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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

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			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

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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.

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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.

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

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Project description:Voltage-gated Kv7.2 potassium channels regulate neuronal excitability. The gating of Kv7 channels is regulated by various mediators and neurotransmitters acting via G protein-coupled receptors; the underlying signalling cascades involve phosphatidylinositol-4,5-bisphosphate (PIP2), Ca2+/Calmodulin and phosphorylation. Recent studies have reported that PIP2 sensitivity of Kv7.2 channels is affected by two PTMs, phosphorylation and methylation, harboured in the PIP2 binding domains. Here this project aimed to update phosphorylation and methylation sites on Kv7.2 from heterologous cells, the rat brain and GST-fusion Kv7.2 N- and C-terminal ends proteins.

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