Francesc Lopez-Giraldez, PhD
Research Scientist in GeneticsDownloadHi-Res Photo
Cards
Appointments
Genetics
Primary
Additional Titles
YCGA Associate Director of Bioinformatics, Genetics
Contact Info
Appointments
Genetics
Primary
Additional Titles
YCGA Associate Director of Bioinformatics, Genetics
Contact Info
Appointments
Genetics
Primary
Additional Titles
YCGA Associate Director of Bioinformatics, Genetics
Contact Info
About
Titles
Research Scientist in Genetics
YCGA Associate Director of Bioinformatics, Genetics
Appointments
Genetics
Research ScientistPrimary
Other Departments & Organizations
Education & Training
- Post-Doctoral fellowship Beatriu de Pinós
- Generalitat de Catalunya (2009)
- PhD
- Autonomous University of Barcelona, Evolutionary Genetics (2006)
- Graduate student fellowship
- Generalitat de Catalunya (2004)
- MSc
- Pompeu Fabra University, Health and Life Sciences (2004)
- BS
- University of Girona, Biology (2000)
- Undergraduate student fellowship to develop a project on the Phylogeny of the genus Merluccius
- Gobierno de España (2000)
Research
Research at a Glance
Yale Co-Authors
Frequent collaborators of Francesc Lopez-Giraldez's published research.
Publications Timeline
A big-picture view of Francesc Lopez-Giraldez's research output by year.
Jeffrey Townsend, PhD
Kaya Bilguvar, MD, PhD
Zheng Wang, PhD
Murat Gunel, MD, FACS, FAHA, FAANS
James Knight, PhD
Jordan Pober, MD, PhD
91Publications
6,128Citations
Publications
2024
IL-1β Induces Human Endothelial Surface Expression of IL-15 by Relieving let-7c-3p Suppression of Protein Translation.
Mullan C, Summer L, Lopez-Giraldez F, Tobiasova Z, Manes T, Yasothan S, Song G, Jane-Wit D, Saltzman W, Pober J. IL-1β Induces Human Endothelial Surface Expression of IL-15 by Relieving let-7c-3p Suppression of Protein Translation. The Journal Of Immunology 2024, 213: 1338-1348. PMID: 39302113, PMCID: PMC11493510, DOI: 10.4049/jimmunol.2400331.Peer-Reviewed Original ResearchConceptsIL-15Surface expressionIL-1BIL-15 transcriptsEndothelial cellsCD8 T cell activationExpression of IL-15EC surface expressionIL-15 transpresentationComplement activationGraft endothelial cellsActivity of CTLT cell activationIL-15 mRNAEndothelial surface expressionAbsence of complement activationCultured human endothelial cellsIL-1-mediated activationIL-15RAProtein translationAllograft rejectionRNA polymerase II-mediated transcriptionHuman endothelial cellsSuppression of protein translationmTORC1 Signaling in Brain Endothelial Progenitors Contributes to CCM Pathogenesis
Min W, Qin L, Zhang H, López-Giráldez F, Jiang N, Kim Y, Mohan V, Su M, Murray K, Grutzendler J, Zhou J. mTORC1 Signaling in Brain Endothelial Progenitors Contributes to CCM Pathogenesis. Circulation Research 2024, 135: e94-e113. PMID: 38957991, PMCID: PMC11293987, DOI: 10.1161/circresaha.123.324015.Peer-Reviewed Original ResearchAltmetricConceptsCerebral vascular malformationsEndothelial progenitor cellsBlood-brain barrier integritySingle-cell RNA sequencing analysisDisruption of blood-brain barrier integrityBarrier integrityResident endothelial progenitor cellsRNA sequencing analysisTissue immunofluorescence analysisEndothelial cellsEPC clustersStem cell markersFocal neurological deficitsBrain's neurovascular unitMTOR signalingHuman CCM lesionsMTORC1 signalingBlood-brain barrierCapillary endothelial cellsCCM pathogenesisVascular malformationsLesion signaturesNeurological deficitsCell markersClonal expansionmTORC1 signaling in brain endothelial progenitors contributes to CCM pathogenesis
Min W, Qin L, Zhang H, López-Giráldez F, Kim Y, Jiang N, Mohan VK, Su M, Murray KN, Grutzendler J, Zhou JH. mTORC1 signaling in brain endothelial progenitors contributes to CCM pathogenesis. Circulation Research 2024Peer-Reviewed Original ResearchASCL1 Drives Tolerance to Osimertinib in EGFR Mutant Lung Cancer in Permissive Cellular Contexts.
Hu B, Wiesehöfer M, de Miguel F, Liu Z, Chan L, Choi J, Melnick M, Arnal Estape A, Walther Z, Zhao D, Lopez-Giraldez F, Wurtz A, Cai G, Fan R, Gettinger S, Xiao A, Yan Q, Homer R, Nguyen D, Politi K. ASCL1 Drives Tolerance to Osimertinib in EGFR Mutant Lung Cancer in Permissive Cellular Contexts. Cancer Research 2024, 84: 1303-1319. PMID: 38359163, PMCID: PMC11142404, DOI: 10.1158/0008-5472.can-23-0438.Peer-Reviewed Original ResearchCitationsAltmetricConceptsTyrosine kinase inhibitorsPatient-derived xenograftsEGFR mutant lung cancerMutant lung cancerPre-treatment tumorsResidual diseaseDrug toleranceLung cancerResidual tumor cells in vivoEGFR mutant lung adenocarcinomaTyrosine kinase inhibitor osimertinibEGFR tyrosine kinase inhibitorsTyrosine kinase inhibitor treatmentTumor cells in vivoMutant lung adenocarcinomaMaximal tumor regressionTranscription factor Ascl1Drug-tolerant cellsTime of maximal responseEvidence of cellsCells in vivoOsimertinib treatmentTumor regressionSingle cell transcriptional profilingTumor cells
2023
LRRC23 truncation impairs radial spoke 3 head assembly and sperm motility underlying male infertility
Hwang J, Chai P, Nawaz S, Choi J, Lopez-Giraldez F, Hussain S, Bilguvar K, Mane S, Lifton R, Ahmad W, Zhang K, Chung J. LRRC23 truncation impairs radial spoke 3 head assembly and sperm motility underlying male infertility. ELife 2023, 12: rp90095. PMID: 38091523, PMCID: PMC10721216, DOI: 10.7554/elife.90095.Peer-Reviewed Original ResearchCitationsAltmetricLRRC23 truncation impairs radial spoke 3 head assembly and sperm motility underlying male infertility
Hwang J, Chai P, Nawaz S, Choi J, Lopez-Giraldez F, Hussain S, Bilguvar K, Mane S, Lifton R, Ahmad W, Zhang K, Chung J. LRRC23 truncation impairs radial spoke 3 head assembly and sperm motility underlying male infertility. ELife 2023, 12 DOI: 10.7554/elife.90095.3.Peer-Reviewed Original ResearchCitationsAltmetricLineage-specific genes are clustered with HET-domain genes and respond to environmental and genetic manipulations regulating reproduction in Neurospora
Wang Z, Wang Y, Kasuga T, Lopez-Giraldez F, Zhang Y, Zhang Z, Wang Y, Dong C, Sil A, Trail F, Yarden O, Townsend J. Lineage-specific genes are clustered with HET-domain genes and respond to environmental and genetic manipulations regulating reproduction in Neurospora. PLOS Genetics 2023, 19: e1011019. PMID: 37934795, PMCID: PMC10684091, DOI: 10.1371/journal.pgen.1011019.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsLineage-specific genesHET domain genesSexual reproductionFunctional roleUnusual carbon sourcesPotential functional roleMating lociAsexual growthGenetic mutantsNeurospora crassaPossible functional roleSexual phaseGenetic manipulationTranscriptomic profilingReproduction regulationGene knockoutPP-1ADV-1Environmental alterationsGenesSexual developmentNeurosporaReproductionCarbon sourceGenetic barrierOrigins of lineage‐specific elements via gene duplication, relocation, and regional rearrangement in Neurospora crassa
Wang Z, Wang Y, Kasuga T, Hassler H, Lopez‐Giraldez F, Dong C, Yarden O, Townsend J. Origins of lineage‐specific elements via gene duplication, relocation, and regional rearrangement in Neurospora crassa. Molecular Ecology 2023 PMID: 37843462, DOI: 10.1111/mec.17168.Peer-Reviewed Original ResearchCitationsAltmetricConceptsLineage-specific genesGene duplicationNew genesLineage-specific elementsWeighted gene correlation network analysisRecent gene duplicationNon-coding DNACell wall integrityCo-regulatory modulesGene correlation network analysisNon-coding sequencesCorrelation network analysisAntifungal toxinsGene syntenyNeurospora speciesGenus NeurosporaEvolutionary biologistsSuch cladesRegulatory machinerySequence repeatsModel speciesAncestral statusNeurospora crassaTranscriptomic dataDiverse functionsMicroRNA-1 protects the endothelium in acute lung injury
Korde A, Haslip M, Pednekar P, Khan A, Chioccioli M, Mehta S, Lopez-Giraldez F, Bermejo S, Rojas M, Dela Cruz C, Matthay M, Pober J, Pierce R, Takyar S. MicroRNA-1 protects the endothelium in acute lung injury. JCI Insight 2023, 8: e164816. PMID: 37737266, PMCID: PMC10561733, DOI: 10.1172/jci.insight.164816.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsAcute respiratory distress syndromeAcute lung injuryVascular endothelial growth factorAngiopoietin-2Lung injuryAcute injuryMiR-1MicroRNA-1Endothelial cell-specific overexpressionSevere endothelial dysfunctionRespiratory distress syndromeSurvival of miceIntrinsic protective effectContext of injuryCell-specific overexpressionEndothelial growth factorFamily member 3Pneumonia cohortMiR-1 targetsEndothelial dysfunctionDistress syndromeBarrier dysfunctionCapillary leakProtective effectSevere formMultiomic analyses implicate a neurodevelopmental program in the pathogenesis of cerebral arachnoid cysts
Kundishora A, Allington G, McGee S, Mekbib K, Gainullin V, Timberlake A, Nelson-Williams C, Kiziltug E, Smith H, Ocken J, Shohfi J, Allocco A, Duy P, Elsamadicy A, Dong W, Zhao S, Wang Y, Qureshi H, DiLuna M, Mane S, Tikhonova I, Fu P, Castaldi C, López-Giráldez F, Knight J, Furey C, Carter B, Haider S, Moreno-De-Luca A, Alper S, Gunel M, Millan F, Lifton R, Torene R, Jin S, Kahle K. Multiomic analyses implicate a neurodevelopmental program in the pathogenesis of cerebral arachnoid cysts. Nature Medicine 2023, 29: 667-678. PMID: 36879130, DOI: 10.1038/s41591-023-02238-2.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsArachnoid cystCerebral arachnoid cystsDe novo variantsAC pathogenesisDevelopmental brain lesionsStructural brain diseaseAppropriate clinical contextPatients' medical recordsDamaging de novo variantsMedical recordsClinical severityBrain lesionsHealthy individualsAC subtypesBrain diseasesGenetic testingNeurodevelopmental pathologyClinical contextPathogenesisPatient phenotypesNeurodevelopmental programsNovo variantsRNA sequencing transcriptomeHuman brainCysts
Academic Achievements & Community Involvement
honor National Cancer Institute Research Specialist Award (R50)
National AwardNational Cancer InstituteDetails08/01/2023United States
Teaching & Mentoring
Mentoring
Duna Domingo
Graduate student2022 - 2023
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The Anlyan Center
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300 Cedar Street, Wing North, Fl 2, Rm 212
New Haven, CT 06519
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203.737.6864