Sodium channel protein type 11 subunit alpha, also known as SCN11A or Nav1.9 is a voltage-gated sodium ion channel protein which is encoded by the SCN11A gene on chromosome 3 in humans. SCN11A encodes a 1765 amino acids protein that shows the least degree of homology to other members of the neuronal VGSC family. The protein consists of 4 domains joined by 3 intracellular loops; each domain consists of 6 transmembrane segments and intracellular and extracellular junctions. The 4th transmembrane segment of each domain is the voltage-sensing region of the channel. The protein is highly expressed in nociceptive neurons of dorsal root ganglia and trigeminal ganglia and is a major effector of peripheral inflammatory pain hypersensitivity.
|Basic Information of SCN11A|
|Protein Name||Sodium channel protein type 11 subunit alpha|
|Aliases||Peripheral nerve sodium channel 5(PN5), Sensory neuron sodium channel 2, Sodium channel protein type XI subunit alpha, Voltage-gated sodium channel, subunit alpha Nav1.9, hNaN|
|Organism||Homo sapiens (Human)|
The voltage-gated sodium channel is a membrane protein complex that plays a fundamental role in the rising phase of the action potential of most excitable cells. Alpha subunits, such as SCN11A, regulate voltage-dependent gating and conductance. However, the auxiliary beta subunit regulates the motion characteristics of the channel and facilitates complex membrane localization. Aberrant alpha subunits expression patterns or mutations of alpha subunits result in several disorders. SCN11A involves nociception, having been linked to the perception of inflammatory, neuropathic and cold-related pain. Moreover, SCN11A regulates resting membrane potentials and prolongs the depolarization response to subthreshold stimuli. Mutant SCN11A channels display excessive activity at resting voltages, causing sustained depolarization of nociceptors, impair generation of action potentials and aberrant synaptic transmission. The diseases include neuropathy, hereditary sensory and autonomic, 7 episodic pain syndrome, familial, 3 (FEPS3), which are caused by mutations affecting the SCN11A gene represented in this entry.
Fig.1 Schematic of a typical VGSC. (Kanellopoulos, 2016)
This article finds that episodic pain disorder may result from gain-of-function mutations in SCN11A.
This article suggests that mutant SCN11A results in continuous depolarization of nociceptors, which may impair action potentials and abnormal synaptic transmission.
This article shows that three patients have marked joint hypermobility found in genetic disorders of connective tissue, indicating a potential role of SCN11A in connective tissues should be investigated.
This article explains the mechanism that mutation S360Y makes NaV1.9 channels sensitive to tetrodotoxin and saxitoxin.
This article suggests that missense mutations of Nav1.9 could be a reason for painful peripheral neuropathy.
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