents, we used Fura-2 imaging to examine calcium (Ca<sup>2+</sup>) handling under naïve and nerve injury conditions. Neuropathic injury is associated with increased intracellular Ca<sup>2+</sup> signaling that in part results from dysregulation of the sarco/endoplasmic reticulum calcium transport ATPase (SERCA). Here we demonstrate that under naïve conditions, PDX1 regulates expression of the SERCA2B isoform in sensory neurons. In response to infraorbital nerve injury, a significant reduction of PDX1 and SERCA2B expression and dysregulation of Ca<sup>2+</sup> handling occurs in PDX1-tom trigeminal ganglia neurons. The identification of PDX1 expression in the somatosensory system and its regulation of SERCA2B and Ca<sup>2+</sup> handling provide a new mechanism to explain pathological changes in primary afferents that may contribute to pain associated with nerve injury.</p></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"120 ","pages":"Article 102884"},"PeriodicalIF":4.0,"publicationDate":"2024-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140341236","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Utilization of the genetically encoded calcium indicator Salsa6F in cardiac applications 基因编码钙指示剂 Salsa6F 在心脏领域的应用
IF 4 2区 生物学
Cell calcium Pub Date : 2024-03-20 DOI: 10.1016/j.ceca.2024.102873
Karla M. Márquez-Nogueras, Elisa Bovo, Jacy E. Neczypor, Quan Cao, Aleksey V. Zima, Ivana Y. Kuo
{"title":"Utilization of the genetically encoded calcium indicator Salsa6F in cardiac applications","authors":"Karla M. Márquez-Nogueras,&nbsp;Elisa Bovo,&nbsp;Jacy E. Neczypor,&nbsp;Quan Cao,&nbsp;Aleksey V. Zima,&nbsp;Ivana Y. Kuo","doi":"10.1016/j.ceca.2024.102873","DOIUrl":"10.1016/j.ceca.2024.102873","url":null,"abstract":"<div><p>Calcium signaling is a critical process required for cellular mechanisms such as cardiomyocyte contraction. The inability of the cell to properly activate or regulate calcium signaling can lead to contractile dysfunction. In isolated cardiomyocytes, calcium signaling has been primarily studied using calcium fluorescent dyes, however these dyes have limited applicability to whole organs. Here, we crossed the Salsa6f mouse which expresses a genetically encoded ratiometric cytosolic calcium indicator with a cardiomyocyte specific inducible cre to temporally-induce expression and studied cytosolic calcium transients in isolated cardiomyocytes and modified Langendorff heart preparations. Isolated cardiomyocytes expressing Salsa6f or Fluo-4AM loaded were compared. We also crossed the Salsa6f mouse with a floxed Polycystin 2 (PC2) mouse to test the feasibility of using the Salsa6f mouse to measure calcium transients in PC2 heterozygous or homozygous knock out mice. Although there are caveats in the applicability of the Salsa6f mouse, there are clear advantages to using the Salsa6f mouse to measure whole heart calcium signals.</p></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"119 ","pages":"Article 102873"},"PeriodicalIF":4.0,"publicationDate":"2024-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140272508","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
STIM2 variants regulate Orai1/TRPC1/TRPC4-mediated store-operated Ca2+ entry and mitochondrial Ca2+ homeostasis in cardiomyocytes STIM2 变异调节心肌细胞中 Orai1/TRPC1/TRPC4 介导的贮存操作 Ca2+ 输入和线粒体 Ca2+ 平衡
IF 4 2区 生物学
Cell calcium Pub Date : 2024-03-19 DOI: 10.1016/j.ceca.2024.102871
Rui Luo , Pauline Le Gourriérec , Fabrice Antigny , Kaveen Bedouet , Séverine Domenichini , Ana-Maria Gomez , Jean-Pierre Benitah , Jessica Sabourin
{"title":"STIM2 variants regulate Orai1/TRPC1/TRPC4-mediated store-operated Ca2+ entry and mitochondrial Ca2+ homeostasis in cardiomyocytes","authors":"Rui Luo ,&nbsp;Pauline Le Gourriérec ,&nbsp;Fabrice Antigny ,&nbsp;Kaveen Bedouet ,&nbsp;Séverine Domenichini ,&nbsp;Ana-Maria Gomez ,&nbsp;Jean-Pierre Benitah ,&nbsp;Jessica Sabourin","doi":"10.1016/j.ceca.2024.102871","DOIUrl":"10.1016/j.ceca.2024.102871","url":null,"abstract":"<div><p>The stromal interaction molecules (STIMs) are the sarcoplasmic reticulum (SR) Ca<sup>2+</sup> sensors that trigger store-operated Ca<sup>2+</sup> entry (SOCE) in a variety of cell types. While STIM1 isoform has been the focus of the research in cardiac pathophysiology, the function of the homolog STIM2 remains unknown. Using Ca<sup>2+</sup> imaging and patch-clamp techniques, we showed that knockdown (KD) of STIM2 by siRNAs increased SOCE and the <em>I</em><sub>SOC</sub> current in neonatal rat ventricular cardiomyocytes (NRVMs). Within this cardiomyocyte model, we identified the transcript expression of <em>Stim2.1</em> and <em>Stim2.2</em> splice variants, with predominance for <em>Stim2.2</em>. Using conventional and super-resolution confocal microscopy (STED), we found that exogenous STIM2.1 and STIM2.2 formed pre-clusters with a reticular organization at rest. Following SR Ca<sup>2+</sup> store depletion, some STIM2.1 and STIM2.2 clusters were translocated to SR-plasma membrane (PM) junctions and co-localized with Orai1. The overexpression strategy revealed that STIM2.1 suppressed Orai1-mediated SOCE and the <em>I</em><sub>SOC</sub> current while STIM2.2 enhanced SOCE. STIM2.2-enhanced SOCE was also dependent on TRPC1 and TRPC4. Even if STIM2 KD or splice variants overexpression did not affect cytosolic Ca<sup>2+</sup> cycling, we observed, using Rhod-2/AM Ca<sup>2+</sup> imaging, that Orai1 inhibition or STIM2.1 overexpression abolished the mitochondrial Ca<sup>2+</sup> (mCa<sup>2+</sup>) uptake, as opposed to STIM2 KD. We also found that STIM2 was present in the mitochondria-associated endoplasmic reticulum (ER) membranes (MAMs) by interacting with the inositol trisphosphate receptors (IP<sub>3</sub>Rs), voltage-dependent anion channel (VDAC), mitochondrial Ca<sup>2+</sup> uniporter (MCU), and mitofusin-2 (MNF2). Our results suggested that, in NRVMs, STIM2.1 constitutes the predominant functional variant that negatively regulates Orai1-generated SOCE. It participates in the control of mCa<sup>2+</sup> uptake capacity possibly via the STIM2-IP<sub>3</sub>Rs-VDAC-MCU and MNF2 complex.</p></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"119 ","pages":"Article 102871"},"PeriodicalIF":4.0,"publicationDate":"2024-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0143416024000290/pdfft?md5=11d1caa8cf0ca123f3dc1df14867cc62&pid=1-s2.0-S0143416024000290-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140169337","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Ruthenium red: Blocker or antagonist of TRPV channels? 钌红:TRPV 通道的阻断剂还是拮抗剂?
IF 4 2区 生物学
Cell calcium Pub Date : 2024-03-18 DOI: 10.1016/j.ceca.2024.102874
Andrés Jara-Oseguera
{"title":"Ruthenium red: Blocker or antagonist of TRPV channels?","authors":"Andrés Jara-Oseguera","doi":"10.1016/j.ceca.2024.102874","DOIUrl":"10.1016/j.ceca.2024.102874","url":null,"abstract":"<div><p>Ruthenium red (RR) is a widely used inhibitor of Transient Receptor Potential (TRP) cation channels and other types of ion channels. Although RR has been generally accepted to inhibit TRP channels by physically blocking the ion permeation pathway, recent structural evidence suggests that it might also function as an antagonist, inducing conformational changes in the channel upon binding that result in closure of the pore. In a recent manuscript published in EMBO Reports, Ruth A. Pumroy and collaborators solve structures of TRPV2 and TRPV5 channels in the presence and absence of activators and RR. The data sheds light on the mechanism of inhibition by RR, while also opening new questions for further investigation.</p></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"119 ","pages":"Article 102874"},"PeriodicalIF":4.0,"publicationDate":"2024-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140154348","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Sleep, calcium and microglia – an (un)expected liaison 睡眠、钙和小胶质细胞--(意想不到的)联系
IF 4 2区 生物学
Cell calcium Pub Date : 2024-03-08 DOI: 10.1016/j.ceca.2024.102872
Olga Garaschuk , Alexei Verkhratsky
{"title":"Sleep, calcium and microglia – an (un)expected liaison","authors":"Olga Garaschuk ,&nbsp;Alexei Verkhratsky","doi":"10.1016/j.ceca.2024.102872","DOIUrl":"10.1016/j.ceca.2024.102872","url":null,"abstract":"","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"119 ","pages":"Article 102872"},"PeriodicalIF":4.0,"publicationDate":"2024-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140105219","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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