T-type calcium channels in differentiation and proliferation

Lory, Philippe; Bidaud, Isabelle; Chemin, Jean

doi:10.1016/j.ceca.2006.04.017

Cited by 117 publications

(118 citation statements)

References 145 publications

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“…In contrast, down-regulation of Cav3.2, or its blockade with various inhibitors, slows cell proliferation [118]. This is in agreement with many articles showing the participation of T-type calcium channels in various aspects of cell growth, including cell proliferation or cell apoptosis (for a review see [114] or [58]). Since NE cells of the prostate may proliferate rapidly in some forms of prostate carcinomas (SCPCa), it will be of great interest to assess whether Cav3.2 channels, involved in both proliferation and NE differentiation, in combination with a p53 inactivation, are indeed involved in the development of SCPCa.…”

Section: Ne Differentiation In Cancer Progression-perspectives On Thesupporting

confidence: 69%

“…It has been shown in the literature that in many neuronal models, T-type calcium channels are expressed in the early stages of development and may participate in the differentiation process [56,57]. The involvement of calcium channels, notably T-type calcium channels, in neuronal development has been reviewed thoroughly elsewhere [58].…”

Section: Expression Of Voltage-dependent Calcium Channelsmentioning

confidence: 99%

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Expression and Role of T-type Calcium Channels during Neuroendocrine Differentiation

Warnier¹,

Gackière²,

Roudbaraki³

et al. 2017

J Cell Signal

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Neuroendocrine cells release their secretion into the extracellular environment through calcium-dependent signalling pathways. These cells share common morphological and molecular features such as the expression of specific biomarkers, neurite outgrowth and dense core secretory granules. In order to elucidate the signalling pathways leading from undifferentiated to differentiated neuroendocrine cells, the role of voltage-dependent calcium channels, central actors in the excitation-secretion coupling, has been comprehensively investigated. T-type calcium channels appear to belong to the most important ion channel family involved in the neuroendocrine differentiation process. They could also participate in the development of neuroendocrine tumours.

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Section: Ne Differentiation In Cancer Progression-perspectives On Thesupporting

confidence: 69%

Section: Expression Of Voltage-dependent Calcium Channelsmentioning

confidence: 99%

Expression and Role of T-type Calcium Channels during Neuroendocrine Differentiation

Warnier¹,

Gackière²,

Roudbaraki³

et al. 2017

J Cell Signal

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“…Although T-type calcium channels are differentially distributed in the brain (Talley et al, 1999), and their density changes in neurons during development (Lory et al, 2006), very little is known about transcriptional regulation of T-type channel genes, including Cacna1g. The human CACNA1G promoter is hypermethylated in various tumors, which results in its repression (Toyota et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

LEF1/β-Catenin Complex Regulates Transcription of the Cav3.1 Calcium Channel Gene (Cacna1g) in Thalamic Neurons of the Adult Brain

Wisniewska

Misztal²,

Michowski³

et al. 2010

J. Neurosci.

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␤-Catenin, together with LEF1/TCF transcription factors, activates genes involved in the proliferation and differentiation of neuronal precursor cells. In mature neurons, ␤-catenin participates in dendritogenesis and synaptic function as a component of the cadherin cell adhesion complex. However, the transcriptional activity of ␤-catenin in these cells remains elusive. In the present study, we found that in the adult mouse brain, ␤-catenin and LEF1 accumulate in the nuclei of neurons specifically in the thalamus. The particular electrophysiological properties of thalamic neurons depend on T-type calcium channels. Cav3.1 is the predominant T-type channel subunit in the thalamus, and we hypothesized that the Cacna1g gene encoding Cav3.1 is a target of the LEF1/␤-catenin complex. We demonstrated that the expression of Cacna1g is high in the thalamus and is further increased in thalamic neurons treated in vitro with LiCl or WNT3A, activators of ␤-catenin. Luciferase reporter assays confirmed that the Cacna1G promoter is activated by LEF1 and ␤-catenin, and footprinting analysis revealed four LEF1 binding sites in the proximal region of this promoter. Chromatin immunoprecipitation demonstrated that the Cacna1g proximal promoter is occupied by ␤-catenin in vivo in the thalamus, but not in the hippocampus. Moreover, WNT3A stimulation enhanced T-type current in cultured thalamic neurons. Together, our data indicate that the LEF1/␤-catenin complex regulates transcription of Cacna1g and uncover a novel function for ␤-catenin in mature neurons. We propose that ␤-catenin contributes to neuronal excitability not only by a local action at the synapse but also by activating gene expression in thalamic neurons.

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“…T-type Ca 2+ channels are highly expressed in many developing tissues and are implicated in regulating cellular events leading to cell proliferation and differentiation (50). Calcium influx through T-type Ca 2+ channels activates several cellular pathways, including calcineurin/NFAT (29,39), extracellular signal-regulated kinase (31,(51)(52)(53), nitric oxide synthase 3 (54), and Ca 2+ /calmodulindependent protein kinase II (55).…”

Section: Discussionmentioning

confidence: 99%

Ca _v 3.2 T-type calcium channel is required for the NFAT-dependent Sox9 expression in tracheal cartilage

Lin

Tzeng

Lee

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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Significance The tracheal cartilage rings are important for protecting and maintaining the airway. However, the chondrogenesis of tracheal cartilage is not completely understood. We demonstrate that the Ca v 3.2 T-type calcium channel is required for normal tracheal cartilage ring formation. Calcium influx via Ca v 3.2 induces chondrogenesis and up-regulates a chondrogenic master gene, sex determination region of Y chromosome (SRY)-related high-mobility group-Box gene 9 (Sox9), via a calcium and calcineurin-dependent pathway. Ca v 3.2-dependent regulation of Sox9 is mediated by a newly identified nuclear factor of activated T-cell binding site on the Sox9 promoter. Our study provides novel insight into the roles of Ca v 3.2 T-type calcium channels in tracheal development. Moreover, CACNA1H , the human homolog of the mouse Ca v 3.2-encoding gene, may be a potential candidate gene involved in congenital tracheal stenosis in humans.

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T-type calcium channels in differentiation and proliferation

Cited by 117 publications

References 145 publications

Expression and Role of T-type Calcium Channels during Neuroendocrine Differentiation

Expression and Role of T-type Calcium Channels during Neuroendocrine Differentiation

LEF1/β-Catenin Complex Regulates Transcription of the Cav3.1 Calcium Channel Gene (Cacna1g) in Thalamic Neurons of the Adult Brain

Ca _v 3.2 T-type calcium channel is required for the NFAT-dependent Sox9 expression in tracheal cartilage

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T-type calcium channels in differentiation and proliferation

Cited by 117 publications

References 145 publications

Expression and Role of T-type Calcium Channels during Neuroendocrine Differentiation

Expression and Role of T-type Calcium Channels during Neuroendocrine Differentiation

LEF1/β-Catenin Complex Regulates Transcription of the Cav3.1 Calcium Channel Gene (Cacna1g) in Thalamic Neurons of the Adult Brain

Ca v 3.2 T-type calcium channel is required for the NFAT-dependent Sox9 expression in tracheal cartilage

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Ca _v 3.2 T-type calcium channel is required for the NFAT-dependent Sox9 expression in tracheal cartilage