Our Anti-Pan-Nav1 sodium channel mouse monoclonal primary antibody from NeuroMab is produced in-house from hybridoma clone N419/40. It detects human, mouse, and rat Pan-Nav1 sodium channel, and is purified by Protein A chromatography. It is great for use in IHC, ICC, WB.
Immunofluorescence staining of adult rat cortex with N419/40 (red), K89/34 (green) and Hoechst nuclear stain (blue).
The family of voltage gated sodium channels comprise a large alpha subunit and auxiliary beta subunits. Nav1 channels are members of the voltage gated sodium ion channel family and form the alpha type, pore-forming subunit of the channel. There are nine known members of this family. These alpha subunits vary in their function and tissue expression.
Synthetic peptide amino acids 1501-1518 (TEEQKKYYNAMKKLGSKK, cytoplasmic loop between repeat III and IV) of human Nav1.1 (accession number P35498)
Human, Mouse, Rat
AB_2491098
Aliquot and store at ≤ -20°C for long term storage. For short term storage, store at 2-8°C. For maximum recovery of product, centrifuge the vial prior to removing the cap.
Liquid
Produced by in vitro bioreactor culture of hybridoma line followed by Protein A affinity chromatography. Purified mAbs are >90% specific antibody.
10 mM Tris, 50 mM Sodium Chloride, 0.065% Sodium Azide pH 7.125
WB: 1:500
IHC: 1:250
ICC: 1:250
Unconjugated
Cross-reacts with multiple Nav1 channels
Each new lot of antibody is quality control tested on cells overexpressing target protein and confirmed to give the expected staining pattern.
These antibodies are to be used as research laboratory reagents and are not for use as diagnostic or therapeutic reagents in humans.
United States
24 months from date of receipt
Shipped on ice packs
Sodium channel protein type 2 subunit alpha (HBSC II) (Sodium channel protein brain II subunit alpha) (Sodium channel protein type II subunit alpha) (Voltage-gated sodium channel subunit alpha Nav1.2) Sodium channel protein type 1 subunit alpha (Sodium channel protein brain I subunit alpha) (Sodium channel protein type I subunit alpha) (Voltage-gated sodium channel subunit alpha Nav1.1) Sodium channel protein type 9 subunit alpha (Neuroendocrine sodium channel) (hNE-Na) (Peripheral sodium channel 1) (PN1) (Sodium channel protein type IX subunit alpha) (Voltage-gated sodium channel subunit alpha Nav1.7) Sodium channel protein type 5 subunit alpha (HH1) (Sodium channel protein cardiac muscle subunit alpha) (Sodium channel protein type V subunit alpha) (Voltage-gated sodium channel subunit alpha Nav1.5) Sodium channel protein type 3 subunit alpha (Sodium channel protein brain III subunit alpha) (Sodium channel protein type III subunit alpha) (Voltage-gated sodium channel subtype III) (Voltage-gated sodium channel subunit alpha Nav1.3) Sodium channel protein type 8 subunit alpha (Sodium channel protein type VIII subunit alpha) (Voltage-gated sodium channel subunit alpha Nav1.6) Sodium channel protein type 10 subunit alpha (Peripheral nerve sodium channel 3) (PN3) (hPN3) (Sodium channel protein type X subunit alpha) (Voltage-gated sodium channel subunit alpha Nav1.8) Sodium channel protein type 4 subunit alpha (SkM1) (Sodium channel protein skeletal muscle subunit alpha) (Sodium channel protein type IV subunit alpha) (Voltage-gated sodium channel subunit alpha Nav1.4) 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)
da Silva, T.F., et al. 2021. Plasmalogens regulate the AKT-ULK1 signaling pathway to control the position of the axon initial segment. Progress in Neurobiology, 102123.
Hefting, L.L., et al. 2020. Multiple Domains in the Kv7.3 C-Terminus Can Regulate Localization to the Axon Initial Segment. Frontiers in Cellular Neuroscience, 10.
Solé, L., et al. 2019. The MAP1B Binding Domain of Nav1.6 Is Required for Stable Expression at the Axon Initial Segment. Journal of Neuroscience, 4238-4251.
Kaneko, K., et al. 2022. Developmentally regulated impairment of parvalbumin interneuron synaptic transmission in an experimental model of Dravet syndrome. Cell reports, 110580.
Alshammari, M.A., et al. 2019. Changes in the Fluorescence Tracking of NaV1.6 Protein Expression in a BTBR T+Itpr3tf/J Autistic Mouse Model. Neural Plasticity, 4893103.
Hosoi, N., et al. 2019. Deletion of Class II ADP-Ribosylation Factors in Mice Causes Tremor by the Nav1.6 Loss in Cerebellar Purkinje Cell Axon Initial Segments. Journal of Neuroscience, 6339-6353.
Alshammari, M.A., et al. 2019. Changes in the Fluorescence Tracking of NaV1.6 Protein Expression in a BTBR T+Itpr3tf/J Autistic Mouse Model. Neural Plasticity, 4893103.
Roberts, A.J., et al. 2019. Increased IL-6 expression in astrocytes is associated with emotionality, alterations in central amygdala GABAergic transmission, and excitability during alcohol withdrawal. . Brain, Behavior, and Immunity., 188-202.
Gong, B., et al. 2016. Developing high-quality mouse monoclonal antibodies for neuroscience research - approaches, perspectives and opportunities. New Biotechnology, 551-564.
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