Plasma membrane Ca
 2+
 -ATPases can shape the pattern of Ca
 2+
 transients induced by store-operated Ca
 2+
 entry

Pászty, Katalin; Caride, Ariel J.; Bajzer, Željko; Offord, Chetan P.; Padányi, Rita; Hegedűs, Luca; Varga, Karolina; Strehler, Emanuel E.; Enyedi, Ágnes

doi:10.1126/scisignal.2005672

Cited by 47 publications

(26 citation statements)

References 71 publications

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“…). Ca 2+ ‐activated cell functions rely on the amplitude and spatio‐temporal patterning of the Ca 2+ signal (Paszty et al ., ). The general increased expression in channel genes involved in the increase in cytosolic Ca 2+ concentration ( CaV , Orai , LGC , CNG , TRP ) and in channel genes involved in Ca 2+ removal from the cytoplasm (PMCA and NCKX ) suggest up‐regulated Ca 2+ signalling in regulating some diapause processes.…”

Section: Resultsmentioning

confidence: 97%

Transcriptome and proteome analyses reveal complex mechanisms of reproductive diapause in the two‐spotted spider mite, Tetranychus urticae

Zhao

Sun

et al. 2016

Insect Molecular Biology

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Although a variety of factors underlying diapause have been identified in arthropods and other organisms, the molecular mechanisms regulating diapause are still largely unknown. Here, to better understand this process, we examined diapause-associated genes in the two-spotted spider mite, Tetranychus urticae, by comparing the transcriptomes and proteomes of early diapausing and reproductive adult females. Amongst genes underlying diapause revealed by the transcriptomic and proteomic data sets, we described the noticeable change in Ca -associated genes, including 65 Ca -binding protein genes and 23 Ca transporter genes, indicating that Ca signalling has a substantial role in diapause regulation. Other interesting changes in diapause included up-regulation of (1) glutamate receptors that may be involved in synaptic plasticity changes, (2) genes involved in cytoskeletal reorganization including genes encoding each of the components of thick and thin filaments, tubulin and members of integrin signalling and (3) genes involved in anaerobic energy metabolism, which reflects a shift to anaerobic energy metabolism in early diapausing mites.

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Section: Resultsmentioning

confidence: 97%

Transcriptome and proteome analyses reveal complex mechanisms of reproductive diapause in the two‐spotted spider mite, Tetranychus urticae

Zhao

Sun

et al. 2016

Insect Molecular Biology

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“…In fact, it is well-established that frequent Ca 2+ oscillations are particularly efficient in maintaining nuclear NFAT 4 , 5 , 37 . Moreover, recent studies on non-immune cells demonstrated that PMCAs actively shape SOCE-induced Ca 2+ oscillations in an isoform-specific manner 38 and silencing of PMCA1 and 4 was found to increase Ca 2+ oscillations and nuclear translocation of NFATc1 in osteoclasts 39 . Thus, while our FACS-based Ca 2+ measurements did not resolve oscillations, we assume that reduced PMCA levels in both Nptn −/− and Pmca1 +/− T cells exert their effects on NFAT and cytokine production at least in part via increased Ca 2+ oscillation.…”

Section: Discussionmentioning

confidence: 99%

A complex of Neuroplastin and Plasma Membrane Ca2+ ATPase controls T cell activation

Korthals

Langnaese

Smalla

et al. 2017

Sci Rep

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The outcome of T cell activation is determined by mechanisms that balance Ca2+ influx and clearance. Here we report that murine CD4 T cells lacking Neuroplastin (Nptn −/−), an immunoglobulin superfamily protein, display elevated cytosolic Ca2+ and impaired post-stimulation Ca2+ clearance, along with increased nuclear levels of NFAT transcription factor and enhanced T cell receptor-induced cytokine production. On the molecular level, we identified plasma membrane Ca2+ ATPases (PMCAs) as the main interaction partners of Neuroplastin. PMCA levels were reduced by over 70% in Nptn −/− T cells, suggesting an explanation for altered Ca2+ handling. Supporting this, Ca2+ extrusion was impaired while Ca2+ levels in internal stores were increased. T cells heterozygous for PMCA1 mimicked the phenotype of Nptn −/− T cells. Consistent with sustained Ca2+ levels, differentiation of Nptn −/− T helper cells was biased towards the Th1 versus Th2 subset. Our study thus establishes Neuroplastin-PMCA modules as important regulators of T cell activation.

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“…Previously, we demonstrated that PMCA activity can reduce the SOCE-mediated Ca 2+ signal (37) and most recently that PMCA4b can inhibit melanoma cell migration. A direct role of PMCA4b in the regulation of migration was also demonstrated in VEGF-treated endothelial cells (38), which involved the NFAT pathway.…”

Section: Discussionmentioning

confidence: 99%

Histone Deacetylase Inhibitor Treatment Increases the Expression of the Plasma Membrane Ca2+ Pump PMCA4b and Inhibits the Migration of Melanoma Cells Independent of ERK

et al. 2017

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Several new therapeutic options emerged recently to treat metastatic melanoma; however, the high frequency of intrinsic and acquired resistance among patients shows a need for new therapeutic options. Previously, we identified the plasma membrane Ca2+ ATPase 4b (PMCA4b) as a metastasis suppressor in BRAF-mutant melanomas and found that mutant BRAF inhibition increased the expression of the pump, which then inhibited the migratory and metastatic capability of the cells. Earlier it was also demonstrated that histone deacetylase inhibitors (HDACis) upregulated PMCA4b expression in gastric, colon, and breast cancer cells. In this study, we treated one BRAF wild-type and two BRAF-mutant melanoma cell lines with the HDACis, SAHA and valproic acid, either alone, or in combination with the BRAF inhibitor, vemurafenib. We found that HDACi treatment strongly increased the expression of PMCA4b in all cell lines irrespective of their BRAF mutational status, and this effect was independent of ERK activity. Furthermore, HDAC inhibition also enhanced the abundance of the housekeeping isoform PMCA1. Combination of HDACis with vemurafenib, however, did not have any additive effects on either PMCA isoform. We demonstrated that the HDACi-induced increase in PMCA abundance was coupled to an enhanced [Ca2+]i clearance rate and also strongly inhibited both the random and directional movements of A375 cells. The primary role of PMCA4b in these characteristic changes was demonstrated by treatment with the PMCA4-specific inhibitor, caloxin 1c2, which was able to restore the slower Ca2+ clearance rate and higher motility of the cells. While HDAC treatment inhibited cell motility, it decreased only modestly the ratio of proliferative cells and cell viability. Our results show that in melanoma cells the expression of both PMCA4b and PMCA1 is under epigenetic control and the elevation of PMCA4b expression either by HDACi treatment or by the decreased activation of the BRAF-MEK-ERK pathway can inhibit the migratory capacity of the highly motile A375 cells.

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Plasma membrane Ca ²⁺ -ATPases can shape the pattern of Ca ²⁺ transients induced by store-operated Ca ²⁺ entry

Cited by 47 publications

References 71 publications

Transcriptome and proteome analyses reveal complex mechanisms of reproductive diapause in the two‐spotted spider mite, Tetranychus urticae

Transcriptome and proteome analyses reveal complex mechanisms of reproductive diapause in the two‐spotted spider mite, Tetranychus urticae

A complex of Neuroplastin and Plasma Membrane Ca2+ ATPase controls T cell activation

Histone Deacetylase Inhibitor Treatment Increases the Expression of the Plasma Membrane Ca2+ Pump PMCA4b and Inhibits the Migration of Melanoma Cells Independent of ERK

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Plasma membrane Ca 2+ -ATPases can shape the pattern of Ca 2+ transients induced by store-operated Ca 2+ entry

Cited by 47 publications

References 71 publications

Transcriptome and proteome analyses reveal complex mechanisms of reproductive diapause in the two‐spotted spider mite, Tetranychus urticae

Transcriptome and proteome analyses reveal complex mechanisms of reproductive diapause in the two‐spotted spider mite, Tetranychus urticae

A complex of Neuroplastin and Plasma Membrane Ca2+ ATPase controls T cell activation

Histone Deacetylase Inhibitor Treatment Increases the Expression of the Plasma Membrane Ca2+ Pump PMCA4b and Inhibits the Migration of Melanoma Cells Independent of ERK

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Resources

About

Plasma membrane Ca ²⁺ -ATPases can shape the pattern of Ca ²⁺ transients induced by store-operated Ca ²⁺ entry