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TranscriptomicsThe molecular basis of analgesia in congenital insensitivity to pain associated with loss of Nav1.7 function
Loss of function mutations in the SCN9a gene encoding voltage-gated sodium channel Nav1.7 cause congenital insensitivity to pain (CIP) and anosmia in otherwise normal humans and mice, suggesting that this channel may be a good analgesic drug target. Surprisingly, potent selective antagonists of ...
ORGANISM(S): Mus musculus 
2014-09-13 | E-GEOD-61373 | biostudies-arrayexpress
ProteomicsMapping protein interactions of sodium channel NaV1.7 using epitope-tagged gene targeted mice
The voltage-gated sodium channel NaV1.7 plays a critical role in pain pathways. As well as action potential propagation, NaV1.7 regulates neurotransmitter release, integrates depolarizing inputs over long periods and regulates transcription. In order to better understand these functions, we generate...
ORGANISM(S): Mus musculus (Mouse) 
2018-01-15 | PXD005155 | Pride
Pain Epitope-tagged nav1.7 mouse Mice The voltage-gated sodium channel nav1.7 Nav1.7 complexes affinity-purification Lc-ms/ms 
GenomicsBulk RNAseq analysis of dorsal root ganglia from global Nav1.7 knockout mice
Bulk RNAseq analysis of dorsal root ganglia from global Nav1.7 knockout mice
PRJNA882499 | ENA
GenomicsLong-lasting Analgesia via Targeted in situ Repression of NaV1.7
Long-lasting Analgesia via Targeted in situ Repression of NaV1.7
PRJNA670519 | ENA
TranscriptomicsBulk RNAseq analysis of dorsal root ganglia from global Nav1.7 knockout mice
We investigated changes in gene expression of dorsal root ganglia (DRG) isolated from global (pCAGG-CreER x Nav1.7 floxed) Nav1.7 knockout mice using bulk RNA sequencing. We found an upregulation of Penk and downregulation of Ceacam10 in Nav1.7 knockouts compared to controls, as well as other gene e...
ORGANISM(S): Mus musculus 
2023-05-22 | GSE213826 | GEO
Proteomicsrotein expression in Nav1.7 embryonic null mice – mechanisms of compensation
Mice and humans who have lost the expression of functional sodium channel Nav1.7 are pain-free, but otherwise normal. This is the result of a loss of neurotransmitter release such as glutamate and Substance P from primary sensory neurons. The sensory neurons are otherwise normal apart from loss of n...
ORGANISM(S): Mus musculus (Mouse) 
2024-10-17 | PXD052513 | Pride
Two mechanisms of analgesia Drugs Pain Humans Autonomic side-effects Embryonic and adult nulls Sodium channels Mice Nav1.7 Opioid signalling 
GenomicsSingle cell RNAseq analysis of dorsal root ganglia from global and cLTMR-specific Nav1.7 knockout mice
Single cell RNAseq analysis of dorsal root ganglia from global and cLTMR-specific Nav1.7 knockout mice
PRJNA882495 | ENA
ProteomicsDevelopment of Photocrosslinking Probes Based on Huwentoxin-IV to Map the Site of Interaction on Nav1.7
This study reports on the design of a library of photoprobes based on the potent spider toxin Huwentoxin-IV and the determination of the toxin binding interface on VSD2 of Nav1.7 through a photocrosslinking and tandem mass spectrometry approach. Our Huwentoxin-IV probes selectively crosslink to extr...
ORGANISM(S): Homo sapiens (Human) 
2019-11-18 | PXD015037 | Pride
Nav1.7 Photoaffinity labelling Huwentoxin-iv Diazirine Peptide mapping 
TranscriptomicsThe molecular basis of analgesia in congenital insensitivity to pain associated with loss of Nav1.7 function
Loss of function mutations in the SCN9a gene encoding voltage-gated sodium channel Nav1.7 cause congenital insensitivity to pain (CIP) and anosmia in otherwise normal humans and mice, suggesting that this channel may be a good analgesic drug target. Surprisingly, potent selective antagonists of Nav1...
ORGANISM(S): Mus musculus 
2014-09-13 | GSE61373 | GEO
ProteomicsMice brain tissue IP experiment
This is a experment want to fish out the proteins in the mice brain can interact with sodium chanel protein Nav1.7, immuno precipatation and lab free mass spectrmetry were used to identify Nav1.7 Interation parter proteins.
ORGANISM(S): Mus musculus (Mouse) 
2018-01-15 | PXD004926 | Pride
Mice brain 
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