Pub Date : 2025-01-01DOI: 10.1016/j.ceca.2024.102989
M. Raza Zaidi , Jonathan Soboloff
Recent findings by Abrahamian et al. (2024) provides new insights into the relationship between Two Pore Channel 2 (TPC2) activity and the development and progression of melanoma. Melanocyte inducing transcription factor (MITF) is a critical regulator of both melanocyte and melanoma behavior. Abrahamian et al. (2024) show that MITF-high melanoma requires BOTH Rab7a and TPC2 for proliferation, invasion and metastasis. They further identify Wnt signaling as the mediator of this phenomenon; Rab7a induces TPC2 activity in lysosomes and melanosomes, which regulates GSK-3β stability, thereby determining whether β-catenin escapes degradation and translocates to the nucleus to transcribe the MITF gene. These observations provide new insights into the relationship between ion channel function, lysosomal/melanosomal activity and control for oncogenesis and disease progression in melanoma.
{"title":"TPC2 controls MITF expression and metastasis in melanoma","authors":"M. Raza Zaidi , Jonathan Soboloff","doi":"10.1016/j.ceca.2024.102989","DOIUrl":"10.1016/j.ceca.2024.102989","url":null,"abstract":"<div><div>Recent findings by Abrahamian et al. (2024) provides new insights into the relationship between Two Pore Channel 2 (TPC2) activity and the development and progression of melanoma. Melanocyte inducing transcription factor (MITF) is a critical regulator of both melanocyte and melanoma behavior. Abrahamian et al. (2024) show that MITF-high melanoma requires BOTH Rab7a and TPC2 for proliferation, invasion and metastasis. They further identify Wnt signaling as the mediator of this phenomenon; Rab7a induces TPC2 activity in lysosomes and melanosomes, which regulates GSK-3β stability, thereby determining whether β-catenin escapes degradation and translocates to the nucleus to transcribe the <em>MITF</em> gene. These observations provide new insights into the relationship between ion channel function, lysosomal/melanosomal activity and control for oncogenesis and disease progression in melanoma.</div></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"125 ","pages":"Article 102989"},"PeriodicalIF":4.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142909490","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}
Pub Date : 2025-01-01DOI: 10.1016/j.ceca.2024.102990
Salah A. Baker , Manushri Karwa , Ji Yeon Lee , Sarah Riar , Bernard T. Drumm , Kenton M. Sanders
Interstitial cells of Cajal in the plane of the myenteric plexus (ICC-MY) serve as electrical pacemakers in the stomach and small intestine. A similar population of cells is found in the colon, but these cells do not appear to generate regular slow wave potentials, as characteristic in more proximal gut regions. Ca2+ handling mechanisms in ICC-MY of the mouse proximal colon were studied using confocal imaging of muscles from animals expressing GCaMP6f exclusively in ICC. ICC-MY displayed stochastic, localized Ca2+ transients that seldom propagated between cells. Colonic ICC express ANO1 channels, so Ca2+ transients likely couple to activation of spontaneous transient inward currents (STICs) in these cells. The Ca2+ transients were due to Ca2+ release and blocked by cyclopiazonic acid (CPA), thapsigargin and caffeine, but unaffected by tetracaine. Antagonists of L- and T-type Ca2+ channels and reduction in extracellular Ca2+ had minimal effects on Ca2+ transients. We reasoned that STICs may not activate regenerative Ca2+ waves in ICC-MY because voltage-dependent Ca2+ conductances are largely inactivated at the relatively depolarized potentials of colonic muscles. We tested the effects of hyperpolarization with pinacidil, a KATP agonist. Ca2+ waves were initiated in some ICC-MY networks when muscles were hyperpolarized, and these events were blocked by a T-type Ca2+ channel antagonist, NNC 55–0396. Ca2+ waves activated by excitatory nerve stimulation were significantly enhanced by hyperpolarization. Our data suggest that colonic ICC-MY are conditional pacemaker cells that depend upon preparative hyperpolarization, produced physiologically by inputs from enteric inhibitory neurons and necessary for regenerative pacemaker activity.
{"title":"Ca²⁺ signaling in myenteric interstitial cells of Cajal (ICC-MY) and their role as conditional pacemakers in the colon","authors":"Salah A. Baker , Manushri Karwa , Ji Yeon Lee , Sarah Riar , Bernard T. Drumm , Kenton M. Sanders","doi":"10.1016/j.ceca.2024.102990","DOIUrl":"10.1016/j.ceca.2024.102990","url":null,"abstract":"<div><div>Interstitial cells of Cajal in the plane of the myenteric plexus (ICC-MY) serve as electrical pacemakers in the stomach and small intestine. A similar population of cells is found in the colon, but these cells do not appear to generate regular slow wave potentials, as characteristic in more proximal gut regions. Ca<sup>2+</sup> handling mechanisms in ICC-MY of the mouse proximal colon were studied using confocal imaging of muscles from animals expressing GCaMP6f exclusively in ICC. ICC-MY displayed stochastic, localized Ca<sup>2+</sup> transients that seldom propagated between cells. Colonic ICC express ANO1 channels, so Ca<sup>2+</sup> transients likely couple to activation of spontaneous transient inward currents (STICs) in these cells. The Ca<sup>2+</sup> transients were due to Ca<sup>2+</sup> release and blocked by cyclopiazonic acid (CPA), thapsigargin and caffeine, but unaffected by tetracaine. Antagonists of L- and T-type Ca<sup>2+</sup> channels and reduction in extracellular Ca<sup>2+</sup> had minimal effects on Ca<sup>2+</sup> transients. We reasoned that STICs may not activate regenerative Ca<sup>2+</sup> waves in ICC-MY because voltage-dependent Ca<sup>2+</sup> conductances are largely inactivated at the relatively depolarized potentials of colonic muscles. We tested the effects of hyperpolarization with pinacidil, a K<sub>ATP</sub> agonist. Ca<sup>2+</sup> waves were initiated in some ICC-MY networks when muscles were hyperpolarized, and these events were blocked by a T-type Ca<sup>2+</sup> channel antagonist, NNC 55–0396. Ca<sup>2+</sup> waves activated by excitatory nerve stimulation were significantly enhanced by hyperpolarization. Our data suggest that colonic ICC-MY are conditional pacemaker cells that depend upon preparative hyperpolarization, produced physiologically by inputs from enteric inhibitory neurons and necessary for regenerative pacemaker activity.</div></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"125 ","pages":"Article 102990"},"PeriodicalIF":4.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11737426/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142926791","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}
Pub Date : 2025-01-01DOI: 10.1016/j.ceca.2024.102987
Kriti Ahuja, Sharon Raju, Sakshi Dahiya, Rajender K Motiani
Pigmentation is a protective phenomenon that shields skin cells from UV-induced DNA damage. Perturbations in pigmentation pathways predispose to skin cancers and lead to pigmentary disorders. These ailments impart psychological trauma and severely affect the patients’ quality of life. Emerging literature suggests that reactive oxygen species (ROS) and calcium (Ca2+) signaling modules regulate physiological pigmentation. Further, pigmentary disorders are associated with dysregulated ROS homeostasis and changes in Ca2+ dynamics. Here, we systemically review the literature that demonstrates key role of ROS and Ca2+ signaling in pigmentation and pigmentary disorders. Further, we discuss recent studies, which have revealed that organelle-specific Ca2+ transport mechanisms are critical determinant of pigmentation. Importantly, we deliberate upon the possibility of clinical management of pigmentary disorders by therapeutically targeting ROS generation and cellular Ca2+ handling toolkit. Finally, we highlight the key outstanding questions in the field that demand critical and timely attention. Although an important role of ROS and Ca2+ signaling in regulating skin pigmentation has emerged, the underlying molecular mechanisms remain poorly understood. In future, it would be vital to investigate in detail the signaling cascades that connect perturbed ROS homeostasis and Ca2+ signaling to human pigmentary disorders.
{"title":"ROS and calcium signaling are critical determinant of skin pigmentation","authors":"Kriti Ahuja, Sharon Raju, Sakshi Dahiya, Rajender K Motiani","doi":"10.1016/j.ceca.2024.102987","DOIUrl":"10.1016/j.ceca.2024.102987","url":null,"abstract":"<div><div>Pigmentation is a protective phenomenon that shields skin cells from UV-induced DNA damage. Perturbations in pigmentation pathways predispose to skin cancers and lead to pigmentary disorders. These ailments impart psychological trauma and severely affect the patients’ quality of life. Emerging literature suggests that reactive oxygen species (ROS) and calcium (Ca<sup>2+</sup>) signaling modules regulate physiological pigmentation. Further, pigmentary disorders are associated with dysregulated ROS homeostasis and changes in Ca<sup>2+</sup> dynamics. Here, we systemically review the literature that demonstrates key role of ROS and Ca<sup>2+</sup> signaling in pigmentation and pigmentary disorders. Further, we discuss recent studies, which have revealed that organelle-specific Ca<sup>2+</sup> transport mechanisms are critical determinant of pigmentation. Importantly, we deliberate upon the possibility of clinical management of pigmentary disorders by therapeutically targeting ROS generation and cellular Ca<sup>2+</sup> handling toolkit. Finally, we highlight the key outstanding questions in the field that demand critical and timely attention. Although an important role of ROS and Ca<sup>2+</sup> signaling in regulating skin pigmentation has emerged, the underlying molecular mechanisms remain poorly understood. In future, it would be vital to investigate in detail the signaling cascades that connect perturbed ROS homeostasis and Ca<sup>2+</sup> signaling to human pigmentary disorders.</div></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"125 ","pages":"Article 102987"},"PeriodicalIF":4.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142871458","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}
Pub Date : 2025-01-01DOI: 10.1016/j.ceca.2024.102983
Rebecca Frank Hayward , Adam E. Cohen
Calcium mediates many important signals in dendrites. However, the basic transport properties of calcium in dendrites have been difficult to measure: how far and how fast does a local influx of calcium propagate? We developed an all-optical system for simultaneous targeted Ca2+ import and Ca2+ concentration mapping. We co-expressed a blue light-activated calcium selective channelrhodopsin, CapChR2, with a far-red calcium sensor, FR-GECO1c, in cultured rat hippocampal neurons, and used patterned optogenetic stimulation to introduce calcium into cells with user-defined patterns of space and time. We determined a mean steady-state length constant for Ca2+ transport ϕ ∼ 5.8 μm, a half-life for return to baseline t1/2 ∼ 1.7 s, and an effective diffusion coefficient D ∼ 20 μm2/s, though there were substantial differences in Ca2+ dynamics between proximal and distal dendrites. At high Ca2+ concentration, distal dendrites showed nonlinear activation of Ca2+ efflux, which we pharmacologically ascribed to the NCX1 antiporter. Genetically encoded tools for all-optical mapping of Ca2+ transport and handling provide a powerful capability for studying this important messenger.
{"title":"All-optical mapping of Ca2+ transport and homeostasis in dendrites","authors":"Rebecca Frank Hayward , Adam E. Cohen","doi":"10.1016/j.ceca.2024.102983","DOIUrl":"10.1016/j.ceca.2024.102983","url":null,"abstract":"<div><div>Calcium mediates many important signals in dendrites. However, the basic transport properties of calcium in dendrites have been difficult to measure: how far and how fast does a local influx of calcium propagate? We developed an all-optical system for simultaneous targeted Ca<sup>2+</sup> import and Ca<sup>2+</sup> concentration mapping. We co-expressed a blue light-activated calcium selective channelrhodopsin, CapChR2, with a far-red calcium sensor, FR-GECO1c, in cultured rat hippocampal neurons, and used patterned optogenetic stimulation to introduce calcium into cells with user-defined patterns of space and time. We determined a mean steady-state length constant for Ca<sup>2+</sup> transport <em>ϕ</em> ∼ 5.8 μm, a half-life for return to baseline <em>t</em><sub>1/2</sub> ∼ 1.7 s, and an effective diffusion coefficient <em>D</em> ∼ 20 μm<sup>2</sup>/s, though there were substantial differences in Ca<sup>2+</sup> dynamics between proximal and distal dendrites. At high Ca<sup>2+</sup> concentration, distal dendrites showed nonlinear activation of Ca<sup>2+</sup> efflux, which we pharmacologically ascribed to the NCX1 antiporter. Genetically encoded tools for all-optical mapping of Ca<sup>2+</sup> transport and handling provide a powerful capability for studying this important messenger.</div></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"125 ","pages":"Article 102983"},"PeriodicalIF":4.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11735331/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142812032","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}
Pub Date : 2025-01-01DOI: 10.1016/j.ceca.2024.102988
Julio C. Sánchez , Laura V. Muñoz , Barbara E. Ehrlich
{"title":"Corrigendum to “Modulating TRPV4 channels with paclitaxel and lithium” [Cell Calcium 91 (2020) 102266]","authors":"Julio C. Sánchez , Laura V. Muñoz , Barbara E. Ehrlich","doi":"10.1016/j.ceca.2024.102988","DOIUrl":"10.1016/j.ceca.2024.102988","url":null,"abstract":"","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"125 ","pages":"Article 102988"},"PeriodicalIF":4.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142920904","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}
Pub Date : 2025-01-01DOI: 10.1016/j.ceca.2024.102985
Xiao-Hua Zhang, Martin Morad
Rationale & methods
While signaling of cardiac SR by surface membrane proteins (ICa & INCX) is well studied, the regulation of mitochondrial Ca2+ by plasmalemmal proteins remains less explored. Here we have examined the signaling of mitochondria and SR by surface-membrane calcium-transporting proteins, using genetically engineered targeted fluorescent probes, mito-GCamP6 and R-CEPIA1er.
Results
In voltage-clamped and TIRF-imaged cardiomyocytes, low Na+ induced SR Ca2+ release was suppressed by short pre-exposures to ∼100 nM FCCP, suggesting mitochondrial Ca2+ contribution to low Na+ triggered SR Ca2+release. Even though low Na+- or caffeine-triggered SR Ca2+ release activated global mitochondrial Ca2+ uptake, focal mitochondrial Ca2+ signals varied in kinetics and magnitude, showing uptake or release of calcium, depending on cellular location of mitochondria. In spontaneously pacing cells, sustained caffeine exposures depleted the SR Ca2+ content activating mitochondrial Ca2+ uptake followed by sustained mitochondrial pacing. Spontaneous hiPSCCMs pacing was strongly suppressed by L-type calcium channels blockers, but not by inhibiting SERCA2a by CPA.
Conclusion
Spontaneous hiPSCCMs pacing is triggered by influx of calcium through L-type Ca2+ channel that gates the release of SR pools supplemented by NCX-mediated mitochondrial calcium contribution.
{"title":"Regulation of SR and mitochondrial Ca2+ signaling by L-type Ca2+ channels and Na/Ca exchanger in hiPSC–CMs","authors":"Xiao-Hua Zhang, Martin Morad","doi":"10.1016/j.ceca.2024.102985","DOIUrl":"10.1016/j.ceca.2024.102985","url":null,"abstract":"<div><h3>Rationale & methods</h3><div>While signaling of cardiac SR by surface membrane proteins (I<sub>Ca</sub> & I<sub>NCX</sub>) is well studied, the regulation of mitochondrial Ca<sup>2+</sup> by plasmalemmal proteins remains less explored. Here we have examined the signaling of mitochondria and SR by surface-membrane calcium-transporting proteins, using genetically engineered targeted fluorescent probes, mito-GCamP6 and R-CEPIA1er.</div></div><div><h3>Results</h3><div>In voltage-clamped and TIRF-imaged cardiomyocytes, low Na<sup>+</sup> induced SR Ca<sup>2+</sup> release was suppressed by short pre-exposures to ∼100 nM FCCP, suggesting mitochondrial Ca<sup>2+</sup> contribution to low Na<sup>+</sup> triggered SR Ca<sup>2+</sup>release. Even though low Na<sup>+</sup>- or caffeine-triggered SR Ca<sup>2+</sup> release activated <em><u>global</u></em> mitochondrial Ca<sup>2+</sup> uptake, <u>f</u><em><u>ocal</u></em> mitochondrial Ca<sup>2+</sup> signals varied in kinetics and magnitude, showing uptake or release of calcium, depending on cellular location of mitochondria. In spontaneously pacing cells, sustained caffeine exposures depleted the SR Ca<sup>2+</sup> content activating mitochondrial Ca<sup>2+</sup> uptake followed by sustained mitochondrial pacing. Spontaneous hiPSC<img>CMs pacing was strongly suppressed by L-type calcium channels blockers, but not by inhibiting SERCA2a by CPA.</div></div><div><h3>Conclusion</h3><div>Spontaneous hiPSC<img>CMs pacing is triggered by influx of calcium through L-type Ca<sup>2+</sup> channel that gates the release of SR pools supplemented by NCX-mediated mitochondrial calcium contribution.</div></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"125 ","pages":"Article 102985"},"PeriodicalIF":4.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142853112","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}
Pub Date : 2024-12-01DOI: 10.1016/j.ceca.2024.102972
Ana M. Hernández-Vega , Refugio García-Villegas , Tamara Rosenbaum
The transient receptor potential vanilloid 4 (TRPV4) ion channel is a ubiquitously expressed Ca2+-permeable ion channel that controls intracellular calcium ([Ca2+]i) homeostasis in various types of cells. The physiological roles for TRPV4 are tissue specific and the mechanisms behind this specificity remain mostly unclarified. It is noteworthy that mutations in the TRPV4 channel have been associated to a broad spectrum of congenital diseases, with most of these mutations mainly resulting in gain-of-function. Mutations have been identified in human patients showing a variety of phenotypes and symptoms, mostly related to skeletal and neuromuscular disorders. Since TRPV4 is so widely expressed throughout the body, it comes as no surprise that the literature is growing in evidence linking this protein to malfunction in systems other than the skeletal and neuromuscular. In this review, we summarize the expression patterns of TRPV4 in several tissues and highlight findings of recent studies that address critical structural and functional features of this channel, particularly focusing on its interactions and signaling pathways related to Ca2+ entry. Moreover, we discuss the roles of TRPV4 mutations in some diseases and pinpoint some of the mechanisms underlying pathological states where TRPV4’s malfunction is prominent.
{"title":"Roles for TRPV4 in disease: A discussion of possible mechanisms","authors":"Ana M. Hernández-Vega , Refugio García-Villegas , Tamara Rosenbaum","doi":"10.1016/j.ceca.2024.102972","DOIUrl":"10.1016/j.ceca.2024.102972","url":null,"abstract":"<div><div>The transient receptor potential vanilloid 4 (TRPV4) ion channel is a ubiquitously expressed Ca<sup>2+</sup>-permeable ion channel that controls intracellular calcium ([Ca<sup>2+</sup>]<sub>i</sub>) homeostasis in various types of cells. The physiological roles for TRPV4 are tissue specific and the mechanisms behind this specificity remain mostly unclarified. It is noteworthy that mutations in the TRPV4 channel have been associated to a broad spectrum of congenital diseases, with most of these mutations mainly resulting in gain-of-function. Mutations have been identified in human patients showing a variety of phenotypes and symptoms, mostly related to skeletal and neuromuscular disorders. Since TRPV4 is so widely expressed throughout the body, it comes as no surprise that the literature is growing in evidence linking this protein to malfunction in systems other than the skeletal and neuromuscular. In this review, we summarize the expression patterns of TRPV4 in several tissues and highlight findings of recent studies that address critical structural and functional features of this channel, particularly focusing on its interactions and signaling pathways related to Ca<sup>2+</sup> entry. Moreover, we discuss the roles of TRPV4 mutations in some diseases and pinpoint some of the mechanisms underlying pathological states where TRPV4’s malfunction is prominent.</div></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"124 ","pages":"Article 102972"},"PeriodicalIF":4.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142749679","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}
Pub Date : 2024-11-20DOI: 10.1016/j.ceca.2024.102970
Vikas Arige, David I. Yule
{"title":"PIP2 primes IP3 receptor activity: It takes at least three IP3s to open!","authors":"Vikas Arige, David I. Yule","doi":"10.1016/j.ceca.2024.102970","DOIUrl":"10.1016/j.ceca.2024.102970","url":null,"abstract":"","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"124 ","pages":"Article 102970"},"PeriodicalIF":4.3,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142721672","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}
Pub Date : 2024-11-17DOI: 10.1016/j.ceca.2024.102969
Qianru Mu , Jade L. Harris , David I. Yule , James T. Slama , Jonathan S. Marchant , Sandip Patel
{"title":"NAADP signaling: Master manipulation","authors":"Qianru Mu , Jade L. Harris , David I. Yule , James T. Slama , Jonathan S. Marchant , Sandip Patel","doi":"10.1016/j.ceca.2024.102969","DOIUrl":"10.1016/j.ceca.2024.102969","url":null,"abstract":"","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"124 ","pages":"Article 102969"},"PeriodicalIF":4.3,"publicationDate":"2024-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142695392","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}
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