J. Cox

发表

A Gain-of-Function Mutation in TRPA1 Causes Familial Episodic Pain Syndrome

G. Bedoya, A. Ruiz-Linares, C. Woods, 2010, Neuron.

Microdeletion in a FAAH pseudogene identified in a patient with high anandamide concentrations and pain insensitivity

David L. Bennett, A. M. Habib, J. Bras, 2019, British journal of anaesthesia.

A role for Piezo2 in EPAC1-dependent mechanical allodynia

J. M. Torres, Y. Ishikawa, A. Dickenson, 2013, Nature Communications.

INPP 5 E mutations cause primary cilium signaling defects , ciliary instability and ciliopathies in human and mouse

S. Schiffmann, C. Woods, S. Schurmans, 2009 .

INPP5E mutations cause primary cilium signaling defects, ciliary instability and ciliopathies in human and mouse

S. Schiffmann, C. Woods, S. Schurmans, 2009, Nature Genetics.

Sodium channels and pain.

A. M. Habib, J. Cox, J. Wood, 2019, Handbook of experimental pharmacology.

No pain, more gain

J. Cox, J. Wood, 2013, Nature Genetics.

Rare NaV1.7 variants associated with painful diabetic peripheral neuropathy

Andreas C. Themistocleous, A. Rice, D. Bennett, 2017, Pain.

Genetic pain loss disorders

David L. Bennett, T. Hornemann, Y. Parman, 2022, Nature Reviews Disease Primers.

The Tarantula Venom Peptide Eo1a Binds to the Domain II S3-S4 Extracellular Loop of Voltage-Gated Sodium Channel NaV1.8 to Enhance Activation

I. Vetter, G. King, S. Robinson, 2022, Frontiers in Pharmacology.

Rare Na V 1.7 variants associated with painful diabetic peripheral neuropathy

Andreas C. Themistocleous, A. Rice, S. Tesfaye, 2018 .

A novel NGF mutation clarifies the molecular mechanism and extends the phenotypic spectrum of the HSAN5 neuropathy

C. Woods, H. Houlden, L. Al-Gazali, 2010, Journal of Medical Genetics.

JMEDGENET81455 1..5

H. Houlden, L. Al-Gazali, J. Cox, 2022 .

Low potency inhibition of NaV1.7 by externally applied QX-314 via a depolarizing shift in the voltage-dependence of activation.

I. Vetter, T. Durek, D. Carter, 2022, European journal of pharmacology.

AmpliTaq Gold DNA Polymerase The Most Referenced Brand of DNA Polymerase in the World Date : 2005-05

J. J. Breen, Minetta C. Liu, M. Madsen, 2005 .

Novel Mutations Mapping to the Fourth Sodium Channel Domain of Nav1.7 Result in Variable Clinical Manifestations of Primary Erythromelalgia

David L. Bennett, R. Cregg, H. Houlden, 2013, NeuroMolecular Medicine.

Molecular basis of FAAH-OUT-associated human pain insensitivity

A. M. Habib, H. Houlden, J. Cox, 2022, bioRxiv.

A new Nav1.7 sodium channel mutation I234T in a child with severe pain

C. Woods, S. Dib-Hajj, S. Waxman, 2010, European journal of pain.

Null mutation in SCN9A in which noxious stimuli can be detected in the absence of pain

S. McMahon, A. M. Habib, D. Bennett, 2014, Neurology.

Mexiletine as a treatment for primary erythromelalgia: normalization of biophysical properties of mutant L858F NaV1.7 sodium channels

R. Cregg, D. Bennett, J. Cox, 2014, British journal of pharmacology.

Mexiletine as a Treatment for Primary Erythromelalgia: Normalization of Biophysical Properties of Mutant L858f Na V 1.7 Sodium Channels Background and Purpose Experimental Approach Conclusion and Implications

R. Cregg, D. Bennett, J. Cox, 2022 .

Congenital Insensitivity to Pain: Novel SCN9A Missense and In-Frame Deletion Mutations

C. Woods, F. Reimann, E. Manor, 2010, Human mutation.

WDR62 is associated with the spindle pole and is mutated in human microcephaly

C. Woods, F. Gergely, S. Lindsay, 2010, Nature Genetics.

Regulation of Nav1.7: A Conserved SCN9A Natural Antisense Transcript Expressed in Dorsal Root Ganglia

J. Zhao, C. Woods, A. M. Habib, 2015, PloS one.

An SCN9A channelopathy causes congenital inability to experience pain

Hussain Jafri, Emma Roberts, Enza Maria Valente, 2006, Nature.

CRISPR interference at the FAAH-OUT genomic region reduces FAAH expression

A. M. Habib, J. Cox, J. Wood, 2019, bioRxiv.

The Genetics of Pain: Implications for Therapeutics.

J. Cox, J. Wood, Jing Zhao, 2018, Annual review of pharmacology and toxicology.

Loss‐of‐function mutations in the Nav1.7 gene underlie congenital indifference to pain in multiple human populations

M. Dubé, D. Bowsher, E. Boltshauser, 2007, Clinical genetics.

Pain perception is altered by a nucleotide polymorphism in SCN9A

Minna Männikkö, Jaro Karppinen, Dmitri V Zaykin, 2010, Proceedings of the National Academy of Sciences.

The mechanism of analgesia in NaV1.7 null mutants

F. Zufall, F. Mancini, G. Iannetti, 2020, bioRxiv.

Endogenous opioids contribute to insensitivity to pain in humans and mice lacking sodium channel Nav1.7

Flavia Mancini, John N. Wood, Vanessa Pereira, 2015, Nature Communications.

Gain-of-function mutations in the mechanically activated ion channel PIEZO2 cause a subtype of Distal Arthrogryposis

Alexander Hoischen, Gunnar Houge, Matthew S. Lebo, 2013, Proceedings of the National Academy of Sciences.

Rare NaV 1 . 7 variants associated with painful diabetic peripheral neuropathy

Andreas C. Themistocleous, A. Rice, S. Tesfaye, 2017 .

Novel SCN9A Mutations Underlying Extreme Pain Phenotypes: Unexpected Electrophysiological and Clinical Phenotype Correlations

C. Woods, A. M. Habib, F. Reimann, 2015, The Journal of Neuroscience.

Sodium channel genes in pain-related disorders: phenotype–genotype associations and recommendations for clinical use

C. Woods, S. Dib-Hajj, S. Waxman, 2014, The Lancet Neurology.

A central mechanism of analgesia in mice and humans lacking the sodium channel NaV1.7

F. Zufall, F. Mancini, G. Iannetti, 2021, Neuron.

Functional analysis of an alternatively spliced estrogen receptor lacking exon 4 isolated from MCF-7 breast cancer cells and meningioma tissue

M. Blankenstein, J. Burbach, J. Thijssen, 1994, Molecular and Cellular Endocrinology.

TRPC3 and TRPC6 are essential for normal mechanotransduction in subsets of sensory neurons and cochlear hair cells

Nerissa K. Kirkwood, J. Ashmore, A. Forge, 2012, Open Biology.

A novel human pain insensitivity disorder caused by a point mutation in ZFHX2

A. Aloisi, Y. Komine, T. Yamamori, 2017, Brain : a journal of neurology.

Sensory neuron–derived NaV1.7 contributes to dorsal horn neuron excitability

M. Beato, R. Luján, J. Cox, 2020, Science Advances.

Sensory neuron-derived Nav1.7 contributes to dorsal horn neuron excitability

M. Beato, R. Luján, Jing Zhao, 2019, bioRxiv.

Mapping protein interactions of sodium channel NaV1.7 using epitope‐tagged gene‐targeted mice

F. Zufall, A. Dolphin, B. Kessler, 2017, bioRxiv.

The essential role of centrosomal NDE1 in human cerebral cortex neurogenesis.

C. Woods, M. Crosier, Tanyeri Barak, 2011, American journal of human genetics.

Distinct transcriptional responses of mouse sensory neurons in models of human chronic pain conditions

J. Cox, J. Wood, F. ter Heegde, 2018, Wellcome open research.

Pain-causing stinging nettle toxins target TMEM233 to modulate NaV1.7 function

Samantha J. Stehbens, S. Dib-Hajj, S. Waxman, 2023, Nature communications.

Transcriptomic profiling reveals a pro-nociceptive role for Angiotensin II in inflammatory bowel disease

T. Raine, J. Cox, J. Wood, 2023, bioRxiv.

Tools for analysis and conditional deletion of subsets of sensory neurons

Federico Iseppon, J. Cox, J. Wood, 2021, Wellcome open research.

Novel Mutations Mapping to the Fourth Sodium Channel Domain of Nav1.7 Result in Variable Clinical Manifestations of Primary Erythromelalgia

R. Cregg, H. Houlden, M. Kinali, 2013, NeuroMolecular Medicine.

TRPC 3 and TRPC 6 are essential for normal mechanotransduction in subsets of sensory neurons and cochlear hair cells

Nerissa K. Kirkwood, J. Ashmore, A. Forge, 2012 .

Pain in Fabry disease: Plasma lipids sensitise nociceptors

J. Cox, A. Habib, 2015, Neuroscience Letters.

Splice Variants of NaV1.7 Sodium Channels Have Distinct β Subunit-Dependent Biophysical Properties

C. Woods, S. Schorge, Emily V. Fletcher, 2012, PloS one.

Peripheral sensory neuropathies – pain loss vs. pain gain

C. Woods, I. Kurth, J. Cox, 2020, Medizinische Genetik.

Chemogenetic Silencing of NaV1.8-Positive Sensory Neurons Reverses Chronic Neuropathic and Bone Cancer Pain in FLEx PSAM4-GlyR Mice

Jing Zhao, J. Cox, J. Wood, 2023, eNeuro.

The essential role of centrosomal NDE1 in human cerebral cortex neurogenesis.

C. Woods, M. Crosier, Mehmet Bakırcıoğlu, 2011, American journal of human genetics.

Sodium channels and pain.

J. Cox, J. Wood, A. Habib, 2015, Handbook of experimental pharmacology.