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Expression data from unactivated vs. activated PBMCs

ABSTRACT: Long-lasting activation of T cells requires up-regulation of many genes, for example of transcription factors, cytoskeletal proteins and cell surface proteins including ion channels. An increase of ion channel density at the cell surface reflects the needs to manage increased Ca2+ influx into the activated T cell. Using oligonucleotide-based arrays we have surveyed changes in ion channel mRNA expression that occur upon T cell activation. We used Affymetrix Analysis to confirm our data achieved by self-designed glass array analysis. We isolated PBMCs from blood of healthy donors and divided those into two parts. One was activated for 72 hr by adding PHA-L whereas the other part was incubated in the same way but not stimulated.

ORGANISM(S): Homo sapiens

SUBMITTER: Christoph Ogrodowczyk

PROVIDER: E-GEOD-21837 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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A truncation variant of the cation channel P2RX5 is upregulated during T cell activation.

Abramowski Pierre P Ogrodowczyk Christoph C Martin Roland R Pongs Olaf O

PloS one 20140902 9

Members of the P2X family of ligand-gated cation channels (P2RX) are expressed by various cell types including neurons, smooth- and cardiac muscle cells, and leukocytes. The channels mediate signalling in response to extracellular ATP. Seven subunit isoforms (P2RX1-P2RX7) have been identified and these can assemble as homo- and heterotrimeric molecules. In humans, P2RX5 exists as a natural deletion mutant lacking amino acids 328-349 of exon 10, which are part of transmembrane (TM) 2 and pre-TM2 ...[more]

PMID: 25181038

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Expression data from unactivated vs. activated PBMCs (ion array)

Project description:Long-lasting activation of T cells requires up-regulation of many genes, for example of transcription factors, cytoskeletal proteins and cell surface proteins encluding ion channels. An increase of ion channel density at the cell surface reflects the needs to manage increased Ca2+ influx into the activated T cell. Using oligonucleotide-based arrays we have surveyed changes in ion channel mRNA expression that occur upon T cell activation. We isolated PBMCs from blood of healthy donors and divided those into two parts. One was activated for 72 hr by adding PHA-L whereas the other part was incubated in the same way but not stimulated.

2010-06-17 | E-GEOD-22387 | biostudies-arrayexpress

Expression data from unactivated vs. activated PBMCs (ion array)

2010-06-17 | GSE22387 | GEO

Expression data from unactivated vs. activated PBMCs

Project description:Long-lasting activation of T cells requires up-regulation of many genes, for example of transcription factors, cytoskeletal proteins and cell surface proteins encluding ion channels. An increase of ion channel density at the cell surface reflects the needs to manage increased Ca2+ influx into the activated T cell. Using oligonucleotide-based arrays we have surveyed changes in ion channel mRNA expression that occur upon T cell activation. We used Affymetrix Analysis to confirmate our data achieved by self-designed glass array analysis.

2010-05-14 | GSE21837 | GEO

Schölzel2021 - Modelica implementation of the one-dimensional model of the rabbit atrioventricular node in Inada2009 (InaMo)

Project description:This project contains a reusable, reproducible, understandable, and extensible reimplementation of the one-dimensional model of the rabbit atrioventricular node by Inada et al. (Inada2009) in the language Modelica. The Inada model was the first detailed electrophysiological model of the atrioventricular node. It consists of 10 ion channels (background channel I_b, L-type calcium channel I_Ca,L, rapid delayed rectifier channel I_K,r, inward rectifier channel I_K,1, sodium channel I_Na, transient outward channel I_to, hyperpolarization-activated channel I_f, sustained outward channel I_st), two ion pumps (sodium calcium exchanger I_NaCa, sodium potassium pump I_p/I_NaK), and four compartments containing variable Ca2+ concentrations (cytoplasm [Ca 2+ ]_i, junctional sarcoplasmic reticulum [Ca2+]_jsr, network sarcoplasmic reticulum [Ca2+]_nsr, “fuzzy” subspace [Ca ]_sub - which is the “functionally restricted intracellular space accessible to the Na + /Ca 2+ exchanger as well as to the L-type Ca 2+ channel and the Ca 2+ -gated Ca 2+ channel in the SR”). A current version of this model can be found at https://github.com/CSchoel/inamo .

2021-07-22 | MODEL2102090002 | BioModels

Transcription Factor Acj6 Controls Dendrite Targeting via Combinatorial Cell-Surface Codes

Project description:Transcription factors specify the fate and connectivity of developing neurons. We investigate how a lineage-specific transcription factor, Acj6, controls the precise dendrite targeting of Drosophila olfactory projection neurons (PNs) by regulating the expression of cell-surface proteins. Quantitative cell-surface proteomic profiling of wild-type and acj6 mutant PNs in intact developing brains and a proteome-informed genetic screen identified PN surface proteins that execute Acj6-regulated wiring decisions. These include canonical cell adhesion molecules and proteins previously not associated with wiring, such as Piezo, whose mechanosensitive ion channel activity is dispensable for its function in PN dendrite targeting. Comprehensive genetic analyses revealed that Acj6 employs unique sets of cell-surface proteins in different PN types for dendrite targeting. Combinatorial expression of Acj6 wiring executors rescued acj6 mutant phenotypes with higher efficacy and breadth than expression of individual executors. Thus, Acj6 controls wiring specificity of different neuron types by specifying distinct combinatorial expression of cell-surface executors.

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Developmental gene expression differences between neonatal and adult mouse atria and ventricles

Project description:We study the role of glycosylation in ion channel function. Specfically, we are focusing on how ion channel glycosylation modulates, controls, and impacts cardiac, skeletal muscle, and neuronal electrical activity. We wish to determine differences in gene expression through development and between the atria and ventricles of the mouse heart. Our data indicate differential sialylation directly affects voltage-gated sodium channel function through the developing heart in a chamber-specific manner. We wish to expand our findings to include other ion channels involved in the cardiac action potential, and to eventually create a map of the cardiac conduction system that details the role of differential glycosylation in cardiac excitability. Determining differential expression of the genes that regulate ion channel glycosylation is vital to these goals.

2011-03-02 | GSE27589 | GEO

Establishing and improving retroviral episome transfer of transcription factors to achieve cell fate conversion and reprogramming

Project description:Gene transfer of distinct cocktails of transcription factors enables the targeted modification of cell fate. Reprogramming somatic cells to induced pluripotent stem cells (iPSCs) via ectopic expression of the transcription factors Oct4, Sox2, Klf4 and c-Myc allows creation of pluripotent cells with the potential to differentiate into any cell type of the body. To achieve a high degree of biosafety for future application of converted cells, technologies are required to express the required transcription factors without affecting the target cell genome. Retroviral vectors are widely employed gene transfer vehicles and can be converted into transient gene delivery vehicles by mutation of the viral integrase, thus avoiding risks associated with retroviral integration. We improved the retroviral episome transfer system by identifying the most suitable vector architecture, by enhancing episomal expression and by tuning the activity of the transcription factor Oct4. Repeated episomal transductions allowed establishment of stable, fully reversible expression levels over time. Providing proof-of-principle in the reprogramming context, we were able to generate human iPSCs following retroviral episomal transfer of Oct4 in fibroblasts stably expressing Klf4, Sox2 and c-Myc, with a high percentage of clones not carrying residually integrated vector copies. RNA obtained from human embryonic stem cells, fibroblasts and induced pluripotent stem cell lines reprogrammed with the mentioned reprogramming protocol

2015-05-06 | E-GEOD-57378 | biostudies-arrayexpress

Wnt signaling regulates ion channel expression to promote smooth muscle and cartilage formation in developing mouse trachea

Project description:Ion channels play critical roles in the physiology and function of the nervous system and contractile tissue; however, their role in non-contractile tissue and embryonic development has yet to be understood. Tracheobronchomalacia (TBM) and complete tracheal rings (CTR) are disorders affecting the muscle and cartilage of the trachea and bronchi, whose etiology remains poorly understood. We demonstrated that trachealis muscle organization and polarity are disrupted after epithelial ablation of Wls, a cargo receptor critical for the Wnt signaling pathway, in developing trachea. The phenotype resembles the anomalous trachealis muscle observed after deletion of ion channel encoding genes in developing mouse trachea. We sought to investigate whether and how the deletion ofWlsaffects ion channels during tracheal development. We hypothesize that Wnt signaling influences the expression of ion channels to promote trachealis muscle cell assembly and patterning. Deleting Wls in developing trachea causes differential regulation of genes mediating actin binding, cytoskeleton organization, and potassium ion channel activity. Wnt signaling regulated expression of Kcnj13, Kcnd3, Kcnj8, and Abcc9 as demonstrated by in vitro studies and in vivo analysis in Wnt5a and b-catenin deficient tracheas. Pharmacological inhibition of potassium ion channels and Wnt signaling impaired contractility of developing trachealis smooth muscle and formation of cartilaginous mesenchymal condensation. Thus, in mice, epithelial-induced Wnt/b-catenin signaling mediates trachealis muscle and cartilage development via modulation of ion channel expression, promoting trachealis muscle architecture, contractility, and cartilaginous extracellular matrix. In turn, ion channel activity may influence tracheal morphogenesis underlying TBM and CTR.

2023-11-06 | GSE241175 | GEO

EAG2 potassium channel with evolutionarily conserved function as a brain tumor target

Project description:Characterizing the impact of pharmacological and shRNA-mediated silencing of EAG2 in medulloblastoma. Medulloblastoma (MB) is the most common pediatric CNS malignancy. Previously, we demonstrated that overexpression of the ion channel EAG2, identified in a subset of histological and molecular subtypes of this disease, functionally contributes to tumor progression (PMID: 22855790). Here, we demonstrate the evolutionarily conserved function of EAG2 potassium channel in promoting brain tumor growth and metastasis, delineate downstream pathways and uncover a co-option mechanism for different potassium channels to regulate mitotic cell volume and tumor progression. We show that EAG2 potassium channel is enriched at the trailing edge of migrating MB cells to regulate local cell volume dynamics, thereby facilitating cell motility. We identify the FDA- approved antipsychotic drug thioridazine as an EAG2 channel blocker that reduces xenografted MB growth and metastasis, and present a case report of repurposing thioridazine for treating a human patient. Our findings thus illustrate the potential of targeting ion channels in cancer treatment.

2015-07-08 | GSE70576 | GEO

Transgenic NUP98-HOXA9 Zebrafish Embryos: Unactivated ('lGl') vs. Cre-activated ('NHA9')

Project description:Transcriptional profiling of zebrafish embryos at 28 hours post fertilization, comparing control 'unactivated' Tg(spi1::lox-eGFP-lox::NHA9) embryos with experimental 'Cre-activated' Tg(spi1::NHA9) embryos. Goal was to determine the effects of expressing NUP98-HOXA9 oncogene on global and blood cell-specific gene expression in early zebrafish development.

2014-10-30 | GSE62793 | GEO

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