Carolina Gomis Perez, PhD
Cards
About
Titles
Associate Research Scientist
Appointments
Cellular & Molecular Physiology
Associate Research ScientistPrimary
Other Departments & Organizations
Education & Training
- PhD
- University of Siena, Cellular Physiology (2009)
- MSc
- University of Murcia, Biology and Reproductive Technology (2005)
- BS
- Univesity of Miguel Hernandez, Biochemistry (2004)
Research
Publications
2024
Cell Membrane Tension Gradients, Membrane Flows, and Cellular Processes
Yan Q, Gomis Perez C, Karatekin E. Cell Membrane Tension Gradients, Membrane Flows, and Cellular Processes. Physiology 2024, 39: 231-245. PMID: 38501962, DOI: 10.1152/physiol.00007.2024.Peer-Reviewed Original ResearchNav1.8 in small dorsal root ganglion neurons contributes to vincristine-induced mechanical allodynia
Nascimento de Lima A, Zhang H, Chen L, Effraim P, Gomis-Perez C, Cheng X, Huang J, Waxman S, Dib-Hajj S. Nav1.8 in small dorsal root ganglion neurons contributes to vincristine-induced mechanical allodynia. Brain 2024, awae071. PMID: 38447953, DOI: 10.1093/brain/awae071.Peer-Reviewed Original ResearchDorsal root ganglion neuronsDorsal root ganglionVincristine-induced mechanical allodyniaVincristine-induced peripheral neuropathyMechanical allodyniaVincristine treatmentNav1.8 channelsSmall dorsal root ganglion neuronsDevelopment of mechanical allodyniaTTX-R current densityVoltage-gated sodium channel Nav1.6Vincristine-treated animalsCurrent-clamp recordingsSodium channel Nav1.8Voltage-clamp recordingsReducing current thresholdSodium channel Nav1.6Investigate pathophysiological mechanismsTTX-RHyperpolarizing shiftRoot ganglionAllodyniaGanglion neuronsVincristine administrationPeripheral neuropathy
2022
Membrane fission during bacterial spore development requires cellular inflation driven by DNA translocation
Landajuela A, Braun M, Martínez-Calvo A, Rodrigues CDA, Gomis Perez C, Doan T, Rudner DZ, Wingreen NS, Karatekin E. Membrane fission during bacterial spore development requires cellular inflation driven by DNA translocation. Current Biology 2022, 32: 4186-4200.e8. PMID: 36041438, PMCID: PMC9730832, DOI: 10.1016/j.cub.2022.08.014.Peer-Reviewed Original ResearchConceptsMother cell membraneMembrane fissionMother cellsDNA translocationMembrane tensionLarger mother cellMother cell cytoplasmCell membraneHigh membrane tensionSmaller foresporeDNA translocaseEnergy-limited conditionsForespore compartmentAsymmetric divisionEndospore formationMembrane compartmentsMembrane necksSpore developmentCell divisionMolecular basisForesporeMembrane flowBacillus subtilisCell cytoplasmFisBRapid propagation of membrane tension at retinal bipolar neuron presynaptic terminals
Gomis Perez C, Dudzinski NR, Rouches M, Landajuela A, Machta B, Zenisek D, Karatekin E. Rapid propagation of membrane tension at retinal bipolar neuron presynaptic terminals. Science Advances 2022, 8: eabl4411. PMID: 34985955, DOI: 10.1126/sciadv.abl4411.Peer-Reviewed Original ResearchMembrane tensionMembrane flowStimulation of exocytosisSynaptic vesicle turnoverNeuroendocrine adrenal chromaffin cellsCell divisionVesicle turnoverCellular activitiesCell migrationCell typesAdrenal chromaffin cellsChromaffin cellsGlobal decreasePresynaptic terminalsRapid propagationEndocytosisExocytosisNeuronal terminalsPhagocytosisTurnoverGradientCellsDivisionMigration
2021
An epilepsy-causing mutation leads to co-translational misfolding of the Kv7.2 channel
Urrutia J, Aguado A, Gomis-Perez C, Muguruza-Montero A, Ballesteros OR, Zhang J, Nuñez E, Malo C, Chung HJ, Leonardo A, Bergara A, Villarroel A. An epilepsy-causing mutation leads to co-translational misfolding of the Kv7.2 channel. BMC Biology 2021, 19: 109. PMID: 34020651, PMCID: PMC8138981, DOI: 10.1186/s12915-021-01040-1.Peer-Reviewed Original ResearchConceptsKv7.2 channelsChannel functionSequences of proteinsNon-native configurationsNascent chainsProper foldingEpilepsy-causing mutationsIQ motifResponsive domainHuman diseasesHelix ANative conformationFolding routeIon channelsKCNQ2 geneMutationsNeuronal compartmentsFoldingMisfoldingProteinKey pathogenic mechanismsPathogenic variantsSilico studiesPathogenic mechanismsSide chains
2020
A 49-residue sequence motif in the C terminus of Nav1.9 regulates trafficking of the channel to the plasma membrane
Sizova D, Huang J, Akin E, Estacion M, Gomis-Perez C, Waxman S, Dib-Hajj S. A 49-residue sequence motif in the C terminus of Nav1.9 regulates trafficking of the channel to the plasma membrane. Journal Of Biological Chemistry 2020, 295: 1077-1090. DOI: 10.1016/s0021-9258(17)49917-0.Peer-Reviewed Original ResearchPlasma membraneC-terminusHEK293 cellsHigh-resolution live microscopyC-terminal motifHeterologous expression systemC-terminal chimerasHigh-throughput assaysSequence motifsCytoplasmic faceHeterologous systemsVoltage-gated sodium channel Nav1.9Live microscopyRecombinant expressionExpression systemLong motifsMechanistic basisFunctional expressionFunctional studiesTerminusLow functional expressionMotifChannel chimeraExpression levelsChimeras
2018
Homomeric Kv7.2 current suppression is a common feature in KCNQ2 epileptic encephalopathy
Gomis‐Pérez C, Urrutia J, Marcé‐Grau A, Malo C, López‐Laso E, Felipe‐Rucián A, Raspall‐Chaure M, Macaya A, Villarroel A. Homomeric Kv7.2 current suppression is a common feature in KCNQ2 epileptic encephalopathy. Epilepsia 2018, 60: 139-148. PMID: 30478917, DOI: 10.1111/epi.14609.Peer-Reviewed Original ResearchConceptsKv7.2 channelsDe novo mutantsWild type Kv7.2Dominant-negative behaviorGenotype-phenotype relationshipsGenetic balanceBisphosphate depletionMutantsHomomeric channelsDNA ratioSubunitsKv7.3 subunitsKv7.2Kv7.3Milder phenotypeMutationsM-currentKCNQ2Common featureNeuronal connectionsRescueKv7.2/Kv7.3 channelsPhenotypeKv7.3 channelsCellsResilience to Pain: A Peripheral Component Identified Using Induced Pluripotent Stem Cells and Dynamic Clamp
Mis MA, Yang Y, Tanaka BS, Gomis-Perez C, Liu S, Dib-Hajj F, Adi T, Garcia-Milian R, Schulman BR, Dib-Hajj SD, Waxman SG. Resilience to Pain: A Peripheral Component Identified Using Induced Pluripotent Stem Cells and Dynamic Clamp. Journal Of Neuroscience 2018, 39: 382-392. PMID: 30459225, PMCID: PMC6335750, DOI: 10.1523/jneurosci.2433-18.2018.Peer-Reviewed Original ResearchMeSH KeywordsAdultChildChronic PainErythromelalgiaExcitatory Postsynaptic PotentialsExomeFemaleGanglia, SpinalHumansImmunohistochemistryIndividualityInduced Pluripotent Stem CellsKCNQ Potassium ChannelsMaleMembrane PotentialsNAV1.7 Voltage-Gated Sodium ChannelPain MeasurementPatch-Clamp TechniquesResilience, PsychologicalSensory Receptor CellsConceptsWhole-exome sequencingPeripheral sensory neuronsSensory neuronsSpecific gene variantsGene variantsPluripotent stem cell-derived sensory neuronsInterindividual differencesDorsal root ganglion neuronsExome sequencingDifferent pain profilesDRG neuron excitabilityDynamic clampPeripheral nervous systemStem cellsPain ProfilePluripotent stem cellsChronic painPeripheral mechanismsGanglion neuronsNeuron excitabilityPainNervous systemHuman genetic modelsNeuronsDifferent gene variantsStructural basis and energy landscape for the Ca2+ gating and calmodulation of the Kv7.2 K+ channel
Bernardo-Seisdedos G, Nuñez E, Gomis-Perez C, Malo C, Villarroel Á, Millet O. Structural basis and energy landscape for the Ca2+ gating and calmodulation of the Kv7.2 K+ channel. Proceedings Of The National Academy Of Sciences Of The United States Of America 2018, 115: 2395-2400. PMID: 29463698, PMCID: PMC5873240, DOI: 10.1073/pnas.1800235115.Peer-Reviewed Original ResearchConceptsC-lobeKey biological signalsPrincipal molecular componentsAssociation of helicesTransmembrane regionStructural basisFunction of CaKv7.2 channelsBasal cytosolic CaConformational rearrangementsN-lobeInactive stateKey controllerMolecular componentsCytosolic CaIntracellular CaKv7.2HelixInactive channelsM-currentBiological signalsCalcification stateMillisecond timeNeuronal excitabilityPopulated excited statesLack of correlation between surface expression and currents in epileptogenic AB-calmodulin binding domain Kv7.2 potassium channel mutants
Alaimo A, Etxeberria A, Gómez-Posada JC, Gomis-Perez C, Fernández-Orth J, Malo C, Villarroel A. Lack of correlation between surface expression and currents in epileptogenic AB-calmodulin binding domain Kv7.2 potassium channel mutants. Channels 2018, 12: 299-310. PMID: 30126342, PMCID: PMC6161613, DOI: 10.1080/19336950.2018.1511512.Peer-Reviewed Original Research
Links & Media
News
- December 04, 2018
Scientists Identify Method to Study Resilience to Pain