Nav1.5 Rabbit anti-Human, Mouse, Polyclonal, Proteintech

Description

• Scn5a is an integral membrane protein and tetrodotoxin-resistant voltage-gated sodium channel subunit
• Scn5a is found primarily in cardiac muscle and is responsible for the initial upstroke of the action potential in an electrocardiogram
• Defects in Scn5a are a cause of long QT syndrome type 3 (LQT3), an autosomal domit cardiac disease
• Alternative splicing results in several transcript variants encoding different isoforms of Scn5a
• Voltage-gated sodium channesl (VGSCs) mediate regenerative cell membrane depolarization and conduction of electrical signalling in nerves and muscles
• Expression of Scn5a is also detected in lymphocytes, glia, and fibroblasts
• Further, Scn5a mediates the voltage-dependent sodium ion permeability of excitable membranes
• Assuming opened or closed conformations in response to the voltage difference across the membrane, Scn5a forms a sodium-selective channel through which Na(+) ions may pass in accordance with their electrochemical gradient
• Functionally, Scn5a is responsible for the initial upstroke of the action potential and the channel inactivation is regulated by intracellular calcium levels
• Voltage-gated sodium channels (NaV) are responsible for action potential initiation and propagation in excitable cells, including nerve, muscle, and neuroendocrine cell types
• Scn5a are also expressed at low levels in non-excitable cells, where their physiological role is unclear
• Diseases associated with SCN5A include Long Qt Syndrome-3 and Brugada Syndrome 1.