TRPM8 and Nav1.8 sodium channels are required for transthyretin-induced calcium influx in growth cones of small-diameter TrkA-positive sensory neurons (Q34677515)

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English	TRPM8 and Nav1.8 sodium channels are required for transthyretin-induced calcium influx in growth cones of small-diameter TrkA-positive sensory neurons	scientific article

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scholarly article

1 reference

Europe PubMed Central

3 August 2017

TRPM8 and Nav1.8 sodium channels are required for transthyretin-induced calcium influx in growth cones of small-diameter TrkA-positive sensory neurons (English)

1 reference

Europe PubMed Central

3 August 2017

1

object named as

Robert J Gasperini

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Europe PubMed Central

3 August 2017

object named as

Lisa C Foa

7

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author name string

Xu Hou

2

1 reference

Europe PubMed Central

3 August 2017

Helena Parkington

3

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Europe PubMed Central

3 August 2017

Harry Coleman

4

1 reference

Europe PubMed Central

3 August 2017

David W Klaver

5

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Europe PubMed Central

3 August 2017

Adele J Vincent

6

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Europe PubMed Central

3 August 2017

David H Small

8

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Europe PubMed Central

3 August 2017

publication date

4 March 2011

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Europe PubMed Central

3 August 2017

Molecular Neurodegeneration

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Europe PubMed Central

3 August 2017

6

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Europe PubMed Central

3 August 2017

1

1 reference

Europe PubMed Central

3 August 2017

19

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Europe PubMed Central

3 August 2017

describes a project that uses

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Europe PubMed Central

11 June 2022

https://www.ebi.ac.uk/europepmc/webservices/rest/PMC3058062/fullTextXML

based on heuristic

inferred from PubMed Central ID database lookup

https://scigraph.springernature.com/pub.10.1186/1750-1326-6-19

0 references

Neurotrophin receptors TrkA and TrkC cause neuronal death whereas TrkB does not

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Caspase activation precedes and leads to tangles

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Homer regulates calcium signalling in growth cone turning.

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Role of neurotrophin signalling in the differentiation of neurons from dorsal root ganglia and sympathetic ganglia

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Phosphoinositide regulation of non-canonical transient receptor potential channels

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Lipid raft segregation modulates TRPM8 channel activity

1 reference

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The role of GDNF family ligand signalling in the differentiation of sympathetic and dorsal root ganglion neurons

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Quantification of the thermodynamically linked quaternary and tertiary structural stabilities of transthyretin and its disease-associated variants: the relationship between stability and amyloidosis.

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Sensory neuron sodium channel Nav1.8 is essential for pain at low temperatures

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Transient receptor potential channels in Alzheimer's disease.

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Attenuated cold sensitivity in TRPM8 null mice

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Transthyretin and familial amyloidotic polyneuropathy. Recent progress in understanding the molecular mechanism of neurodegeneration

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Bidirectional shifts of TRPM8 channel gating by temperature and chemical agents modulate the cold sensitivity of mammalian thermoreceptors.

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Transthyretin oligomers induce calcium influx via voltage-gated calcium channels.

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Carbamazepine interacts with a slow inactivation state of NaV1.8-like sodium channels

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In vitro inhibition of transthyretin aggregate-induced cytotoxicity by full and peptide derived forms of the soluble receptor for advanced glycation end products (RAGE)

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Comparison of the effects of four Na+ channel analgesics on TTX-resistant Na+ currents in rat sensory neurons and recombinant Nav1.2 channels

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Binding of amyloidogenic transthyretin to the plasma membrane alters membrane fluidity and induces neurotoxicity

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Transthyretin-related familial amyloidotic polyneuropathy

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Early painful diabetic neuropathy is associated with differential changes in tetrodotoxin-sensitive and -resistant sodium channels in dorsal root ganglion neurons in the rat.

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Prevention of transthyretin amyloid disease by changing protein misfolding energetics.

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Inherent toxicity of aggregates implies a common mechanism for protein misfolding diseases

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Identification of a cold receptor reveals a general role for TRP channels in thermosensation

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Deposition of transthyretin in early stages of familial amyloidotic polyneuropathy: evidence for toxicity of nonfibrillar aggregates

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The most pathogenic transthyretin variant, L55P, forms amyloid fibrils under acidic conditions and protofilaments under physiological conditions

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Family studies of the genetic abnormality in transthyretin (prealbumin) in Portuguese patients with familial amyloidotic polyneuropathy

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inferred from PubMed ID database lookup

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10.1186/1750-1326-6-19

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Europe PubMed Central

3 August 2017

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Europe PubMed Central

3 August 2017

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Europe PubMed Central

3 August 2017

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