2017
FGF13 Selectively Regulates Heat Nociception by Interacting with Nav1.7
Yang L, Dong F, Yang Q, Yang P, Wu R, Wu Q, Wu D, Li C, Zhong Y, Lu Y, Cheng X, Xu F, Chen L, Bao L, Zhang X. FGF13 Selectively Regulates Heat Nociception by Interacting with Nav1.7. Neuron 2017, 93: 806-821.e9. PMID: 28162808, DOI: 10.1016/j.neuron.2017.01.009.Peer-Reviewed Original ResearchConceptsDorsal root gangliaAction potential firingHeat nociceptionFibroblast growth factorDRG neuronsSustained action potential firingTransient receptor potential cation channel V1Intracellular fibroblast growth factorsNoxious heat stimulationNoxious heat stimuliMouse DRG neuronsNociceptive neuronsNociceptive behaviorSodium channel NaRoot gangliaHeat stimuliNociceptionAction potentialsSodium currentHeat stimulationGrowth factorFGF13NeuronsChannel NaCurrent knowledge
2015
ASIC3 Mediates Itch Sensation in Response to Coincident Stimulation by Acid and Nonproton Ligand
Peng Z, Li W, Huang C, Jiang Y, Wang X, Zhu M, Cheng X, Xu T. ASIC3 Mediates Itch Sensation in Response to Coincident Stimulation by Acid and Nonproton Ligand. Cell Reports 2015, 13: 387-398. PMID: 26440887, DOI: 10.1016/j.celrep.2015.09.002.Peer-Reviewed Original ResearchConceptsAcid-sensing ion channel 3Itch sensationPrimary sensory neuronsIon channel 3ASIC3 geneSL-NH2Concomitant inflammationScratching behaviorPathological changesCoincident stimulationTissue acidosisASIC3 channelsSensory neuronsAcidosisNonproton ligandPruritogensSensationIle-GlyChannel 3Arg-LeuInflammationItchMiceNeuronsDesensitization
2009
Alternative splicing of Cav1.2 channel exons in smooth muscle cells of resistance-size arteries generates currents with unique electrophysiological properties
Cheng X, Pachuau J, Blaskova E, Asuncion-Chin M, Liu J, Dopico A, Jaggar J. Alternative splicing of Cav1.2 channel exons in smooth muscle cells of resistance-size arteries generates currents with unique electrophysiological properties. AJP Heart And Circulatory Physiology 2009, 297: h680-h688. PMID: 19502562, PMCID: PMC2724194, DOI: 10.1152/ajpheart.00109.2009.Peer-Reviewed Original ResearchAlternative SplicingAmino Acid SequenceAnimalsBase SequenceCalcium Channels, L-TypeCells, CulturedCerebral ArteriesCerebrovascular CirculationExonsMolecular Sequence DataMuscle, Smooth, VascularMyocytes, Smooth MusclePatch-Clamp TechniquesProtein Structure, TertiaryRatsRats, Sprague-DawleyVascular Resistance
2002
Carbon Monoxide Dilates Cerebral Arterioles by Enhancing the Coupling of Ca2+ Sparks to Ca2+-Activated K+ Channels
Jaggar J, Leffler C, Cheranov S, Tcheranova D, E S, Cheng X. Carbon Monoxide Dilates Cerebral Arterioles by Enhancing the Coupling of Ca2+ Sparks to Ca2+-Activated K+ Channels. Circulation Research 2002, 91: 610-617. PMID: 12364389, DOI: 10.1161/01.res.0000036900.76780.95.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsArteriolesCalcium Channel BlockersCalcium SignalingCarbon MonoxideCells, CulturedCerebral ArteriesCulture TechniquesElectric ConductivityHemeKineticsLysineMuscle, Smooth, VascularPotassium Channels, Calcium-ActivatedRyanodineRyanodine Receptor Calcium Release ChannelSignal TransductionSwineVasodilationVasodilator AgentsConceptsCerebral arteriolesArteriole smooth muscle cellsRelease channel blockerSmooth muscle cellsLarge-conductance Ca2Ryanodine-sensitive Ca2Enzyme heme oxygenasePial arteriolesCerebral circulationChannel blockersCoupling of Ca2Cellular signaling mechanismsPotent effectsArteriolesMuscle cellsHeme oxygenaseVasodilatorsPotent activatorControl conditionDilationPresent studySignaling mechanismCa2Source of controversyPercentage of Ca2