Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Voltage-gated sodium channel (VGSC) beta1 subunit-intracellular domain (Beta1-ICD) overexpression in Chinese hamster lung cells

ABSTRACT: Voltage-gated sodium channel (VGSC) beta1 subunit-intracellular domain (Beta1-ICD) overexpression in Chinese hamster lung cells

PROVIDER: PRJNA564074 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10072401_1.fastq.gz	Fastqsanger.gz
	SRR10072401_2.fastq.gz	Fastqsanger.gz
	SRR10072402_1.fastq.gz	Fastqsanger.gz
	SRR10072402_2.fastq.gz	Fastqsanger.gz
	SRR10072403_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

Regulation of fin regeneration by a voltage-gated sodium channel

Project description:Regulation of fin regeneration by a voltage-gated sodium channel

| PRJNA775662 | ENA

Voltage-gated sodium channel (VGSC) beta1 subunit-intracellular domain (Beta1-ICD) overexpression in Chinese hamster lung cells

Project description:Overexpression of hypothesized transcriptional regulator in a cell line to compare gene expression changes to in vivo knockout of upstream signaling pathway component. All samples are from Chinese hamster lung cells.

2020-02-08 | GSE136927 | GEO

Impact of the Voltage-Gated Calcium Channel Antagonist Nimodipinedipine on the Development of Oligodendrocyte Precursor Cells

Project description:We investigated the effects of nimodipine, a L-type voltage-gated calcium channel antagonist, on the expression profile of myelin genes in the oligodendrocyte precursor cell (OPC) line Oli-Neu. We performed gene expression profiling analysis using data obtained from RNA-seq of four biological replicates for treatment and four replicates for control condition.

2023-03-30 | GSE221939 | GEO

Severe deficiency of voltage-gated sodium channel NaV1.2 elevates neuronal excitability in adult mice

Project description:Scn2a encodes voltage-gated sodium channel NaV1.2, a main mediator of neuronal action potential firing. The current paradigm suggests that NaV1.2 gain-of-function variants enhance neuronal excitability resulting in epilepsy, whereas NaV1.2 deficiency impairs excitability contributing to autism. This paradigm, however, does not explain why 20~30% of patients with NaV1.2 deficiency still develop seizures. Here we report a counterintuitive finding that severe NaV1.2 deficiency results in increased neuronal excitability. Using a unique NaV1.2-deficient mouse model, we found enhanced intrinsic excitabilities of principal neurons in the prefrontal cortex and striatum, brain regions known to be involved in Scn2a-related seizures. This increased excitability is autonomous, and is reversible by the genetic restoration of Scn2a expression in adult mice. RNA-sequencing revealed that the downregulation of multiple potassium channels including KV1.1, and KV channel openers alleviated hyperexcitability of NaV1.2-deficient neurons. This unexpected neuronal hyperexcitability may serve as a cellular basis underlying NaV1.2 deficiency-related seizures.

2021-07-13 | GSE179818 | GEO

Severe deficiency of voltage-gated sodium channel NaV1.2 elevates neuronal excitability in adult mice

Project description:Severe deficiency of voltage-gated sodium channel NaV1.2 elevates neuronal excitability in adult mice

| PRJNA745173 | ENA

Impact of the Voltage-Gated Calcium Channel Antagonist Nimodipinedipine on the Development of Oligodendrocyte Precursor Cells

Project description:Impact of the Voltage-Gated Calcium Channel Antagonist Nimodipinedipine on the Development of Oligodendrocyte Precursor Cells

| PRJNA916927 | ENA

Transcriptional profiling analysis of pre-selected DP thymocytes in response to positive and negative selection signals

Project description:Sustained Ca2+ entry into CD4+CD8+ double-positive thymocytes is required for positive selection. We identified a voltage-gated Na+ channel (VGSC), essential for positive selection of CD4+ T cells. Pharmacological inhibition of VGSC activity inhibited sustained Ca2+ influx induced by positive-selecting ligands and in vitro positive selection of CD4+ but not CD8+ T cells. In vivo shRNA knockdown of Scn5a specifically inhibited positive selection of CD4+ T cells. Ectopic expression of VGSC in peripheral AND CD4+ T cells bestowed the ability to respond to a positively selecting ligand, directly demonstrating VGSC expression was responsible for increased sensitivity. Thus active VGSCs in thymocytes provides a mechanism by which a weak positive selecting signal can induce sustained Ca2+ signals required for CD4+ T cell development.

2012-07-01 | GSE38909 | GEO

Larval application of sodium channel homologous dsRNA restores pyrethroid insecticide susceptibility in a resistant adult mosquito population

Project description:Mosquitoes host and pass on to humans a variety of disease-causing pathogens such as infectious viruses and other parasitic microorganisms. The emergence and spread of insecticide resistance is threatening the effectiveness of current control measures for common mosquito vector borne diseases, such as malaria, dengue and Zika. Therefore, the emerging resistance to the widely used pyrethroid insecticides is an alarming problem for public health. Among the new approaches implemented for pest control, one of the most promising is RNA interference (RNAi). The aim of this study was to provide a feasible RNAi solution that can be applied on wild pyrethroid resistant mosquito populations in the near future. To achieve this, high dsRNA efficacy at economic quantities is required. It is recognized that the sodium channel transcript variability governs its functional diversity including the emergence of insecticide resistance. Therefore, to maximize the RNAi effect, we tiled a number of overlapping dsRNA constructs that together target about half of the voltage-gated sodium channel (VGSC) transcript variants annotated in this work. This strategy provided a refined dsRNA trigger that increased mortality with a three-fold decrease in dsRNA amounts compared to the primary VGSC dsRNA construct. Thus, we demonstrated the use of RNA interference (RNAi) to increase susceptibility of adult mosquitoes to a widely used pyrethroid insecticide. Small RNA sequences from 5 mosquitoes treated with Random or VGSC dsRNAs were generated using Illumina HiSeq 2500.

2016-07-06 | E-GEOD-84030 | biostudies-arrayexpress

Voltage-gated Sodium Channel SCN5A Promotes Tumor Progression and Enhances Chemosensitivity to 5-Fluorouracil in Colorectal Cancer

Project description:Voltage-gated Sodium Channel SCN5A Promotes Tumor Progression and Enhances Chemosensitivity to 5-Fluorouracil in Colorectal Cancer

| PRJNA631241 | ENA

Peptide toxins that target vertebrate voltage-gated sodium channels underly the painful stings of harvester ants

Project description:Harvester ants (genus Pogonomyrmex) are notable for their stings which cause intense, long-lasting pain and other neurotoxic symptoms in vertebrates. Here we show that harvester ant venoms are relatively simple and composed largely of peptide toxins. One class of peptides is primarily responsible for the long-lasting local pain of envenomation. These hydrophobic, cysteine-free peptides activate mammalian sensory neurons via potent modulation of voltage-gated sodium (NaV) channels, reducing voltage threshold for activation and inhibiting channel inactivation. These toxins appear to have evolved specifically as deterrents against vertebrates.

2024-06-16 | PXD043773 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data