Journal of Cellular Physiology最新文献

{"title":"Mg2+ Supplementation Mitigates Metabolic Deficits Associated With TRPM7 Disruption","authors":"Severin Boulassel,&nbsp;Pascale C. F. Schreier,&nbsp;Anna M. Melyshi,&nbsp;Johanna Berger,&nbsp;Peter S. Reinach,&nbsp;Katharina Jacob,&nbsp;Ingrid Boekhoff,&nbsp;Andreas Breit,&nbsp;Timo D. Müller,&nbsp;Susanna Zierler,&nbsp;Thomas Gudermann,&nbsp;Noushafarin Khajavi","doi":"10.1002/jcp.70042","DOIUrl":"https://doi.org/10.1002/jcp.70042","url":null,"abstract":"<p>Transient receptor potential channel subfamily M member 7 (TRPM7) regulates cellular and systemic Mg²⁺ homeostasis through its channel domain and induces protein phosphorylation via its kinase domain. We recently found that mice with selective deletion of <i>Trpm7</i> in β-cells develop glucose intolerance and declines in insulin secretion, primarily due to the impaired enzymatic activity of this protein. Accumulating evidence suggests that Mg²⁺ supplementation effectively mitigates the detrimental effects of TRPM7 disruption in various cell types. However, the impact of Mg²⁺ supplementation on metabolic impairments caused by TRPM7 inactivation remains unclear. In the present study, we found that Mg²⁺ supplementation significantly ameliorates glucose intolerance observed in high-fat-fed TRPM7 kinase-deficient mice (<i>Trpm7</i>^<i>R/R</i>). However, our ex vivo analysis of islets isolated from <i>Trpm7</i>^<i>R/R</i> mice revealed that Mg²⁺ supplementation does not enhance glucose-induced insulin secretion. Instead, the improvement appears to be partially driven by enhanced insulin sensitivity and increased β-cell proliferation. The pharmacological analysis in MIN6 cells showed that inhibiting TRPM7 with either NS8593 or VER155008 disrupts β-cell proliferation. These effects mimicked the phenotype seen in <i>Trpm7</i>^<i>R/R</i> mice. We attribute this impairment to diminished ERK1/2 signaling, which suppressed PDX1 expression, while Mg²⁺ supplementation in vitro partially restored ERK1/2 phosphorylation levels. Collectively, Mg²⁺ supplementation enhances glucose metabolism in <i>Trpm7</i>^<i>R/R</i> mice and mitigates the ERK1/2 signaling disruptions and proliferation arrest induced by TRPM7 inactivation in vitro. These findings provide compelling evidence that Mg²⁺ supplementation can reverse the adverse metabolic and cellular phenotypes associated with the loss of TRPM7 function.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70042","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143871560","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}

{"title":"Nestin(+)- and Nestin(−)-Ventricular Cardiomyocytes Reenter the Cell Cycle In Vitro but Are Reciprocally Regulated in the Partial Apex-Resected 7-Day Neonatal Rat Heart","authors":"Adrien Aubry,&nbsp;Mariana Kebbe,&nbsp;Patrice Naud,&nbsp;Louis Villeneuve,&nbsp;Charles Alexandre Leblanc,&nbsp;Angelino Calderone","doi":"10.1002/jcp.70040","DOIUrl":"https://doi.org/10.1002/jcp.70040","url":null,"abstract":"<p>The 1-day-old neonatal rat heart contains two subpopulations of ventricular cardiomyocytes (NNVMs) that reenter the cell cycle in vitro and in vivo distinguished by the absence or de novo expression of the intermediate filament protein nestin. Furthermore, de novo nestin expression in NNVMs directly facilitated cell cycle reentry and elicited a morphological migratory phenotype. Previous studies have reported that ventricular cardiomyocytes failed to reenter the cell cycle following damage to the 7-day-old rodent heart. The present study tested the hypothesis that cell cycle reentry of one or both of the NNVM subpopulations of 7-day-old neonatal rat pups was compromised in vitro and/or in vivo following cardiac damage. Three-day treatment of 7-day-old NNVMs with the protein kinase C activator phorbol 12,13-dibutyrate and the serine/threonine p38α/β MAPK kinase inhibitor SB203580 facilitated cell cycle reentry into the S phase and G₂–M phase of the cell cycle. Two distinct subpopulations of 7-day NNVMs reentered the cell cycle, and the predominant subpopulation was distinguished by de novo nestin expression. Three days following the sham-operation of 7-day-old neonatal rat hearts, cell cycle reentry was detected exclusively in NNVMs lacking nestin expression. Partial apex resection of 7-day-old neonatal rat hearts led to the de novo appearance of nestin⁽⁺⁾-NNVMs preferentially bordering the damaged region and a subpopulation reentered the S-phase and G₂–M phase of the cell cycle in the absence of p38α/β MAPK inhibition. By contrast, cell cycle reentry of nestin⁽⁻⁾-NNVMs identified adjacent to the apex-resected region was significantly reduced. These data highlight the disparate in vivo regulation of the two subpopulations of NNVMs following damaged to the 7-day-old neonatal rat heart and reaffirm the premise that targeting the subpopulation of nestin⁽⁺⁾-ventricular cardiomyocytes identified in the ischemically damaged adult mammalian heart represents a plausible first step to initiate cell cycle reentry.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70040","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143871647","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}

{"title":"Erratum to “Taurine Improves Low-Level Inorganic Arsenic-Induced Insulin Resistance by Activating PPARγ-mTORC2 Signalling and Inhibiting Hepatic Autophagy”","authors":"","doi":"10.1002/jcp.70015","DOIUrl":"https://doi.org/10.1002/jcp.70015","url":null,"abstract":"<p>Gao, N., Yao, X., Jiang, L., et al. 2019. “Taurine Improves Low-Level Inorganic Arsenic-Induced Insulin Resistance by Activating PPARγ-mTORC2 Signalling and Inhibiting Hepatic Autophagy. <i>Journal of Cellular Physiology</i> 234, no. 4: 5143–5152. https://doi.org/10.1002/jcp.27318</p><p>An incorrect PAS staining image for the 1 mg/L iAs3+ group in Figure 1i was used inadvertently during compilation. The corrected figure is shown below.</p><p>We apologize for this error.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70015","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143866040","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}

{"title":"Correction to “The Effect of lncRNA-ARAP1-AS2/ARAP1 on High Glucose-Induced Cytoskeleton Rearrangement and Epithelial–Mesenchymal Transition in Human Renal Tubular Epithelial Cells”","authors":"","doi":"10.1002/jcp.70041","DOIUrl":"https://doi.org/10.1002/jcp.70041","url":null,"abstract":"<p>Li, L., L. Xu, S. Wen, Y. Yang, X. Li, and Q. Fan. 2020. “The Effect of lncRNA-ARAP1-AS2/ARAP1 on High Glucose-Induced Cytoskeleton Rearrangement and Epithelial-Mesenchymal Transition in Human Renal Tubular Epithelial Cells.” <i>Journal of Cellular Physiology</i> 235, no. 7–8: 5787–5795. https://10.1002/jcp.29512.</p><p>Figure 3d was mistakenly replaced with an incorrect version, here is the picture to be corrected.</p><p></p><p><b>Figure 3d</b></p><p>During the image processing, due to my oversight, the image for the ARAP1-shRNA-NG group was mistakenly used for the NG group. This error occurred entirely because of my carelessness in data organization and image labeling, and I deeply regret it. I take full responsibility for this mistake. I understand that such an error may significantly affect the accuracy of the research findings, mislead readers, and compromise the credibility of the article. Therefore, I sincerely apologize for any negative consequences this may have caused.</p><p>To rectify this issue, I have carefully reviewed all the raw data and identified the correct images. The new images are consistent with the original experimental results, and we have confirmed that they do not affect the conclusions of the article.</p><p>Once again, I sincerely apologize for this mistake. I will take this as a serious lesson to exercise greater diligence in my future research to prevent similar occurrences.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70041","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143850974","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}

{"title":"CBLB Regulates MAPK-P38 Pathway via MAP3K9 Ubiquitination to Inhibit GBM Cell Invasion and Migration","authors":"Yuankun Liu,&nbsp;Kaixiang Ni,&nbsp;Songyun Zhao,&nbsp;Jingjing Zhao,&nbsp;Mengmeng Zhong,&nbsp;Chao Cheng,&nbsp;Wei Ji,&nbsp;Jiantong Jiao,&nbsp;Junfei Shao","doi":"10.1002/jcp.70037","DOIUrl":"https://doi.org/10.1002/jcp.70037","url":null,"abstract":"<div>\u0000 \u0000 <p>Glioma cells exhibit high invasiveness and have the ability to evade surgical resection, radiotherapy, and chemotherapy, which are major factors contributing to the challenges in effective treatment and recurrence. The ubiquitin-proteasome system (UPS) plays a crucial role in posttranslational modification, significantly contributing to the aggressive progression of glioblastoma (GBM). This study identified the E3 ubiquitin ligase CBLB as a crucial and abnormally regulated component of the UPS in GBM, noting its significant downregulation compared to normal brain tissue and its negative correlation with malignant phenotypes and poor prognosis. Experimental studies, both in vitro and in vivo, have shown that CBLB can inhibit the migration and invasion of GBM cells. Mechanistically, CBLB directly interacts with MAP3K9 through its RING domain, leading to K48-K63-linked polyubiquitination at the Lys 193 site, thereby promoting MAP3K9 proteasomal-mediated degradation. MAP3K9 downregulation suppresses MAPK-P38 pathway activation. This study identifies CBLB as a tumor suppressor that modulates the MAPK-P38 signaling pathway by promoting the polyubiquitination and degradation of MAP3K9, offering a new therapeutic approach for GBM treatment.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143852872","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}

{"title":"EXPRESSION OF CONCERN: EW-7197 Prevents Ulcerative Colitis-Associated Fibrosis and Inflammation","authors":"","doi":"10.1002/jcp.70028","DOIUrl":"https://doi.org/10.1002/jcp.70028","url":null,"abstract":"<p><b>EXPRESSION OF CONCERN</b>: M. M. Binabaj, F. Asgharzadeh, A. Avan, F. Rahmani, A. Soleimani, M. R. Parizadeh, et al., “EW-7197 Prevents Ulcerative Colitis-Associated Fibrosis and Inflammation,” <i>Journal of Cellular Physiology</i> 234, no. 7 (2018): 11654-11661, https://doi.org/10.1002/jcp.27823.</p><p>This Expression of Concern is for the above article, published online on 27 November 2018 in Wiley Online Library (wileyonlinelibrary.com), and has been published by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. The Expression of Concern has been agreed due to concerns raised by the third party, which revealed inappropriate figure overlap in Figure 2(a), by the similar group of authors in different articles. While the corresponding author provided original data during the investigation, the reproduced control and colitis data (Figure 2a) are indeed considered unreliable as they were published elsewhere in a different scientific context. However, the authors have explained they conducted these experiments of the murine model of colitis using mice with the uniform characteristics including their age, species, and gender. More importantly, these experiments were conducted simultaneously by the same researchers in the same location, with the same molecular weight DSS, contributing to the consistency in the patterns observed. Furthermore, the Chair, Research Integrity Committee of the institution (Mashhad University of Medical Sciences, Mashhad, Iran) has contacted the journal and confirmed that this article was a thesis independently conducted with different research aims, methodologies, and datasets in their university. Nevertheless, the Editor-in-Chief and the Publisher's Research Integrity team have decided to publish this Expression of Concern to inform readers that concerns about the reliability of the presented results remain.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70028","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143850973","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}

{"title":"Correction to “SMAD4 Regulates the Expression of LCK Affecting Chimeric Antigen Receptor-T Cells Proliferation Through PI3K/Akt Signaling Pathway”","authors":"","doi":"10.1002/jcp.70039","DOIUrl":"https://doi.org/10.1002/jcp.70039","url":null,"abstract":"<p>Wan, R., Fu, B., Fu, X., et al. 2025. “SMAD4 Regulates the Expression of LCK Affecting Chimeric Antigen Receptor-T Cells Proliferation Through PI3K/Akt Signaling Pathway.” <i>Journal of Cellular Physiology</i> 240, no. 1: e31520.</p><p>In the author list part of the paper, Rongxue Wan and Bowen Fu are co-first authors who contributed equally to the paper, however, there was no sign to reflect this, which was incorrect. To correct, the sentence “Rongxue Wan and Bowen Fu contributed equally to this study” should be added under the author list part.</p><p>We apologize for this error.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70039","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143845917","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}

{"title":"Copper Impedes Calcification of Human Aortic Vascular Smooth Muscle Cells Through Inhibition of Osteogenic Transdifferentiation and Promotion of Extracellular Matrix Stability","authors":"Iurii Orlov,&nbsp;Gaëlle Lenglet,&nbsp;Carine Avondo,&nbsp;John H. Beattie,&nbsp;Said Kamel,&nbsp;Irina Korichneva","doi":"10.1002/jcp.70035","DOIUrl":"https://doi.org/10.1002/jcp.70035","url":null,"abstract":"<p>Vascular calcification (VC), a common pathological condition, is a strong predictor of cardiovascular events and associated mortality. Development and progression of VC heavily rely on vascular smooth muscle cells (VSMCs) and are closely related to oxidative stress, inflammation, and remodelling of extracellular matrix (ECM). Copper (Cu), an essential microelement, participates in these processes, but its involvement in pathophysiology of VC and VSMCs physiology remains poorly investigated. In the present study, we analysed the impact of Cu on the calcification of human aortic primary VSMCs induced in vitro by treatment with high calcium and phosphate levels. Supplementation with physiological micromolar doses of Cu significantly reduced the amount of calcium deposited on VSMCs as compared to moderate deficiency, Cu restriction with chelators or Cu excess. Moreover, optimal concentrations of Cu ions increased protein production by VSMCs, stimulated their metabolic activity, inhibited alkaline phosphatase activity associated with cell-conditioned medium and cellular lysates, and prevented osteogenic differentiation of VSMCs. RNA-seq results indicated that high calcium and phosphate treatments activated many pathways related to oxidative stress and inflammation in VSMCs at the initial stage of calcification. At the same time, expression of VSMCs-specific markers and certain components of ECM were downregulated. Supplementation of calcifying cells with 10 μM Cu prevented most of the transcriptomic alterations induced by high calcium and phosphate while chelation-mediated restriction of Cu greatly aggravated them. In summary, physiological concentration of Cu impedes in vitro calcification of VSMCs, prevents their osteogenic transition and minimises early phenotypic alterations induced by high calcium and phosphate, thereby underlining the importance of Cu homeostasis for the physiology of VSMCs, one of the cornerstones of cardiovascular health. Our data suggest that features of Cu metabolism and its status should be considered when developing preventive and therapeutic approaches for cardiovascular diseases.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70035","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143845916","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}

{"title":"Piezo1 Is Related to the Enamel Matrix Formation in Mouse Tooth Germ Development","authors":"Hiroko Wada,&nbsp;Misaki Abe,&nbsp;Naohisa Wada,&nbsp;Shohei Yoshimoto,&nbsp;Shinsuke Fujii,&nbsp;Masafumi Moriyama,&nbsp;Yoshihide Mori,&nbsp;Mizuho A. Kido,&nbsp;Tamotsu Kiyoshima","doi":"10.1002/jcp.70036","DOIUrl":"https://doi.org/10.1002/jcp.70036","url":null,"abstract":"<div>\u0000 \u0000 <p>Cellular responses to mechanical stimulation are involved in tissue development and the maintenance of biological functions. Teeth function as receptors for mastication and occlusal pressure. During tooth development, the tooth germ begins with an invagination of the epithelium, and its morphology matures through dynamic interactions between epithelial cells and mesenchymal cells, suggesting that mechanosensors may play an important role in this process. We analyzed the expression and function of Piezo1, a mechanically activated ion channel, during tooth development and clarified the involvement of Piezo1 in tooth morphogenesis. The expression of Piezo1 was observed in both the enamel organ and the surrounding mesenchymal cells at the early stage and in the ameloblasts and odontoblasts during enamel and dentin matrix formation. Yoda1, a Piezo1 activator, inhibited cell proliferation in mouse dental epithelial (mDE6) cells and E15 tooth germs, and suppressed cell migration in mDE6 cells. Meanwhile, GsMTx4, a Piezo1 inactivator, showed opposite results. Furthermore, in the organ culture of E15 tooth germs, the activation and inactivation of Piezo1 were found to affect the expression of ameloblast differentiation marker genes and control the arrangement of ameloblasts. Interestingly, the expression of E-cadherin was reduced in the cell membrane of ameloblasts at the cusp in the GsMTx4-treated tooth germs of organ culture, and enamel formation was significantly decreased. Yoda1-treated mDE6 cells showed upregulated E-cadherin expression, which was downregulated by calpain inhibitor. These findings suggest that Piezo1 may be involved in tooth morphogenesis during ameloblast development by playing an essential role in cell proliferation, migration, arrangement, differentiation, and mineralization.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143836467","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}

{"title":"Methods to Assess Neuronal Primary Cilia Electrochemical Signaling","authors":"Paul G. DeCaen,&nbsp;Louise F. Kimura","doi":"10.1002/jcp.70034","DOIUrl":"https://doi.org/10.1002/jcp.70034","url":null,"abstract":"<p>Primary cilia are polymodal sensory organelles which project from the apical side of polarized cells. They are found in all brain hemispheres but are most pronounced in neurons, which comprise the granular layers of the hippocampus and cerebellum. Pathogenic variants in genes which encode primary cilia components are responsible for neuronal ciliopathies—a group of central nervous system disorders characterized by neurodevelopmental conditions such as intellectual disability, seizure, ataxia, and sensory deficits. In the hippocampus, neuronal primary cilia form chemical synapses with axons and their membranes are populated with unique sets of ion channels and G protein-coupled receptors (GPCRs). Primary cilia are small and privileged compartments that are challenging organelles to study. In detail, we describe cilia electrophysiology methods and the use of cilia-specific fluorescent sensors to assay neuronal polycystin channel function and serotonergic receptor signaling, respectively. These tools allow researchers to assay calcium, cAMP and channel-related signaling pathways in isolated neurons in real-time and in semi-quantitative terms, while enhancing our understanding of this understudied organelle and its dysregulation in ciliopathy disease states.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70034","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143831116","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}