Anti-SCN11A Antibody Picoband® Fluoro550 Conjugated

Sodium channel, voltage-gated, type XI, alpha subunit 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. Voltage-gated sodium channels are transmembrane glycoprotein complexes composed of a large alpha subunit with 24 transmembrane domains and one or more regulatory beta subunits. They are responsible for the generation and propagation of action potentials in neurons and muscle. This gene encodes one member of the sodium channel alpha subunit gene family, and is highly expressed in nociceptive neurons of dorsal root ganglia and trigeminal ganglia. It mediates brain-derived neurotrophic factor-evoked membrane depolarization and is a major effector of peripheral inflammatory pain hypersensitivity. Mutations in this gene have been associated with hereditary sensory and autonomic neuropathy type VII and familial episodic pain syndrome-3. Alternative splicing results in multiple transcript variants.

Sodium channel protein type 11 subunit alpha; 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; SCN11A; SCN12A, SNS2

A synthetic peptide corresponding to a sequence at the N-terminus of human SCN11A, which shares 87.2% and 89.7% amino acid (aa) sequence identity with mouse and rat SCN11A, respectively.

Expressed in the dorsal root ganglia and trigeminal ganglia, olfactory bulb, hippocampus, cerebellar cortex, spinal cord, spleen, small intestine and placenta.

This protein mediates the voltage-dependent sodium ion permeability of excitable membranes. Assuming opened or closed conformations in response to the voltage difference across the membrane, the protein forms a sodium-selective channel through which sodium ions may pass in accordance with their electrochemical gradient. It is a tetrodotoxin-resistant sodium channel isoform. Also involved, with the contribution of the receptor tyrosine kinase NTRK2, in rapid BDNF-evoked neuronal depolarization.

1. Dib-Hajj S, Black JA, Cummins TR, Waxman SG (May 2002) . NaN/Nav1.9: a sodium channel with unique properties. Trends in Neurosciences. 25 (5) : 253–9. 2. Dib-Hajj SD, Tyrrell L, Waxman SG (2002) . Structure of the sodium channel gene SCN11A: evidence for intron-to-exon conversion model and implications for gene evolution. Molecular Neurobiology. 26 (2–3) : 235–50. 3. Dib-Hajj SD, Black JA, Waxman SG (September 2015) . NaV1.9: a sodium channel linked to human pain. Nature Reviews. Neuroscience. 16 (9) : 511–9.