Cell calcium最新文献

Endoplasmic reticulum-mitochondria lockdown in Wolfram syndrome 沃尔夫拉姆综合征中的内质网-线粒体锁定现象

IF 4.3 2区生物学

Cell calcium Pub Date : 2024-09-12 DOI: 10.1016/j.ceca.2024.102955

引用次数: 0

In memoriam of Shun-ichi Miyazaki 1941–2024 悼念宫崎顺一 1941-2024

IF 4.3 2区生物学

Cell calcium Pub Date : 2024-09-03 DOI: 10.1016/j.ceca.2024.102948

引用次数: 0

The quest to map STIM1 activation in granular detail 绘制 STIM1 激活细节图的探索

IF 4.3 2区生物学

Cell calcium Pub Date : 2024-08-23 DOI: 10.1016/j.ceca.2024.102946

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Unveiling the intricate role of S100A1 in regulating RyR1 activity: A commentary on “Structural insights into the regulation of RyR1 by S100A1” 揭示 S100A1 在调节 RyR1 活性中的复杂作用：关于 "S100A1调控RyR1的结构见解 "的评论文章

IF 4.3 2区生物学

Cell calcium Pub Date : 2024-08-23 DOI: 10.1016/j.ceca.2024.102947

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ELD607 specifically traffics Orai1 to the lysosome leading to inhibition of store operated calcium entry ELD607 能特异性地将 Orai1 运送到溶酶体，从而抑制储存操作的钙离子输入

IF 4.3 2区生物学

Cell calcium Pub Date : 2024-08-14 DOI: 10.1016/j.ceca.2024.102945

{"title":"ELD607 specifically traffics Orai1 to the lysosome leading to inhibition of store operated calcium entry","authors":"","doi":"10.1016/j.ceca.2024.102945","DOIUrl":"10.1016/j.ceca.2024.102945","url":null,"abstract":"<div><p>Orai1 is a plasma membrane Ca<sup>2+</sup> channel involved in store operated calcium entry (SOCE). SOCE can regulate cell growth, exocytosis, gene expression and inflammation. We previously found that short palate lung and nasal epithelial clone 1′s (SPLUNC1) sixth α-helix (α6) bound Orai1 to inhibit SOCE. SPLUNC1 was not proteolytically stable, so we developed ELD607, an 11 amino acid peptide based on SPLUNC1’s α6 region which was more stable and more potent than SPLUNC1/α6. Here, we studied ELD607’s mechanism of action. We overexpressed either Orai1-HA or Orai1-YFP in HEK293T cells to probe ELD607-Orai1 interactions by confocal microscopy. We also measured changes in Fluo-4 fluorescence in a multiplate reader as a marker of cytoplasmic Ca<sup>2+</sup> levels. ELD607 internalized Orai1 independently of STIM1. Both 15 min and 3 h exposure to ELD607 similarly depleted Orai1 in the plasma membrane. However, 3 h exposure to ELD607 yielded greater inhibition of SOCE. ELD607 continued to colocalize with Orai1 after internalization and this process was dependent on the presence of the ubiquitin ligase NEDD4.2. Similarly, ELD607 increased the colocalization between Orai1 and ubiquitin. ELD607 also increased the colocalization between Orai1 and Rab5 and 7, but not Rab11, suggesting that Orai1 trafficked through early and late but not recycling endosomes. Finally, ELD607 caused Orai1, but not Orai2, Orai3, or STIM1 to traffic to lysosomes. We conclude that ELD607 rapidly binds to Orai1 and works in an identical fashion as full length SPLUNC1 by internalizing Orai1 and sending it to lysosomes, leading to a decrease in SOCE.</p></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":null,"pages":null},"PeriodicalIF":4.3,"publicationDate":"2024-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0143416024001039/pdfft?md5=fb9b28cebc700529d56816f0ae473c7a&pid=1-s2.0-S0143416024001039-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142075753","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

Duchenne muscular dystrophy skeletal muscle cells derived from human induced pluripotent stem cells recapitulate various calcium dysregulation pathways 从人类诱导多能干细胞中提取的杜氏肌营养不良症骨骼肌细胞再现了各种钙失调途径

IF 4.3 2区生物学

Cell calcium Pub Date : 2024-08-13 DOI: 10.1016/j.ceca.2024.102943

{"title":"Duchenne muscular dystrophy skeletal muscle cells derived from human induced pluripotent stem cells recapitulate various calcium dysregulation pathways","authors":"","doi":"10.1016/j.ceca.2024.102943","DOIUrl":"10.1016/j.ceca.2024.102943","url":null,"abstract":"<div><p>Duchenne muscular dystrophy (DMD) is an X-linked progressive muscle degenerative disease, caused by mutations in the dystrophin gene and resulting in premature death. As a major secondary event, an abnormal elevation of the intracellular calcium concentration in the dystrophin-deficient muscle contributes to disease progression in DMD. In this study, we investigated the specific functional features of induced pluripotent stem cell-derived muscle cells (hiPSC-skMCs) generated from DMD patients to regulate intracellular calcium concentration. As compared to healthy hiPSC-skMCs, DMD hiPSC-skMCs displayed specific spontaneous calcium signatures with high levels of intracellular calcium concentration. Furthermore, stimulations with electrical field or with acetylcholine perfusion induced higher calcium response in DMD hiPSC-skMCs as compared to healthy cells. Finally, Mn2+ quenching experiments demonstrated high levels of constitutive calcium entries in DMD hiPSC-skMCs as compared to healthy cells. Our findings converge on the fact that DMD hiPSC-skMCs display intracellular calcium dysregulation as demonstrated in several other models. Observed calcium disorders associated with RNAseq analysis on these DMD cells highlighted some mechanisms, such as spontaneous and activated sarcoplasmic reticulum (SR) releases or constitutive calcium entries, known to be disturbed in other dystrophin-deficient models. However, store operated calcium entries (SOCEs) were not found to be dysregulated in our DMD hiPSC-skMCs model. These results suggest that all the mechanisms of calcium impairment observed in other animal models may not be as pronounced in humans and could point to a preference for certain mechanisms that could correspond to major molecular targets for DMD therapies.</p></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":null,"pages":null},"PeriodicalIF":4.3,"publicationDate":"2024-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0143416024001015/pdfft?md5=8264d1db13ed561425b5160803383264&pid=1-s2.0-S0143416024001015-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141998326","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

Remodeling Ca2+ dynamics by targeting a promising E-box containing G-quadruplex at ORAI1 promoter in triple-negative breast cancer 针对三阴性乳腺癌 ORAI1 启动子中前景看好的含 E-box 的 G- 四叉链，重塑 Ca2+ 动力学

IF 4.3 2区生物学

Cell calcium Pub Date : 2024-08-12 DOI: 10.1016/j.ceca.2024.102944

{"title":"Remodeling Ca2+ dynamics by targeting a promising E-box containing G-quadruplex at ORAI1 promoter in triple-negative breast cancer","authors":"","doi":"10.1016/j.ceca.2024.102944","DOIUrl":"10.1016/j.ceca.2024.102944","url":null,"abstract":"<div><p>ORAI1 is an intrinsic component of store-operated calcium entry (SOCE) that strictly regulates Ca<sup>2+</sup> influx in most non-excitable cells. ORAI1 is overexpressed in a wide variety of cancers, and its signal transduction has been associated with chemotherapy resistance. There is extensive proteomic interaction of ORAI1 with other channels and effectors, resulting in various altered phenotypes. However, the transcription regulation of ORAI1 is not well understood. We have found a putative G-quadruplex (G4) motif, <em>ORAI1-Pu</em>, in the upstream promoter region of the gene, having regulatory functions. High-resolution 3-D NMR structure elucidation suggests that <em>ORAI1-Pu</em> is a stable parallel-stranded G4, having a long 8-nt loop imparting dynamics without affecting the structural stability. The protruded loop further houses an E-box motif that provides a docking site for transcription factors like Zeb1. The G4 structure was also endogenously observed using Chromatin Immunoprecipitation (ChIP) with anti-G4 antibody (BG4) in the MDA-MB-231 cell line overexpressing ORAI1. Ligand-mediated stabilization suggested that the stabilized G4 represses transcription in cancer cell line MDA-MB-231. Downregulation of transcription further led to decreased Ca<sup>2+</sup> entry by the SOCE pathway, as observed by live-cell Fura-2 Ca<sup>2+</sup> imaging.</p></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":null,"pages":null},"PeriodicalIF":4.3,"publicationDate":"2024-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142075790","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

The many facets of TMEM63/OCaR proteins as mechanosensitive channels in lysosomes, NAADP signaling and beyond TMEM63/OCaR 蛋白作为溶酶体、NAADP 信号转导等机械敏感通道的多面性。

IF 4.3 2区生物学

Cell calcium Pub Date : 2024-08-04 DOI: 10.1016/j.ceca.2024.102942

引用次数: 0

Regulating calcium flux through AMPA glutamate receptors 通过 AMPA 谷氨酸受体调节钙通量

IF 4.3 2区生物学

Cell calcium Pub Date : 2024-07-30 DOI: 10.1016/j.ceca.2024.102934

引用次数: 0

TRPC1: The housekeeper of the hippocampus TRPC1：海马的管家

IF 4.3 2区生物学

Cell calcium Pub Date : 2024-07-27 DOI: 10.1016/j.ceca.2024.102933

引用次数: 0