Xiaoyang Cheng

发表

Mutations at opposite ends of the DIII/S4-S5 linker of sodium channel NaV1.7 produce distinct pain disorders

S. Dib-Hajj, S. Waxman, L. Tyrrell, 2010, Molecular pain.

Mutation I136V alters electrophysiological properties of the NaV1.7 channel in a family with onset of erythromelalgia in the second decade

S. Dib-Hajj, S. Waxman, L. Tyrrell, 2008, Molecular pain.

Mini-review - Sodium channels and beyond in peripheral nerve disease: Modulation by cytokines and their effector protein kinases

S. Dib-Hajj, S. Waxman, Jin-Sung Choi, 2020, Neuroscience Letters.

Virus-mediated shRNA knockdown of Na(v)1.3 in rat dorsal root ganglion attenuates nerve injury-induced neuropathic pain.

S. Dib-Hajj, S. Waxman, E. Foster, 2013, Molecular therapy : the journal of the American Society of Gene Therapy.

Virus-mediated shRNA Knockdown of Nav1.3 in Rat Dorsal Root Ganglion Attenuates Nerve Injury-induced Neuropathic Pain.

S. Dib-Hajj, S. Waxman, E. Foster, 2013, Molecular therapy : the journal of the American Society of Gene Therapy.

FGF13 Selectively Regulates Heat Nociception by Interacting with Nav1.7

Liu Yang, P. Yang, Xu Zhang, 2017, Neuron.

Carbon Monoxide Dilates Cerebral Arterioles by Enhancing the Coupling of Ca2+ Sparks to Ca2+-Activated K+ Channels

C. Leffler, J. Jaggar, S. Y. Cheranov, 2002, Circulation research.

Gain-of-function Nav1.8 mutations in painful neuropathy

S. Dib-Hajj, S. Waxman, G. Lauria, 2012, Proceedings of the National Academy of Sciences.

Ancient Chinese Formula Qiong-Yu-Gao Protects Against Cisplatin-Induced Nephrotoxicity Without Reducing Anti-tumor Activity

Xueting Cai, Wu-guang Lu, Chunping Hu, 2015, Scientific Reports.

Gain of function NaV1.7 mutations in idiopathic small fiber neuropathy

S. Dib-Hajj, S. Waxman, G. Lauria, 2012, Annals of neurology.

Sodium-calcium exchanger and multiple sodium channel isoforms in intra-epidermal nerve terminals

S. Waxman, J. A. Black, A. Gasser, 2010, Molecular pain.

Genetic Ablation of Caveolin‐1 Modifies Ca2+ Spark Coupling in Murine Arterial Smooth Muscle Cells

J. Jaggar, Xiaoyang Cheng, 2006, American journal of physiology. Heart and circulatory physiology.

Alternative splicing may contribute to time-dependent manifestation of inherited erythromelalgia.

S. Dib-Hajj, S. Waxman, K. Huehne, 2010, Brain : a journal of neurology.

De novo pathogenic SCN8A mutation identified by whole-genome sequencing of a family quartet affected by infantile epileptic encephalopathy and SUDEP.

K. Veeramah, M. Hammer, E. Eichler, 2012, American journal of human genetics.

Conditional knockout of NaV1.6 in adult mice ameliorates neuropathic pain

S. Dib-Hajj, S. Waxman, F. Dib-Hajj, 2018, Scientific Reports.

Hominini-specific regulation of CBLN2 increases prefrontal spinogenesis

N. Šestan, S. Waxman, Navjot Kaur, 2021, Nature.

A channelopathy contributes to cerebellar dysfunction in a model of multiple sclerosis

S. Dib-Hajj, S. Waxman, S. Shields, 2012, Annals of neurology.

Sodium Channel Nav1.7 Is Essential for Lowering Heat Pain Threshold after Burn Injury

S. Dib-Hajj, S. Waxman, C. Sommer, 2012, The Journal of Neuroscience.

A Novel CaV1.2 N Terminus Expressed in Smooth Muscle Cells of Resistance Size Arteries Modifies Channel Regulation by Auxiliary Subunits*

E. Blaskova, J. Jaggar, A. Dopico, 2007, Journal of Biological Chemistry.

An AnkyrinG-Binding Motif Is Necessary and Sufficient for Targeting Nav1.6 Sodium Channels to Axon Initial Segments and Nodes of Ranvier

S. Dib-Hajj, S. Waxman, M. Rasband, 2012, The Journal of Neuroscience.

Two Nedd4-binding Motifs Underlie Modulation of Sodium Channel Nav1.6 by p38 MAPK*

S. Dib-Hajj, S. Waxman, L. Tyrrell, 2010, The Journal of Biological Chemistry.

Single amino acid deletion in transmembrane segment D4S6 of sodium channel Scn8a (Nav1.6) in a mouse mutant with a chronic movement disorder

S. Dib-Hajj, M. Meisler, J. Dowling, 2016, Neurobiology of Disease.

Alternating Electric Fields and Carcinogenesis: A New Paradigm to Avoid Missing the Elephant in the Room

Kim Sh, Daniel J. Clauw, Robert S. Katz, 2015 .

Kv7-specific activators hyperpolarize resting membrane potential and modulate human iPSC-derived sensory neuron excitability

S. Dib-Hajj, S. Waxman, M. Estacion, 2023, Frontiers in Pharmacology.

Conditional knockout of NaV1.6 in adult mice ameliorates neuropathic pain

S. Dib-Hajj, S. Waxman, F. Dib-Hajj, 2018, Scientific Reports.

Clinical comparison and functional study of the L703P: a recurrent mutation in human SCN4A that causes sodium channel myotonia

R. Griggs, Yuezhou Li, Fang Ji, 2022, Neuromuscular Disorders.

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

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

A Buthus martensii Karsch scorpion sting targets Nav1.7 in mice and mimics a phenotype of human chronic pain.

S. Dib-Hajj, S. Waxman, Juan Ye, 2021, Pain.

CaV1.2 Channel N-terminal Splice Variants Modulate Functional Surface Expression in Resistance Size Artery Smooth Muscle Cells*

Zachary P. Neeb, J. Jaggar, A. Adebiyi, 2011, The Journal of Biological Chemistry.

Mutation I136V alters electrophysiological properties of the NaV1.7 channel in a family with onset of erythromelalgia in the second decade

S. Dib-Hajj, S. Waxman, L. Tyrrell, 2008, Molecular pain.

Ca V 1.2 Channel N-terminal Splice Variants Modulate Functional Surface Expression in Resistance Size Artery

Zachary P. Neeb, J. Jaggar, A. Adebiyi, 2011 .

Deletion mutation of sodium channel Na(V)1.7 in inherited erythromelalgia: enhanced slow inactivation modulates dorsal root ganglion neuron hyperexcitability.

S. Dib-Hajj, S. Waxman, J. Drenth, 2011, Brain : a journal of neurology.

Mutation I136V alters electrophysiological properties of the NaV1.7 channel in a family with onset of erythromelalgia in the second decade

S. Dib-Hajj, L. Tyrrell, Xiaoyang Cheng, 2008, Molecular pain.

The ataxia3 Mutation in the N-Terminal Cytoplasmic Domain of Sodium Channel Nav1.6 Disrupts Intracellular Trafficking

M. Justice, S. Dib-Hajj, S. Waxman, 2009, The Journal of Neuroscience.

Alternative splicing of Cav1.2 channel exons in smooth muscle cells of resistance-size arteries generates currents with unique electrophysiological properties.

E. Blaskova, J. Jaggar, A. Dopico, 2009, American journal of physiology. Heart and circulatory physiology.