Barbara Ehrlich, PhD
Professor of Pharmacology and of Cellular And Molecular PhysiologyDownloadHi-Res Photo
Cards
Appointments
Pharmacology
Primary
Cellular & Molecular Physiology
Secondary
Contact Info
Pharmacology
PO Box 208066, 333 Cedar Street
New Haven, CT 06520-8066
United States
About
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Titles
Professor of Pharmacology and of Cellular And Molecular Physiology
Appointments
Pharmacology
ProfessorPrimaryCellular & Molecular Physiology
ProfessorSecondary
Other Departments & Organizations
- Biochemistry, Quantitative Biology, Biophysics and Structural Biology (BQBS)
- Cellular & Molecular Physiology
- Dean's Workshops
- Developmental Therapeutics
- Graduate Program in Cellular and Molecular Physiology
- Interdepartmental Neuroscience Program
- Laboratory of Molecular Hermeneutics (Ehrlich)
- Molecular Medicine, Pharmacology, and Physiology
- Neuroscience Track
- Pharmacology
- Primary Faculty
- Vascular Biology and Therapeutics Program
- Yale Cancer Center
- Yale Combined Program in the Biological and Biomedical Sciences (BBS)
- Yale Ventures
Education & Training
- PhD
- University of California at Los Angeles (1979)
Research
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Overview
Medical Research Interests
Calcium; Drug-Related Side Effects and Adverse Reactions; Hermeneutics; Pharmacology; Physiology; Polycystic Kidney Diseases
ORCID
0000-0001-9657-9704- View Lab Website
Ehrlich Lab Website
Research at a Glance
Yale Co-Authors
Frequent collaborators of Barbara Ehrlich's published research.
Publications Timeline
A big-picture view of Barbara Ehrlich's research output by year.
Research Interests
Research topics Barbara Ehrlich is interested in exploring.
Declan McGuone, FRCPath Neuro, MBBCh
Emma Kruglov
Michael Mak
Michael H Nathanson, MD, PhD
Mateus Guerra, PhD
Titus Boggon, PhD
66Publications
4,699Citations
Calcium
Polycystic Kidney Diseases
Publications
2026
Blood‐based proteomic profiling reveals context‐dependent changes in BCL2‐associated signaling during taxane therapy in breast cancer patients
Munshani S, Ibrahim E, Rodwin R, Ferrucci L, Blenman K, Lustberg M, Ehrlich B. Blood‐based proteomic profiling reveals context‐dependent changes in BCL2‐associated signaling during taxane therapy in breast cancer patients. FEBS Open Bio 2026 PMID: 41883148, DOI: 10.1002/2211-5463.70239.Peer-Reviewed Original ResearchAltmetricConceptsReverse phase proteomic arraysBreast cancer patientsSide effects of chemotherapyEffects of chemotherapySide effectsCancer patientsKaplan-Meier survival curvesProtein expressionActivation of stress response pathwaysSenescent-associated secretory phenotypeStress response pathwaysLong-term outcomesNon-interventional studyCalcium signaling dysregulationCourse of treatmentSignaling-related proteinsBCL2 familyTaxane therapyProteomic dataChemotherapy timingCancer recurrenceSurvival curvesCancer therapyProteome arrayChemotherapy
2025
Pathological Calcium Signaling in Traumatic Brain Injury and Alzheimer’s Disease: From Acute Neuronal Injury to Chronic Neurodegeneration
Neuschmid S, Schallerer C, Ehrlich B, McGuone D. Pathological Calcium Signaling in Traumatic Brain Injury and Alzheimer’s Disease: From Acute Neuronal Injury to Chronic Neurodegeneration. International Journal Of Molecular Sciences 2025, 26: 9245. PMID: 41009808, PMCID: PMC12471116, DOI: 10.3390/ijms26189245.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsAlzheimer's diseaseCalcium-dependent protease calpainPharmacological inhibitionCalcium signalingTau hyperphosphorylationAmyloid-bLoss of calcium homeostasisProtein misfoldingCalcium-dependent enzymesSignaling proteinsAD riskProtease calpainAD modelProtease networkDisrupted calcium signalingTraumatic brain injuryUpstream driversEnzyme activityPathological calcium signalingSynaptic architectureCalcium dysregulationAxonal transportNeuronal deathEssential scaffoldsCalcium homeostasisCalpain in Traumatic Brain Injury: From Cinderella to Central Player
Schallerer C, Neuschmid S, Ehrlich B, McGuone D. Calpain in Traumatic Brain Injury: From Cinderella to Central Player. Cells 2025, 14: 1253. PMID: 40862734, PMCID: PMC12384584, DOI: 10.3390/cells14161253.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsConceptsTraumatic brain injuryTherapeutic targetCalcium-dependent protease calpainBrain injuryCause of deathSecondary injury cascadesPreclinical efficacyTraumatic brain injury pathologyGlobal health concernClinical dataRegulatory proteinsCalcium homeostasisInjury cascadeCalcium dysregulationProtein fragmentsProtease calpainCalpain substratesCalpain activityMitochondrial dysfunctionProtease activityAxonal integrityNeuronal compartmentsSelective inhibitorsCentral playerSynaptic functionMonomethyl auristatin E and paclitaxel use different mechanisms to alter intracellular calcium signaling
Mendes G, Munshani S, Wachtler N, Wopfner H, Gong X, Sun Z, Mak M, Ehrlich B. Monomethyl auristatin E and paclitaxel use different mechanisms to alter intracellular calcium signaling. Biochemical Pharmacology 2025, 242: 117188. PMID: 40721011, PMCID: PMC12351507, DOI: 10.1016/j.bcp.2025.117188.Peer-Reviewed Original ResearchCitationsAltmetricConceptsMonomethyl auristatin EChemotherapy-induced peripheral neuropathyAntibody-drug conjugatesInositol trisphosphate receptorCalcium signalingCytotoxic agents to cancer cellsAuristatin ECalcium homeostasisAgents to cancer cellsPatients' qualityNCS-1Neurotoxic effectsIntracellular calcium levelsIntracellular calcium signalingPatients' quality of lifeTargeted cancer therapyMicrotubule-targeting agentsLithium co-treatmentPTX treatmentTrisphosphate receptorChemotherapy toleranceClinical successNeuronal calcium sensor-1Peripheral neuropathyCalcium levelsChemotherapy-induced neuropathy in monomethyl Auristatin E treatment: prevention by lithium
Itaborahy M, Feng I, Vieira-Machado U, da Silveira I, Valverde T, Costa G, Guimarães J, Laet-Souza D, Malamut C, Martins M, Marques J, Rezende-Ribeiro J, Gorshkov V, Kjeldsen F, Favalessa M, Acipreste I, Verano-Braga T, Carvalho H, Oliveira A, Dias M, Goes A, Ehrlich B, Leite M. Chemotherapy-induced neuropathy in monomethyl Auristatin E treatment: prevention by lithium. British Journal Of Cancer 2025, 133: 604-614. PMID: 40595283, PMCID: PMC12405523, DOI: 10.1038/s41416-025-03020-6.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsChemotherapy-induced peripheral neuropathyMonomethyl auristatin EAntibody-drug conjugatesChemotherapy-induced cognitive impairmentPeripheral neuropathyAntitumor activityNew drug classesPrevalence of adverse effectsChemotherapy-induced neuropathyPrevalence of neuropathyPeripheral sensitizationCognitive effectsLithium pretreatmentTumor progressionAuristatin EDrug classesMouse modelNeuropathyCalcium signalingCancer cellsCognitive impairmentCancer treatmentQuality of life of cancer survivorsE treatmentLife of cancer survivorsAdaptation to Volumetric Compression Drives an Apoptosis-Resistant and Invasive Phenotype in Liver Cancer
Gong X, Ogino N, Leite M, Zhang D, Chen Z, Nguyen R, Liu R, Kruglov E, Flores K, Cabral A, Moreira de M Mendes G, Ehrlich B, Mak M. Adaptation to Volumetric Compression Drives an Apoptosis-Resistant and Invasive Phenotype in Liver Cancer. Cancer Research 2025, 85: 3156-3175. PMID: 40387600, PMCID: PMC12354003, DOI: 10.1158/0008-5472.can-24-0859.Peer-Reviewed Original ResearchCitationsAltmetricConceptsEpithelial-to-mesenchymal transition genesLiver cancerResistance to apoptosisCell state transitionsProliferation of tumor cellsYAP nuclear translocationCancer cell invasionIntracellular calcium signalingLiver cancer developmentTranscriptional dynamicsRac1 activationCellular protrusionsInhibiting Rac1Apoptosis-resistantTranscriptional changesInvasive phenotypeIntracellular calciumTumor cellsCell invasionNuclear translocationCancer developmentCalcium signalingTransition genesCancer cellsLiver-specific markersExploring Calcium Channels as Potential Therapeutic Targets in Blast Traumatic Brain Injury
Wachtler N, O’Brien R, Ehrlich B, McGuone D. Exploring Calcium Channels as Potential Therapeutic Targets in Blast Traumatic Brain Injury. Pharmaceuticals 2025, 18: 223. PMID: 40006037, PMCID: PMC11859800, DOI: 10.3390/ph18020223.Peer-Reviewed Original ResearchCitationsAltmetricConceptsCalcium signalingCalcium channelsTherapeutic strategiesCalcium homeostasisFunction of calcium channelsDysregulated calcium signalingModulation of injuryTraumatic brain injuryBrain injuryLoss of calcium homeostasisBlast-related traumatic brain injuryDevelopment of neuroprotective interventionsIntracellular calcium dynamicsPlasma membrane stabilityExtracellular calciumBlast traumatic brain injuryPreclinical modelsTherapeutic outcomesNeuroprotective interventionsMembrane abnormalitiesPharmacological inhibitorsNeuronal somataExclusion criteriaCalcium dynamicsSecondary injuryCorrigendum to “Modulating TRPV4 channels with paclitaxel and lithium” [Cell Calcium 91 (2020) 102266]
Sánchez J, Muñoz L, Ehrlich B. Corrigendum to “Modulating TRPV4 channels with paclitaxel and lithium” [Cell Calcium 91 (2020) 102266]. Cell Calcium 2025, 125: 102988. PMID: 39746287, DOI: 10.1016/j.ceca.2024.102988.Peer-Reviewed Original Research
2024
Neutrophils insert elastase into hepatocytes to regulate calcium signaling in alcohol-associated hepatitis
Ogino N, Leite M, Guerra M, Kruglov E, Asashima H, Hafler D, Ito T, Pereira J, Peiffer B, Sun Z, Ehrlich B, Nathanson M. Neutrophils insert elastase into hepatocytes to regulate calcium signaling in alcohol-associated hepatitis. Journal Of Clinical Investigation 2024, 134: e171691. PMID: 38916955, PMCID: PMC11324315, DOI: 10.1172/jci171691.Peer-Reviewed Original ResearchCitationsAltmetricConceptsAlcohol-associated hepatitisReduced cell proliferationCalcium channel expressionCalcium signaling mechanismsIntracellular calcium channelsCell proliferationRegulate calcium signalingNeutrophil extracellular trapsChannel expressionNeutrophil granule proteinsCalcium channelsNeutrophil infiltrationPatient specimensGranule proteasesMouse modelHealthy subjectsLiver diseaseExtracellular trapsCalcium signalingSerpin E2NeutrophilsElastase activityHepatitisTissue remodelingSignaling mechanismsNCS-1 protein regulates TRPA1 channel through the PI3K pathway in breast cancer and neuronal cells
Sánchez J, Alemán A, Henao J, Olaya J, Ehrlich B. NCS-1 protein regulates TRPA1 channel through the PI3K pathway in breast cancer and neuronal cells. Journal Of Physiology And Biochemistry 2024, 80: 451-463. PMID: 38564162, PMCID: PMC11074019, DOI: 10.1007/s13105-024-01016-z.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsTransient receptor potential channel ankyrin 1Breast cancerPI3K pathwayNCS-1Chemotherapy-induced peripheral neuropathyCa2+ channelsK pathwayCa2+ influxNCS-1 expressionBreast cancer cellsCa2+ sensorCa2+ homeostasisCa2+ dynamicsNeuronal calcium sensor-1MDA-MB-231Fura-2Open probabilityPain sensationAnkyrin 1Peripheral neuropathyTRPA1 channelsCo-ImmunoprecipitationChannel functionRegulatory componentsCellular pathways
Academic Achievements & Community Involvement
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Activities
activity NICHD, Board of Scientific Counselors
06/06/2004 - 06/05/2011Peer Review Groups and Grant Study SectionsMemberDetailsChairactivity Marine Biological Laboratory, Woods Hole, MA
07/04/2004 - 07/03/2010CommitteesMemberDetailsElected Member
Honors
honor Washington University Equalize Pitch Competition Finalist
10/15/2020National AwardDetailsUnited Stateshonor Blavatnik Foundation Innovator Awardee
05/13/2020Yale University AwardDetailsUnited Stateshonor K.S. Cole Award for Excellence in Membrane Biophysics
01/01/2005National AwardBiophysical SocietyDetailsUnited Stateshonor Margaret Oakley Dayhoffer Award in Biophysics
02/01/1987National AwardBiophysical SocietyDetailsUnited Stateshonor Pew Scholar
07/01/1986National AwardPew Charitable TrustDetailsUnited States
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Academic Office Number
Lab Number
Mailing Address
Pharmacology
PO Box 208066, 333 Cedar Street
New Haven, CT 06520-8066
United States