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AB196806

Anti-Nav1.7 抗体

Anti-Nav1.7 antibody

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(1 Publication)

Rabbit Polyclonal SCN9A antibody. Suitable for WB, IHC-P and reacts with Mouse, Human samples. Cited in 1 publication. Immunogen corresponding to Synthetic Peptide within Human SCN9A.

別名を表示する

NENA, SCN9A, Sodium channel protein type 9 subunit alpha, Neuroendocrine sodium channel, Peripheral sodium channel 1, Sodium channel protein type IX subunit alpha, Voltage-gated sodium channel subunit alpha Nav1.7, hNE-Na, PN1

2 Images
Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-Nav1.7 antibody (AB196806)
  • IHC-P

Supplier Data

Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-Nav1.7 antibody (AB196806)

Immunohistochemical analysis of paraffin-embedded Human lung carcinoma tissue, labeling Nav1.7 with ab196806 at 1/50 dilution. The image on the right is treated with synthesized peptide.

Western blot - Anti-Nav1.7 antibody (AB196806)
  • WB

Supplier Data

Western blot - Anti-Nav1.7 antibody (AB196806)

All lanes:

Western blot - Anti-Nav1.7 antibody (ab196806) at 1/500 dilution

Lane 1:

RAW cell extract

Lane 2:

RAW cell extract with synthesized peptide

Predicted band size: 226 kDa

false

Key facts

宿主種

Rabbit

クローン性

Polyclonal

アイソタイプ

IgG

キャリアフリー

No

交差種

Mouse, Human

アプリケーション

WB, IHC-P

applications

免疫原

Synthetic Peptide within Human SCN9A. The exact immunogen used to generate this antibody is proprietary information.

Q15858

Reactivity data

{ "title": "Reactivity Data", "filters": { "stats": ["", "Species", "Dilution Info", "Notes"], "tabs": { "all-applications": {"fullname" : "All Applications", "shortname": "All Applications"}, "WB" : {"fullname" : "Western blot", "shortname":"WB"}, "IHCP" : {"fullname" : "Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections)", "shortname":"IHC-P"} }, "product-promise": { "all": "all", "testedAndGuaranteed": "tested", "guaranteed": "expected", "predicted": "predicted", "notRecommended": "not-recommended" } }, "values": { "Human": { "WB-species-checked": "guaranteed", "WB-species-dilution-info": "", "WB-species-notes": "", "IHCP-species-checked": "testedAndGuaranteed", "IHCP-species-dilution-info": "1/50 - 1/100", "IHCP-species-notes": "<p></p>" }, "Mouse": { "WB-species-checked": "testedAndGuaranteed", "WB-species-dilution-info": "1/500 - 1/3000", "WB-species-notes": "<p></p>", "IHCP-species-checked": "guaranteed", "IHCP-species-dilution-info": "", "IHCP-species-notes": "" } } }

出荷温度及び保存条件

製品の状態
Liquid
精製方法
Affinity purification Immunogen
バッファー組成
pH: 7.4 Preservative: 0.02% Sodium azide Constituents: PBS, 50% Glycerol (glycerin, glycerine), 0.87% Sodium chloride
出荷温度
Blue Ice
短期保存期間
1-2 weeks
短期保存温度
+4°C
長期保存温度
-20°C
分注に関する情報
Upon delivery aliquot
保管に関する情報
Avoid freeze / thaw cycle

補足情報

This supplementary information is collated from multiple sources and compiled automatically.

Nav1.7 also known as SCN9A is a voltage-gated sodium channel. This protein has a mass of approximately 260 kDa. It plays a role in the generation and conduction of action potentials in neurons. Nav1.7 is found mainly in peripheral neurons including dorsal root ganglia and sympathetic ganglia. These neurons are part of the sensory pathways responsible for transmitting pain signals.
Biological function summary

Nav1.7 acts as an essential component in neuronal excitability. It is not part of a larger protein complex but operates as an individual unit within the cell membrane. By allowing sodium ions to enter the neuron Nav1.7 contributes to the depolarization phase of action potentials. This function is critical in the propagation of electrical signals in the nervous system specifically in nociceptive neurons that are involved in pain sensation.

Pathways

Nav1.7 is integral to the nociceptive pain pathway. It works with other sodium channels such as Nav1.8 which also play roles in pain sensation. Nav1.7's activity helps to initiate and maintain action potentials facilitating the transmission of pain signals to the central nervous system. Additionally Nav1.7 is linked to neuropathic pain pathways where its function underpins the continuous firing of neurons even in the absence of external stimuli.

Nav1.7 mutations have a significant association with primary erythromelalgia and congenital indifference to pain. Mutations that cause gain-of-function in Nav1.7 can lead to primary erythromelalgia resulting in extreme pain and redness in the body’s extremities. Conversely loss-of-function mutations can cause congenital indifference to pain where individuals experience little to no pain sensation. Nav1.7 works alongside Nav1.8 in these conditions as both are involved in the modulation of pain signals.

製品プロトコール

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ターゲットの情報

Pore-forming subunit of Nav1.7, a voltage-gated sodium (Nav) channel that directly mediates the depolarizing phase of action potentials in excitable membranes. Navs, also called VGSCs (voltage-gated sodium channels) or VDSCs (voltage-dependent sodium channels), operate by switching between closed and open conformations depending on the voltage difference across the membrane. In the open conformation they allow Na(+) ions to selectively pass through the pore, along their electrochemical gradient. The influx of Na(+) ions provokes membrane depolarization, initiating the propagation of electrical signals throughout cells and tissues (PubMed : 15385606, PubMed : 16988069, PubMed : 17145499, PubMed : 17167479, PubMed : 19369487, PubMed : 24311784, PubMed : 25240195, PubMed : 26680203, PubMed : 7720699). Nav1.7 plays a crucial role in controlling the excitability and action potential propagation from nociceptor neurons, thereby contributing to the sensory perception of pain (PubMed : 17145499, PubMed : 17167479, PubMed : 19369487, PubMed : 24311784).
See full target information SCN9A

文献 (1)

Recent publications for all applications. Explore the full list and refine your search

Oncogene 42:911-925 PubMed36725888

2023

METTL3 regulates breast cancer-associated alternative splicing switches.

Applications

Unspecified application

Species

Unspecified reactive species

Cyrinne Achour,Devi Prasad Bhattarai,Paula Groza,Ángel-Carlos Román,Francesca Aguilo
View all publications

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