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Oncostatin M can sensitize sensory neurons in inflammatory pruritus

Science translational medicine, 2021-11, Vol.13 (619), p.eabe3037

2021

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The Cytokine TGF-β Induces Interleukin-31 Expression from Dermal Dendritic Cells to Activate Sensory Neurons and Stimulate Wound Itching

Immunity (Cambridge, Mass.), 2020-08, Vol.53 (2), p.371-383.e5

2020

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Circuit dissection of the role of somatostatin in itch and pain

Nature neuroscience, 2018-05, Vol.21 (5), p.707

2018

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Nppb Neurons Are Sensors of Mast Cell-Induced Itch

Cell reports (Cambridge), 2019-03, Vol.26 (13), p.3561-3573.e4

2019

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Targeting human Mas-related G protein-coupled receptor X1 to inhibit persistent pain

Proceedings of the National Academy of Sciences - PNAS, 2017-03, Vol.114 (10), p.E1996-E2005

2017

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α‐Actinin‐1 promotes activity of the L‐type Ca2+ channel Cav1.2

The EMBO journal, 2020-09, Vol.39 (18), p.e106171-n/a

2020

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Specific β-Defensins Stimulate Pruritus through Activation of Sensory Neurons

Journal of investigative dermatology, 2022-03, Vol.142 (3), p.594-602

2022

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Interactions of the Neuro‒Immune‒Stromal Triad in Itch

Journal of investigative dermatology, 2022-01, Vol.142 (1), p.42-46

2022

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Cytoplasmic ATP inhibition of CLC-1 is enhanced by low pH

The Journal of general physiology, 2007-08, Vol.130 (2), p.217-221

2007

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Molecular Genetics of Kappa Opioids in Pain and Itch Sensations

The Kappa Opioid Receptor, 2022, p.255-274

2022

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Discovery and Characterization of 2-(Cyclopropanesulfonamido)-N-(2-ethoxyphenyl)benzamide, ML382: a Potent and Selective Positive Allosteric Modulator of MrgX1

ChemMedChem, 2015-01, Vol.10 (1), p.57-61

2015

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GPR15L is an epithelial inflammation-derived pruritogen

Science advances, 2022-06, Vol.8 (24), p.eabm7342-eabm7342

2022

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α-Actinin-1 promotes activity of the L-type Ca 2+ channel Ca v 1.2

The EMBO journal, 2020-09, Vol.39 (18), p.e106171

2020

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α‐Actinin‐1 promotes activity of the L‐type Ca2+ channel Cav1.2

The EMBO journal, 2020-03, Vol.39 (5), p.n/a

2020

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α-Actinin-1 promotes activity of the L-type Ca 2+ channel Ca v 1.2

The EMBO journal, 2020-03, Vol.39 (5), p.e102622

2020

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Blocking pore-open mutants of CLC-0 by amphiphilic blockers

The Journal of general physiology, 2009-01, Vol.133 (1), p.43-58

2009

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Spontaneous differentiation of adult rat marrow stromal cells in a long-term culture

Journal of Veterinary Medical Science, 2007, Vol.69(2), pp.95-102

2007

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ATP inhibition of CLC-1 is controlled by oxidation and reduction

The Journal of general physiology, 2008-10, Vol.132 (4), p.421-428

2008

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Binding of ATP to the CBS domains in the C-terminal region of CLC-1

The Journal of general physiology, 2011-04, Vol.137 (4), p.357-368

2011

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Dominantly Inherited Myotonia Congenita Resulting from a Mutation That Increases Open Probability of the Muscle Chloride Channel CLC-1

Neuromolecular medicine, 2012-12, Vol.14 (4), p.328-337

2012

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Competition between α-actinin and Ca²⁺-calmodulin controls surface retention of the L-type Ca²⁺ channel Ca(V)1.2

Neuron (Cambridge, Mass.), 2013-05, Vol.78 (3), p.483-497

2013

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MrgprX1 Mediates Neuronal Excitability and Itch Through Tetrodotoxin-Resistant Sodium Channels

Itch (Philadelphia, Pa.), 2019-07, Vol.4 (3), p.e28-e28

2019

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Alpha-Actinin Promotes Surface Localization and Ion Conducting Activity of the L-Type Ca2+ Channel by Binding to the IQ Region of CaV1.2

Biophysical journal, 2016-02, Vol.110 (3), p.442a-443a

2016

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The inhibition of high-voltage-activated calcium current by activation of MrgC11 involves phospholipase C-dependent mechanisms

Neuroscience, 2015-08, Vol.300, p.393-403

2015

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Analysis of the CLC-1 ATP Binding Site by Structure-Guided Mutagenesis

Biophysical journal, 2010-01, Vol.98 (3), p.320a-320a

2010

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Oncostatin M can sensitize sensory neurons in inflammatory pruritus

The Cytokine TGF-β Induces Interleukin-31 Expression from Dermal Dendritic Cells to Activate Sensory Neurons and Stimulate Wound Itching

Circuit dissection of the role of somatostatin in itch and pain

Nppb Neurons Are Sensors of Mast Cell-Induced Itch

Targeting human Mas-related G protein-coupled receptor X1 to inhibit persistent pain

α‐Actinin‐1 promotes activity of the L‐type Ca2+ channel Cav1.2

Specific β-Defensins Stimulate Pruritus through Activation of Sensory Neurons

Interactions of the Neuro‒Immune‒Stromal Triad in Itch

Cytoplasmic ATP inhibition of CLC-1 is enhanced by low pH

Molecular Genetics of Kappa Opioids in Pain and Itch Sensations

Discovery and Characterization of 2-(Cyclopropanesulfonamido)-N-(2-ethoxyphenyl)benzamide, ML382: a Potent and Selective Positive Allosteric Modulator of MrgX1

GPR15L is an epithelial inflammation-derived pruritogen

α-Actinin-1 promotes activity of the L-type Ca 2+ channel Ca v 1.2

α‐Actinin‐1 promotes activity of the L‐type Ca2+ channel Cav1.2

α-Actinin-1 promotes activity of the L-type Ca 2+ channel Ca v 1.2

Blocking pore-open mutants of CLC-0 by amphiphilic blockers

Spontaneous differentiation of adult rat marrow stromal cells in a long-term culture

ATP inhibition of CLC-1 is controlled by oxidation and reduction

Binding of ATP to the CBS domains in the C-terminal region of CLC-1

Dominantly Inherited Myotonia Congenita Resulting from a Mutation That Increases Open Probability of the Muscle Chloride Channel CLC-1

Competition between α-actinin and Ca²⁺-calmodulin controls surface retention of the L-type Ca²⁺ channel Ca(V)1.2

MrgprX1 Mediates Neuronal Excitability and Itch Through Tetrodotoxin-Resistant Sodium Channels

Alpha-Actinin Promotes Surface Localization and Ion Conducting Activity of the L-Type Ca2+ Channel by Binding to the IQ Region of CaV1.2

The inhibition of high-voltage-activated calcium current by activation of MrgC11 involves phospholipase C-dependent mechanisms

Analysis of the CLC-1 ATP Binding Site by Structure-Guided Mutagenesis

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