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1.A.1.10.6
Tetrodotoxin-resistant voltage-gated Na+ channel of dorsal ganglion sensory neurons, Nav1.8, plays a crucial role in the occurrence and development of chronic pain (Akopian et al., 1996) and is essential for pain at low temperatures (Zimmermann et al., 2007). Nav1.8 is the sole electrical impulse generator in a nociceptor that transmits information to the central nervous system.  Bark scorpion venom induces pain in many mammals (house mice, rats, humans) by activating Nav1.7 but has no effect on Nav1.8. Grasshopper mice Nav1.8 has amino acid variants that bind bark scorpion toxins and inhibit Na+ currents, blocking action potential propagation and inducing analgesia.  These mice thereby can use scorpions as a food source (Zhu et al. 2013; Rowe et al. 2013). Nav1.8 is involved in bull spermatozoa dynamics including motility, membrane integrity, acrosome integrity, capacitation and mitochondrial transmembrane potential (Chauhan et al. 2017). Selective inhibition of NaV1.8 with VX-548 aleviates acute pain in humans (Jones et al. 2023). N-(((1S,3R,5S)-adamantan-1-yl)methyl)-3-((4-chlorophenyl)sulfonyl)benzenesulfonamide is a novel Nav1.8 inhibitor with an analgesic profile (Song et al. 2024).

Accession Number:Q62968
Protein Name:Sodium channel protein type 10 subunit alpha aka Nav1.8
Length:1956
Molecular Weight:219733.00
Species:Rattus norvegicus (Rat) [10116]
Number of TMSs:20
Location1 / Topology2 / Orientation3: Membrane1 / Multi-pass membrane protein2
Substrate sodium(1+)

Cross database links:

RefSeq: NP_058943.1   
Entrez Gene ID: 29571   
Pfam: PF00520    PF06512   
KEGG: rno:29571   

Gene Ontology

GO:0001518 C:voltage-gated sodium channel complex
GO:0005515 F:protein binding
GO:0005248 F:voltage-gated sodium channel activity
GO:0006814 P:sodium ion transport
GO:0055085 P:transmembrane transport

References (9)

[1] “A tetrodotoxin-resistant voltage-gated sodium channel expressed by sensory neurons.”  Akopian A.N.et.al.   8538791
[2] “Structure and function of a novel voltage-gated, tetrodotoxin-resistant sodium channel specific to sensory neurons.”  Sangameswaran L.et.al.   8626372
[3] “Role of auxiliary beta1-, beta2-, and beta3-subunits and their interaction with Na(v)1.8 voltage-gated sodium channel.”  Vijayaragavan K.et.al.   15178439
[4] “Novel isoforms of the sodium channels Nav1.8 and Nav1.5 are produced by a conserved mechanism in mouse and rat.”  Kerr N.C.H.et.al.   15047701
[5] “Unilateral nerve injury down-regulates mRNA for Na+ channel SCN10A bilaterally in rat dorsal root ganglia.”  Oaklander A.L.et.al.   9450690
[6] “Developmental expression of the TTX-resistant voltage-gated sodium channels Nav1.8 (SNS) and Nav1.9 (SNS2) in primary sensory neurons.”  Benn S.C.et.al.   11487631
[7] “Annexin II light chain regulates sensory neuron-specific sodium channel expression.”  Okuse K.et.al.   12050667
[8] “Sensory neuron proteins interact with the intracellular domains of sodium channel NaV1.8.”  Malik-Hall M.et.al.   12591166
[9] “Redistribution of Na(V)1.8 in uninjured axons enables neuropathic pain.”  Gold M.S.et.al.   12514212

External Searches:

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Predict TMSs (Predict number of transmembrane segments)
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FASTA formatted sequence 
1:	MELPFASVGT TNFRRFTPES LAEIEKQIAA HRAAKKARTK HRGQEDKGEK PRPQLDLKAC 
61:	NQLPKFYGEL PAELVGEPLE DLDPFYSTHR TFMVLNKSRT ISRFSATWAL WLFSPFNLIR 
121:	RTAIKVSVHS WFSIFITITI LVNCVCMTRT DLPEKVEYVF TVIYTFEALI KILARGFCLN 
181:	EFTYLRDPWN WLDFSVITLA YVGAAIDLRG ISGLRTFRVL RALKTVSVIP GLKVIVGALI 
241:	HSVRKLADVT ILTVFCLSVF ALVGLQLFKG NLKNKCIRNG TDPHKADNLS SEMAEYIFIK 
301:	PGTTDPLLCG NGSDAGHCPG GYVCLKTPDN PDFNYTSFDS FAWAFLSLFR LMTQDSWERL 
361:	YQQTLRASGK MYMVFFVLVI FLGSFYLVNL ILAVVTMAYE EQSQATIAEI EAKEKKFQEA 
421:	LEVLQKEQEV LAALGIDTTS LQSHSGSPLA SKNANERRPR VKSRVSEGST DDNRSPQSDP 
481:	YNQRRMSFLG LSSGRRRASH GSVFHFRAPS QDISFPDGIT DDGVFHGDQE SRRGSILLGR 
541:	GAGQTGPLPR SPLPQSPNPG RRHGEEGQLG VPTGELTAGA PEGPALDTTG QKSFLSAGYL 
601:	NEPFRAQRAM SVVSIMTSVI EELEESKLKC PPCLISFAQK YLIWECCPKW RKFKMALFEL 
661:	VTDPFAELTI TLCIVVNTVF MAMEHYPMTD AFDAMLQAGN IVFTVFFTME MAFKIIAFDP 
721:	YYYFQKKWNI FDCVIVTVSL LELSASKKGS LSVLRTFRLL RVFKLAKSWP TLNTLIKIIG 
781:	NSVGALGNLT FILAIIVFIF ALVGKQLLSE DYGCRKDGVS VWNGEKLRWH MCDFFHSFLV 
841:	VFRILCGEWI ENMWVCMEVS QKSICLILFL TVMVLGNLVV LNLFIALLLN SFSADNLTAP 
901:	EDDGEVNNLQ LALARIQVLG HRASRAIASY ISSHCRFRWP KVETQLGMKP PLTSSEAKNH 
961:	IATDAVSAAV GNLTKPALSS PKENHGDFIT DPNVWVSVPI AEGESDLDEL EEDMEQASQS 
1021:	SWQEEDPKGQ QEQLPQVQKC ENHQAARSPA SMMSSEDLAP YLGESWKRKD SPQVPAEGVD 
1081:	DTSSSEGSTV DCPDPEEILR KIPELADDLD EPDDCFTEGC TRRCPCCNVN TSKSPWATGW 
1141:	QVRKTCYRIV EHSWFESFII FMILLSSGAL AFEDNYLEEK PRVKSVLEYT DRVFTFIFVF 
1201:	EMLLKWVAYG FKKYFTNAWC WLDFLIVNIS LTSLIAKILE YSDVASIKAL RTLRALRPLR 
1261:	ALSRFEGMRV VVDALVGAIP SIMNVLLVCL IFWLIFSIMG VNLFAGKFSK CVDTRNNPFS 
1321:	NVNSTMVNNK SECHNQNSTG HFFWVNVKVN FDNVAMGYLA LLQVATFKGW MDIMYAAVDS 
1381:	GEINSQPNWE NNLYMYLYFV VFIIFGGFFT LNLFVGVIID NFNQQKKKLG GQDIFMTEEQ 
1441:	KKYYNAMKKL GSKKPQKPIP RPLNKYQGFV FDIVTRQAFD IIIMVLICLN MITMMVETDE 
1501:	QGEEKTKVLG RINQFFVAVF TGECVMKMFA LRQYYFTNGW NVFDFIVVIL SIGSLLFSAI 
1561:	LKSLENYFSP TLFRVIRLAR IGRILRLIRA AKGIRTLLFA LMMSLPALFN IGLLLFLVMF 
1621:	IYSIFGMASF ANVVDEAGID DMFNFKTFGN SMLCLFQITT SAGWDGLLSP ILNTGPPYCD 
1681:	PNLPNSNGSR GNCGSPAVGI IFFTTYIIIS FLIVVNMYIA VILENFNVAT EESTEPLSED 
1741:	DFDMFYETWE KFDPEATQFI AFSALSDFAD TLSGPLRIPK PNQNILIQMD LPLVPGDKIH 
1801:	CLDILFAFTK NVLGESGELD SLKTNMEEKF MATNLSKASY EPIATTLRWK QEDLSATVIQ 
1861:	KAYRSYMLHR SLTLSNTLHV PRAEEDGVSL PGEGYVTFMA NSGLPDKSET ASATSFPPSY 
1921:	DSVTRGLSDR ANINPSSSMQ NEDEVAAKEG NSPGPQ