Cargando…

Contributions of Na(V)1.8 and Na(V)1.9 to excitability in human induced pluripotent stem-cell derived somatosensory neurons

The inhibition of voltage-gated sodium (Na(V)) channels in somatosensory neurons presents a promising novel modality for the treatment of pain. However, the precise contribution of these channels to neuronal excitability, the cellular correlate of pain, is unknown; previous studies using genetic kno...

Descripción completa

Detalles Bibliográficos
Autores principales:	Alsaloum, Matthew, Labau, Julie I. R., Liu, Shujun, Estacion, Mark, Zhao, Peng, Dib-Hajj, Fadia, Waxman, Stephen G.
Formato:	Online Artículo Texto
Lenguaje:	English
Publicado:	Nature Publishing Group UK 2021
Materias:	Article
Acceso en línea:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8688473/ https://www.ncbi.nlm.nih.gov/pubmed/34930944 http://dx.doi.org/10.1038/s41598-021-03608-x

Ejemplares similares

Lacosamide Inhibition of Na(V)1.7 Channels Depends on its Interaction With the Voltage Sensor Domain and the Channel Pore
por: Labau, Julie I. R., et al.
Publicado: (2021)

Effects of ranolazine on wild-type and mutant hNa(v)1.7 channels and on DRG neuron excitability
por: Estacion, Mark, et al.
Publicado: (2010)

Paclitaxel increases axonal localization and vesicular trafficking of Na(v)1.7
por: Akin, Elizabeth J, et al.
Publicado: (2021)

Paclitaxel effects on axonal localization and vesicular trafficking of Na(V)1.8
por: Baker, Christopher A., et al.
Publicado: (2023)

Atypical changes in DRG neuron excitability and complex pain phenotype associated with a Na(v)1.7 mutation that massively hyperpolarizes activation
por: Huang, Jianying, et al.
Publicado: (2018)

The fates of internalized Na(V)1.7 channels in sensory neurons: Retrograde cotransport with other ion channels, axon-specific recycling, and degradation
por: Higerd-Rusli, Grant P., et al.
Publicado: (2022)

Conserved but not critical: Trafficking and function of Na(V)1.7 are independent of highly conserved polybasic motifs
por: Tyagi, Sidharth, et al.
Publicado: (2023)

Building sensory axons: Delivery and distribution of Na(V)1.7 channels and effects of inflammatory mediators
por: Akin, Elizabeth J., et al.
Publicado: (2019)

Conditional knockout of Na(V)1.6 in adult mice ameliorates neuropathic pain
por: Chen, Lubin, et al.
Publicado: (2018)

A novel gain-of-function Na(v)1.7 mutation in a carbamazepine-responsive patient with adult-onset painful peripheral neuropathy
por: Adi, Talia, et al.
Publicado: (2018)

Paroxysmal extreme pain disorder M1627K mutation in human Na(v)1.7 renders DRG neurons hyperexcitable
por: Dib-Hajj, Sulayman D, et al.
Publicado: (2008)

Differential effect of lacosamide on Na(v)1.7 variants from responsive and non-responsive patients with small fibre neuropathy
por: Labau, Julie I R, et al.
Publicado: (2020)

Kv7-specific activators hyperpolarize resting membrane potential and modulate human iPSC-derived sensory neuron excitability
por: Estacion, Mark, et al.
Publicado: (2023)

Preferential Targeting of Na(v)1.6 Voltage-Gated Na(+) Channels to the Axon Initial Segment during Development
por: Akin, Elizabeth J., et al.
Publicado: (2015)

Na(v)1.7 is the predominant sodium channel in rodent olfactory sensory neurons
por: Ahn, Hye-Sook, et al.
Publicado: (2011)

Intra- and interfamily phenotypic diversity in pain syndromes associated with a gain-of-function variant of Na(V)1.7
por: Estacion, Mark, et al.
Publicado: (2011)

Mutation I136V alters electrophysiological properties of the Na(V)1.7 channel in a family with onset of erythromelalgia in the second decade
por: Cheng, Xiaoyang, et al.
Publicado: (2008)

Cold sensing by Na(V)1.8-positive and Na(V)1.8-negative sensory neurons
por: Luiz, A. P., et al.
Publicado: (2019)

KCNQ variants and pain modulation: a missense variant in Kv7.3 contributes to pain resilience
por: Yuan, Jun-Hui, et al.
Publicado: (2021)

Differential roles of Na(V)1.2 and Na(V)1.6 in regulating neuronal excitability at febrile temperature and distinct contributions to febrile seizures
por: Ye, Mingyu, et al.
Publicado: (2018)

Sensory neuron–derived Na(V)1.7 contributes to dorsal horn neuron excitability
por: Alles, Sascha R. A., et al.
Publicado: (2020)

Na(v)1.7 and Na(v)1.8: Role in the pathophysiology of pain
por: Hameed, Shaila
Publicado: (2019)

The trafficking of Na(V)1.8
por: Swanwick, Richard S., et al.
Publicado: (2010)

Complementary roles of murine Na(V)1.7, Na(V)1.8 and Na(V)1.9 in acute itch signalling
por: Kühn, Helen, et al.
Publicado: (2020)

Mutations at opposite ends of the DIII/S4-S5 linker of sodium channel Na(V)1.7 produce distinct pain disorders
por: Cheng, Xiaoyang, et al.
Publicado: (2010)

Rat Na(V)1.7 loss-of-function genetic model: Deficient nociceptive and neuropathic pain behavior with retained olfactory function and intra-epidermal nerve fibers
por: Grubinska, B, et al.
Publicado: (2019)

A Novel Gain-of-Function Nav1.9 Mutation in a Child With Episodic Pain
por: Huang, Jianying, et al.
Publicado: (2019)

Inactivation properties of sodium channel Na(v)1.8 maintain action potential amplitude in small DRG neurons in the context of depolarization
por: Patrick Harty, T, et al.
Publicado: (2007)

Network topology of NaV1.7 mutations in sodium channel-related painful disorders
por: Kapetis, Dimos, et al.
Publicado: (2017)

Neuropathic pain develops normally in mice lacking both Na(v)1.7 and Na(v)1.8
por: Nassar, Mohammed A, et al.
Publicado: (2005)

Acidosis Differentially Modulates Inactivation in Na(V)1.2, Na(V)1.4, and Na(V)1.5 Channels
por: Vilin, Yury Y., et al.
Publicado: (2012)

Protein arginine methyltransferase 7 modulates neuronal excitability by interacting with Na(V)1.9
por: Ma, Tingbin, et al.
Publicado: (2022)

Heat-resistant action potentials require TTX-resistant sodium channels Na(V)1.8 and Na(V)1.9
por: Touska, Filip, et al.
Publicado: (2018)

Loss-of-function mutations of SCN10A encoding Na(V)1.8 α subunit of voltage-gated sodium channel in patients with human kidney stone disease
por: Nettuwakul, Choochai, et al.
Publicado: (2018)

Increased peripheral nerve excitability and local NaV1.8 mRNA up-regulation in painful neuropathy
por: Thakor, Devang Kashyap, et al.
Publicado: (2009)

Na(v) 1.7 gain-of-function mutation I228M triggers age-dependent nociceptive insensitivity and C-LTMR dysregulation
por: Wimalasena, Nivanthika K., et al.
Publicado: (2023)

Structural basis of cytoplasmic Na(V)1.5 and Na(V)1.4 regulation
por: Nathan, Sara, et al.
Publicado: (2020)

Distinctive Properties and Powerful Neuromodulation of Na(v)1.6 Sodium Channels Regulates Neuronal Excitability
por: Zybura, Agnes, et al.
Publicado: (2021)

The Changes in Expression of Na(V)1.7 and Na(V)1.8 and the Effects of the Inhalation of Their Blockers in Healthy and Ovalbumin-Sensitized Guinea Pig Airways
por: Kocmalova, Michaela, et al.
Publicado: (2021)

Na(v)1.8 neurons are involved in limiting acute phase responses to dietary fat
por: Udit, Swalpa, et al.
Publicado: (2017)

Cannot write session to /tmp/vufind_sessions/sess_cm9lk1dqnlop2if3gfdhb8595o