Sodium Voltage-Gated Channel Alpha Subunit 3 (SCN3A): A Promising Drug Target and Biomarker

Target Name: SCN3A

NCBI ID: G6328

SCN3A

Sodium Voltage-Gated Channel Alpha Subunit 3 (SCN3A): A Promising Drug Target and Biomarker

Abstract:
Sodium voltage-gated channel alpha subunit 3 (SCN3A) is a highly expressed gene in the human brain and is involved in the regulation of neuronal excitability. The deregulation of SCN3A has been implicated in various neurological and psychiatric disorders, including epilepsy, schizophrenia, and mood disorders. This article reviews the current understanding of SCN3A, its role in neuronal excitability regulation, and its potential as a drug target and biomarker.

Introduction:
Sodium voltage-gated channel alpha subunit 3 (SCN3A) is a member of the voltage-gated ion channel family, which plays a critical role in the regulation of neuronal excitability. The SCN3A gene is expressed in the brain and is involved in the regulation of neuronal excitability, including the maintenance of action potentials (APs) and the regulation of neurotransmitter release (NMJ release). The deregulation of SCN3A has been implicated in various neurological and psychiatric disorders, including epilepsy, schizophrenia, and mood disorders (2 ). Therefore, targeting SCN3A has the potential to develop new treatments for these disorders.

Current Understanding of SCN3A:
SCN3A is a voltage-gated ion channel that is expressed in the brain and plays a critical role in the regulation of neuronal excitability. The SCN3A channel is composed of four subunits: alpha, beta, gamma, and delta subunits, which are involved in the regulation of Na+ and K+ ions. The alpha subunit is the most abundant and is responsible for the regulation of SCN3A channel function.

SCN3A is involved in the regulation of neuronal excitability by controlling the flow of Na+ and K+ ions into the cell. During the resting state, the SCN3A channel is in an inactivated state, and the alpha subunit is in its open state, allowing Na+ ions to enter the cell. When a neurotransmitter is released, the SCN3A channel is activated, and the alpha subunit is closed, preventing the entry of Na+ ions.

SCN3A has been implicated in various neurological and psychiatric disorders, including epilepsy, schizophrenia, and mood disorders. For example, studies have shown that individuals with theSCN3A gene are more likely to have epilepsy, and that individuals with theSCN3A gene and the risk of developing schizophrenia. Additionally, studies have shown that individuals with the SCN3A gene are more likely to have mood disorders.

Potential as a Drug Target:
The potential of SCN3A as a drug target is due to its involvement in the regulation of neuronal excitability. Drugs that can modulate SCN3A function have the potential to treat various neurological and psychiatric disorders, including epilepsy, schizophrenia, and mood disorders.

One approach to targeting SCN3A is to use small molecules that can modulate the activity of the alpha subunit. For example, inhibitors of Na+ channels, such as amikacin and gabapentin, have been shown to be effective in modulating SCN3A function. Additionally, Modulators of the alpha subunit, such as slope regulators and calcium channel blockers, have also been shown to be effective in modulating SCN3A function.

Another approach to targeting SCN3A is to use antibodies that can specifically bind to the SCN3A channel and modulate its function. For example, studies have shown that antibodies specific for SCN3A can effectively block the regulation of Na+ and K+ ions.

Potential as a Biomarker:
SCN3A is also a potential biomarker for various neurological and psychiatric disorders, including epilepsy, schizophrenia, and mood disorders

Protein Name: Sodium Voltage-gated Channel Alpha Subunit 3

Functions: Mediates the voltage-dependent sodium ion permeability of excitable membranes. Assuming opened or closed conformations in response to the voltage difference across the membrane, forms a sodium-selective channel through which Na(+) ions may pass in accordance with their electrochemical gradient (PubMed:24157691, PubMed:28235671, PubMed:29466837). May contribute to the regulation of serotonin/5-hydroxytryptamine release by enterochromaffin cells (By similarity). In pancreatic endocrine cells, required for both glucagon and glucose-induced insulin secretion (By similarity)

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