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Inositol 1,4,5-trisphosphate Receptor Mutations associated with Human Disease. 肌醇1,4,5-三磷酸受体突变与人类疾病相关。
Messenger (Los Angeles, Calif. : Print) Pub Date : 2018-06-01
Lara E Terry, Kamil J Alzayady, Esraa Furati, David I Yule
{"title":"Inositol 1,4,5-trisphosphate Receptor Mutations associated with Human Disease.","authors":"Lara E Terry,&nbsp;Kamil J Alzayady,&nbsp;Esraa Furati,&nbsp;David I Yule","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Calcium release into the cytosol via the inositol 1,4,5-trisphosphate receptor (IP<sub>3</sub>R) calcium channel is important for a variety of cellular processes. As a result, impairment or inhibition of this release can result in disease. Recently, mutations in all four domains of the IP<sub>3</sub>R have been suggested to cause diseases such as ataxia, cancer, and anhidrosis; however, most of these mutations have not been functionally characterized. In this review we summarize the reported mutations, as well as the associated symptoms. Additionally, we use clues from transgenic animals, receptor stoichiometry, and domain location of mutations to speculate on the effects of individual mutations on receptor structure and function and the overall mechanism of disease.</p>","PeriodicalId":74176,"journal":{"name":"Messenger (Los Angeles, Calif. : Print)","volume":"6 1-2","pages":"29-44"},"PeriodicalIF":0.0,"publicationDate":"2018-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6128530/pdf/nihms-982657.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36474230","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: 0
The Making and Breaking of Inositol 1,4,5-Trisphosphate Receptor Tetramers. 肌醇1,4,5-三磷酸受体四聚体的合成与断裂。
Messenger (Los Angeles, Calif. : Print) Pub Date : 2018-06-01 DOI: 10.1166/msr.2018.1073
Richard J H Wojcikiewicz
{"title":"The Making and Breaking of Inositol 1,4,5-Trisphosphate Receptor Tetramers.","authors":"Richard J H Wojcikiewicz","doi":"10.1166/msr.2018.1073","DOIUrl":"https://doi.org/10.1166/msr.2018.1073","url":null,"abstract":"<p><p>Mammalian cells express three highly conserved inositol 1,4,5-trisphosphate (IP<sub>3</sub>) receptor types (IP<sub>3</sub>R1, IP<sub>3</sub>R2 and IP<sub>3</sub>R3), which have broadly similar characteristics, but markedly different distributions, and form homo- or heterotetrameric Ca<sup>2+</sup> channels in endoplasmic reticulum (ER) membranes. A vast array of published work details how mature, ER membrane-located IP<sub>3</sub> receptor tetramers are regulated, but much less attention has been paid to the intriguing questions of how the tetramers are assembled and destroyed as part of their natural life cycle. Are they assembled at the ER membrane from nascent, or completely translated polypeptides? How are they disassembled and degraded? These questions and other recently defined modes of IP<sub>3</sub> receptor processing will be briefly reviewed.</p>","PeriodicalId":74176,"journal":{"name":"Messenger (Los Angeles, Calif. : Print)","volume":"6 1-2","pages":"45-49"},"PeriodicalIF":0.0,"publicationDate":"2018-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1166/msr.2018.1073","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36853267","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
Maternal Behavior of CD38 Knockout Dams is Improved by Social Support 社会支持改善CD38基因敲除母鼠的母性行为
Messenger (Los Angeles, Calif. : Print) Pub Date : 2018-06-01 DOI: 10.1166/msr.2018.1069
C. Tsuji, H. Higashida, T. Tsuji
{"title":"Maternal Behavior of CD38 Knockout Dams is Improved by Social Support","authors":"C. Tsuji, H. Higashida, T. Tsuji","doi":"10.1166/msr.2018.1069","DOIUrl":"https://doi.org/10.1166/msr.2018.1069","url":null,"abstract":"","PeriodicalId":74176,"journal":{"name":"Messenger (Los Angeles, Calif. : Print)","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46351513","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
Immobile IP3 Receptor Clusters: Building Blocks for IP3-Evoked Ca2+ Signals 固定IP3受体簇:IP3诱发Ca2+信号的构建块
Messenger (Los Angeles, Calif. : Print) Pub Date : 2018-04-09 DOI: 10.17863/CAM.21858
C. Taylor, Negendra Babu Thillaiappan, David L. Prole
{"title":"Immobile IP3 Receptor Clusters: Building Blocks for IP3-Evoked Ca2+ Signals","authors":"C. Taylor, Negendra Babu Thillaiappan, David L. Prole","doi":"10.17863/CAM.21858","DOIUrl":"https://doi.org/10.17863/CAM.21858","url":null,"abstract":"","PeriodicalId":74176,"journal":{"name":"Messenger (Los Angeles, Calif. : Print)","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49254414","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
Deviant lysosomal Ca2+ signalling in neurodegeneration. An introduction. 神经退行性变中溶酶体Ca2+信号异常。一个介绍。
Messenger (Los Angeles, Calif. : Print) Pub Date : 2016-06-01 DOI: 10.1166/msr.2016.1053
Sandip Patel
{"title":"Deviant lysosomal Ca<sup>2+</sup> signalling in neurodegeneration. An introduction.","authors":"Sandip Patel","doi":"10.1166/msr.2016.1053","DOIUrl":"https://doi.org/10.1166/msr.2016.1053","url":null,"abstract":"<p><p>Lysosomes are key acidic Ca<sup>2+</sup> stores. The principle Ca<sup>2+</sup>-permeable channels of the lysosome are TRP mucolipins (TRPMLs) and NAADP-regulated two-pore channels (TPCs). Recent studies, reviewed in this collection, have linked numerous neurodegenerative diseases to both gain and loss of function of TRPMLs/TPCs, as well as to defects in acidic Ca<sup>2+</sup> store content. These diseases span rare lysosomal storage disorders such as Mucolipidosis Type IV and Niemann-Pick disease, type C, through to more common ones such as Alzheimer and Parkinson disease. Cellular phenotypes, underpinned by endo-lysosomal trafficking defects, are reversed by chemical or molecular targeting of TRPMLs and TPCs. Lysosomal Ca<sup>2+</sup> channels therefore emerge as potential druggable targets in combatting neurodegeneration.</p>","PeriodicalId":74176,"journal":{"name":"Messenger (Los Angeles, Calif. : Print)","volume":"5 1-2","pages":"24-29"},"PeriodicalIF":0.0,"publicationDate":"2016-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1166/msr.2016.1053","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35015757","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: 7
Connecting Ca2+ and lysosomes to Parkinson disease. 连接Ca2+和溶酶体与帕金森病。
Messenger (Los Angeles, Calif. : Print) Pub Date : 2016-06-01 DOI: 10.1166/msr.2016.1059
Bethan S Kilpatrick
{"title":"Connecting Ca<sup>2+</sup> and lysosomes to Parkinson disease.","authors":"Bethan S Kilpatrick","doi":"10.1166/msr.2016.1059","DOIUrl":"https://doi.org/10.1166/msr.2016.1059","url":null,"abstract":"The neurodegenerative movement disorder Parkinson disease (PD) is prevalent in the aged population. However, the underlying mechanisms that trigger disease are unclear. Increasing work implicates both impaired Ca2+ signalling and lysosomal dysfunction in neuronal demise. Here I aim to connect these distinct processes by exploring the evidence that lysosomal Ca2+ signalling is disrupted in PD. In particular, I highlight defects in lysosomal Ca2+ content and signalling through NAADP-regulated two-pore channels in patient fibroblasts harbouring mutations in the PD-linked genes, GBA1 and LRRK2. As an emerging contributor to PD pathogenesis, the lysosomal Ca2+ signalling apparatus could represent a novel therapeutic target.","PeriodicalId":74176,"journal":{"name":"Messenger (Los Angeles, Calif. : Print)","volume":"5 1-2","pages":"76-86"},"PeriodicalIF":0.0,"publicationDate":"2016-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1166/msr.2016.1059","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35016191","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
Lysosomal Calcium in Neurodegeneration. 神经变性中的溶酶体钙。
Messenger (Los Angeles, Calif. : Print) Pub Date : 2016-06-01 DOI: 10.1166/msr.2016.1055
Xinghua Feng, Junsheng Yang
{"title":"Lysosomal Calcium in Neurodegeneration.","authors":"Xinghua Feng,&nbsp;Junsheng Yang","doi":"10.1166/msr.2016.1055","DOIUrl":"10.1166/msr.2016.1055","url":null,"abstract":"<p><p>Lysosomes are the central organelles responsible for macromolecule recycling in the cell. Lysosomal dysfunction is the primary cause of lysosomal storage diseases (LSDs), and contributes significantly to the pathogenesis of common neurodegenerative diseases. The lysosomes are also intracellular stores for calcium ions, one of the most common second messenger in the cell. Lysosomal Ca<sup>2+</sup> is required for diverse cellular processes including signal transduction, vesicular trafficking, autophagy, nutrient sensing, exocytosis, and membrane repair. In this review, we first summarize some recent progresses in the studies of lysosome Ca<sup>2+</sup> regulation, with a focus on the newly discovered lysosomal Ca<sup>2+</sup> channels and the mechanisms of lysosomal Ca<sup>2+</sup> store refilling. We then discuss how defects in lysosomal Ca<sup>2+</sup> release and store maintenance cause lysosomal dysfunction and neurodegeneration.</p>","PeriodicalId":74176,"journal":{"name":"Messenger (Los Angeles, Calif. : Print)","volume":"5 1-2","pages":"56-66"},"PeriodicalIF":0.0,"publicationDate":"2016-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1166/msr.2016.1055","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35649151","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: 26
ADP-ribosyl cyclases regulate early development of the sea urchin. ADP-ribosyl cyclases调控海胆的早期发育。
Messenger (Los Angeles, Calif. : Print) Pub Date : 2016-06-01 DOI: 10.1166/msr.2016.1052
Latha Ramakrishnan, Kevin Uhlinger, Leslie Dale, Amro Hamdoun, Sandip Patel
{"title":"ADP-ribosyl cyclases regulate early development of the sea urchin.","authors":"Latha Ramakrishnan, Kevin Uhlinger, Leslie Dale, Amro Hamdoun, Sandip Patel","doi":"10.1166/msr.2016.1052","DOIUrl":"10.1166/msr.2016.1052","url":null,"abstract":"<p><p>ADP-ribosyl cyclases are multifunctional enzymes involved in the metabolism of nucleotide derivatives necessary for Ca<sup>2+</sup> signalling such as cADPR and NAADP. Although Ca<sup>2+</sup> signalling is a critical regulator of early development, little is known of the role of ADP-ribosyl cyclases during embryogenesis. Here we analyze the expression, activity and function of ADP-ribosyl cyclases in the embryo of the sea urchin - a key organism for study of both Ca<sup>2+</sup> signalling and embryonic development. ADP-ribosyl cyclase isoforms (SpARC1-4) showed unique changes in expression during early development. These changes were associated with an increase in the ratio of cADPR:NAADP production. Over-expression of SpARC4 (a preferential cyclase) disrupted gastrulation. Our data highlight the importance of ADP-ribosyl cyclases during embryogenesis.</p>","PeriodicalId":74176,"journal":{"name":"Messenger (Los Angeles, Calif. : Print)","volume":"5 1-2","pages":"100-106"},"PeriodicalIF":0.0,"publicationDate":"2016-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5435102/pdf/emss-72807.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35016190","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: 0
Two-Pore Channels and Parkinson's Disease: Where's the Link? 双孔通道与帕金森病：联系在哪里？
Messenger (Los Angeles, Calif. : Print) Pub Date : 2016-06-01 DOI: 10.1166/msr.2016.1051
Pilar Rivero-Ríos, Belén Fernández, Jesús Madero-Pérez, María Romo Lozano, Sabine Hilfiker
{"title":"Two-Pore Channels and Parkinson's Disease: Where's the Link?","authors":"Pilar Rivero-Ríos, Belén Fernández, Jesús Madero-Pérez, María Romo Lozano, Sabine Hilfiker","doi":"10.1166/msr.2016.1051","DOIUrl":"10.1166/msr.2016.1051","url":null,"abstract":"<p><p>Two-pore channels are endolysosomal Ca<sup>2+</sup> release channels involved in proper trafficking to and from those organelles. They are the likely targets for the Ca<sup>2+</sup>-mobilizing messenger NAADP, and are further regulated by a variety of mechanisms including phosphoinositide levels and Rab proteins. As discussed here, recent studies highlight a role for these channels in the pathomechanism(s) underlying Parkinson's disease, with important implications for possible alternative treatment strategies.</p>","PeriodicalId":74176,"journal":{"name":"Messenger (Los Angeles, Calif. : Print)","volume":"5 1-2","pages":"67-75"},"PeriodicalIF":0.0,"publicationDate":"2016-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5436604/pdf/emss-72808.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35015758","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: 0
Carvedilol inhibits cADPR- and IP3-induced Ca2+ release. 卡维地洛抑制cADPR-和ip3诱导的Ca2+释放。
Messenger (Los Angeles, Calif. : Print) Pub Date : 2016-06-01 DOI: 10.1166/msr.2016.1050
Anthony J Morgan, Konstantina Bampali, Margarida Ruas, Cailley Factor, Thomas G Back, S R Wayne Chen, Antony Galione
{"title":"Carvedilol inhibits cADPR- and IP<sub>3</sub>-induced Ca<sup>2+</sup> release.","authors":"Anthony J Morgan,&nbsp;Konstantina Bampali,&nbsp;Margarida Ruas,&nbsp;Cailley Factor,&nbsp;Thomas G Back,&nbsp;S R Wayne Chen,&nbsp;Antony Galione","doi":"10.1166/msr.2016.1050","DOIUrl":"https://doi.org/10.1166/msr.2016.1050","url":null,"abstract":"<p><p>Spontaneous Ca<sup>2+</sup> waves, also termed store-overload-induced Ca<sup>2+</sup> release (SOICR), in cardiac cells can trigger ventricular arrhythmias especially in failing hearts. SOICR occurs when RyRs are activated by an increase in sarcoplasmic reticulum (SR) luminal Ca<sup>2+</sup>. Carvedilol is one of the most effective drugs for preventing arrhythmias in patients with heart failure. Furthermore, carvedilol analogues with minimal β-blocking activity also block SOICR showing that SOICR-inhibiting activity is distinct from that for β-block. We show here that carvedilol is a potent inhibitor of cADPR-induced Ca<sup>2+</sup> release in sea urchin egg homogenate. In addition, the carvedilol analog VK-II-86 with minimal β-blocking activity also suppresses cADPR-induced Ca<sup>2+</sup> release. Carvedilol appeared to be a non-competitive antagonist of cADPR and could also suppress Ca<sup>2+</sup> release by caffeine. These results are consistent with cADPR releasing Ca<sup>2+</sup> in sea urchin eggs by sensitizing RyRs to Ca<sup>2+</sup> involving a luminal Ca<sup>2+</sup> activation mechanism. In addition to action on the RyR, we also observed inhibition of inositol 1,4,5-trisphosphate (IP<sub>3</sub>)-induced Ca<sup>2+</sup> release by carvedilol suggesting a common mechanism between these evolutionarily related and conserved Ca<sup>2+</sup> release channels.</p>","PeriodicalId":74176,"journal":{"name":"Messenger (Los Angeles, Calif. : Print)","volume":"5 1-2","pages":"92-99"},"PeriodicalIF":0.0,"publicationDate":"2016-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1166/msr.2016.1050","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35367448","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: 2
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