about
A de novo gain-of-function mutation in SCN11A causes loss of pain perceptionAge-related gene expression analysis in enteric ganglia of human colon after laser microdissection.Congenital insensitivity to pain: Fracturing without apparent skeletal pathobiology caused by an autosomal dominant, second mutation in SCN11A encoding voltage-gated sodium channel 1.9.Characteristics of colonic migrating motor complexes in neuronal NOS (nNOS) knockout mice.Transduction and encoding sensory information by skin mechanoreceptors.The voltage-gated sodium channel NaV 1.9 in visceral pain.Control of intrinsic pacemaker frequency and velocity of colonic migrating motor complexes in mouse.The phenotype of congenital insensitivity to pain due to the NaV1.9 variant p.L811P.Activation of TREK-1 by morphine results in analgesia without adverse side effects.No pain, more gain.Voltage-gated sodium channels: (NaV )igating the field to determine their contribution to visceral nociception.
P2860
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P2860
description
2013 nî lūn-bûn
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2013年の論文
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2013年論文
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2013年論文
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2013年論文
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2013年論文
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2013年論文
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2013年论文
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name
The Nav1.9 channel regulates colonic motility in mice.
@ast
The Nav1.9 channel regulates colonic motility in mice.
@en
type
label
The Nav1.9 channel regulates colonic motility in mice.
@ast
The Nav1.9 channel regulates colonic motility in mice.
@en
prefLabel
The Nav1.9 channel regulates colonic motility in mice.
@ast
The Nav1.9 channel regulates colonic motility in mice.
@en
P2093
P2860
P356
P1476
The Nav1.9 channel regulates colonic motility in mice.
@en
P2093
Bruno Mazet
Carine Copel
Nadine Clerc
Nancy Osorio
Patrick Delmas
P2860
P356
10.3389/FNINS.2013.00058
P577
2013-04-15T00:00:00Z