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Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of human B lymphocytes from Scott syndrome patient and daughter, treated with the A23187 calcium ionophore

ABSTRACT: B lymphoblast samples from control individual, Scott syndrome patient and Scott syndrome daughter. From each samples one part was treated with A23187 ca2+ ionophore. Treated and non-treated samples were then cultured further. Each sample was then processed in duplicate for hybridization on the microarray

ORGANISM(S): Homo sapiens

SUBMITTER: Daniele Kerbiriou-Nabias

PROVIDER: E-GEOD-1028 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Identification of genes involved in Ca2+ ionophore A23187-mediated apoptosis and demonstration of a high susceptibility for transcriptional repression of cell cycle genes in B lymphoblasts from a patient with Scott syndrome.

Kozian Detlef D Proulle Valérie V Nitsche Almut A Galitzine Marie M Martinez Marie-Carmen MC Schumann Beatrice B Meyer Dominique D Herrmann Matthias M Freyssinet Jean-Marie JM Kerbiriou-Nabias Danièle D

BMC genomics 20051021

<h4>Background</h4>In contrast to other agents able to induce apoptosis of cultured cells, Ca2+ ionophore A23187 was shown to elicit direct activation of intracellular signal(s). The phenotype of the cells derived from patients having the hemorrhagic disease Scott syndrome, is associated with an abnormally high proportion of apoptotic cells, both in basal culture medium and upon addition of low ionophore concentrations in long-term cultures. These features are presumably related to the mutation ...[more]

PMID: 16242039

Similar Datasets

Scott B cell studies

Project description:B lymphoblast samples from control individual, Scott syndrome patient and Scott syndrome daughter. From each samples one part was treated with A23187 ca2+ ionophore. Treated and non-treated samples were then cultured further. Each sample was then processed in duplicate for hybridization on the microarray Keywords: ordered

2004-03-05 | GSE1028 | GEO

A positive feedback loop mediates crosstalk between calcium, cyclic nucleotide and lipid signaling in Toxoplasma gondii.

Project description:Fundamental processes of obligate intracellular parasites, such as Plasmodium falciparum and Toxoplasma gondii are controlled by a set of plant-like calcium dependent kinases (CDPKs), the conserved cAMP- and cGMP-dependent protein kinases (PKA and PKG), second messengers and lipid signalling. While some major components of the signalling networks have been identified, how these are connected is largely not known. Here, we compare the phospho-signalling networks during Toxoplasma egress from its host cell by artificially raising cGMP or calcium levels to activate PKG or CDPKs, respectively. We show that both these inducers trigger near identical signalling pathways and provide evidence for a feedback loop involving CDPK3. We measure phospho- and lipid signalling in parasites treated with the Ca2+ ionophore A23187 in a sub-minute timecourse and show CDPK3-dependent regulation of diacylglycerol levels and increased phosphorylation of four phosphodiesterases (PDEs), suggesting their function in the feedback loop. Disruption of CDPK3 leads to elevated cAMP levels and inhibition of PKA signalling rescues the egress defect of ΔCDPK3 parasites treated with A23187. Biochemical analysis of the four PDEs identifies PDE2 as the only cAMP-specific PDE among these candidates while the other PDEs are cGMP specific; two of which are inhibited by the predicted PDE inhibitor BIPPO. Conditional deletion of the 4 PDEs supports an important, but non-essential role of PDE1 and PDE2 for growth, while only the latter plays a role in controlling A23187-mediated egress. In summary, we uncover a positive feedback loop that potentiates signalling during egress and links several signalling pathways together.

2022-10-17 | PXD030057 | Pride

Identification of key pathway and genes expression in the activation of mast cell via calcium flux using bioinformatics analysis

Project description:The purpose of the present study is to identify gene signatures with IgE/antigen and calcium ionophore A23187 on the activation of MMCs. The differentially expressed genes between the two types of samples were identified with the Microarray Analysis. The gene ontology functional and pathway enrichment analyses of differentially-expressed genes were performed using the database for annotation, visualization and integrated discovery software.

2020-10-01 | E-MTAB-9508 | biostudies-arrayexpress

P. falciparum (lab strain DD2) treated with A23187 vs untreated [CGH]

2012-07-14 | E-GEOD-33764 | biostudies-arrayexpress

Combined assessment of global proteome, phosphoproteome and N-terminal protein cleavage to characterize altered platelet functions in human Scott syndrome

Project description:The Scott syndrome is a rare bleeding disorder associated with a mutation in the gene encoding anoctamin-6 (TMEM16F). After stimulation of Ca2+-mobilizing agonists, syndromatic platelets show a reduced phosphatidylserine exposure and do not form membrane blebs. Given the central role of anoctamin-6 in the platelet procoagulant response, we used quantitative proteomics to understand the underlying molecular mechanisms and the complex phenotypic changes in Scott platelets compared to control platelets. Therefore, we applied an iTRAQ-based multi-pronged strategy to quantify changes in (i) the global proteome, (ii) the phosphoproteome and (iii) proteolytic events between resting and stimulated Scott and control platelets. Our data indicate a limited number of proteins with decreased (70) or increased (64) expression in Scott platelets, among those we observed the absence of anoctamin-6 and the strong up-regulation of aquaporin-1. Furthermore, the quantification of 1,566 phosphopeptides revealed major differences between Scott and control platelets after stimulation with thrombin/convulxin or ionomycin. Finally, we quantified 1,596 N-terminal peptides in activated Scott and control platelets, 180 of which we identified as calpain-regulated, whereas a distinct set of 23 neo-N-termini was caspase-regulated. In Scott platelets, calpain-induced cleavage of cytoskeleton-linked and signaling proteins was down-regulated, in accordance with an increased phosphorylation state. Thus, multi-pronged proteomic profiling of Scott platelets provides detailed insight into their protection against detrimental Ca2+-dependent changes that are normally associated with phosphatidylserine exposure.

2016-08-24 | PXD002883 | Pride

P. falciparum (lab strain 3d7) schizonts treated with A23187 vs P. falciparum (lab strain 3d7) reference RNA pool

Project description:Calcium is a universal second messenger molecule which plays a significant role in several biological processes. Presence of calcium sensors (calmodulins) and calcium-dependent protein kinases in Plasmodium species suggests an important role of calcium-dependent signaling pathways in the regulation of cellular processes in the malaria parasites. Evidence for the transcriptional response of Plasmodium falciparum asexual blood stages to the well-known calcium ionophore A23187 has been presented here. P. falciparum 3D7 strain was cultured as described by Bozdech Z, Llinas M, Pulliam BL, Wong ED, Zhu J, DeRisi JL: The transcriptome of the intraerythrocytic developmental cycle of Plasmodium falciparum. PLoS Biol 2003, 1(1):E5. Calcium ionophore treatment was done as follows. Parasites at schizont stage were treated with 5 Î¼M of calcium ionophore, A23187 for 30 minutes, 1 hour, 2 hours, 4 hours and 6 hours. Total RNA from each of the time points was isolated and aminoallyl-cDNA was synthesized using reverse transcriptase system (Fermentas). cDNA made from the treated parasites were labeled with Cy5 (GE-Amersham). A reference pool was made by mixing equal amount of cDNA from the parasites collected at 6 hours interval throughout the 48 hours life cycle and was labeled with Cy3 (GE-Amersham). The samples were then hybridized on a spotted cDNA chip platform comprising 10166 MOEs representing 5363 coding sequences as described in Hu G, Cabrera A, Kono M, Mok S, Chaal BK, Haase S, Engelberg K, Cheemadan S, Spielmann T, Preiser PR, Gilberger TW, Bozdech Z: Transcriptional profiling of growth perturbations of the human malaria parasite Plasmodium falciparum. Nat Biotechnol, 2009. 28(1): p. 91-8. The data was normalized and filtered with the condition, signal intensity>background intensity + 2 SD of background intensity) using NOMAD.

2012-07-14 | E-GEOD-33797 | biostudies-arrayexpress

Regulation of mitochondrial Ca2+ uniporter expression and calcium signalling by lncRNA Tug1 in cardiomyocytes

Project description:Cardiomyocyte Ca2+ is buffered by mitochondria via the mitochondrial calcium uniporter (MCU) complex. The MCU complex consists of pore-forming proteins including the mitochondrial calcium uniporter (MCU), and regulatory proteins such as mitochondrial calcium uptake proteins 1 and 2 (MICU1/2). The stoichiometry of these proteins influences the sensitivity to Ca2+ and activity of the complex. However, the factors that regulate their gene expression remain incompletely understood. Long non-coding RNAs (lncRNAs) regulate gene expression through various mechanisms, and we recently found that the lncRNA Tug1 affected the expression of MCU-associated genes. To further explore this, we knocked down Tug1 (Tug1 KD) in H9c2 rat cardiomyocytes using antisense LNA oligo. This led to increased MCU protein expression yet this did not enhance a marker of mitochondrial Ca2+ uptake. RNA-seq revealed that Tug1 KD increased Mcu and led to differential expression of genes and pathways related to Ca2+ regulation in the heart. To understand the effect of this on Ca2+ signalling, we measured phosphorylation of Ca2+/calmodulin-dependent protein kinase II (CaMKII) and its downstream target cAMP Response Element-Binding protein (CREB), a transcription factor known to promote Mcu gene expression. Tug1 KD attenuated the increase in CAMKII and CREB phosphorylation in response to ionomycin, a Ca2+ ionophore. Inhibition of CaMKII, but not CREB, partially prevented the Tug1 KD mediated increase in Mcu. Together, these data suggest that Tug1 modulates MCU expression via a mechanism that may involve CAMKII and CREB. The Tug1 mediated regulation of MCU on mitochondrial Ca2+ uptake, may have functional consequences for cellular Ca2+ handling which could have implications for cardiac disease.

2023-07-22 | GSE237787 | GEO