About
Titles
Research Scientist
Appointments
Nephrology
Research ScientistPrimary
Other Departments & Organizations
- Internal Medicine
- Nephrology
- Somlo Laboratory
Education & Training
- Scholar
- Showa University School of Medicine (1996)
- MD
- Fourth Military Medical University, Medicine (1986)
Research
Research at a Glance
Yale Co-Authors
Frequent collaborators of Ke Dong's published research.
Publications Timeline
A big-picture view of Ke Dong's research output by year.
Stefan Somlo, MD
Yiqiang Cai, PhD, MD
Sorin Fedeles, PhD, MBA
Xin Tian, MD
John Geibel, DSc, MD, AGAF, MS, FRS
Hongying Shen, PhD
19Publications
266Citations
Publications
2024
Glis2 is an early effector of polycystin signaling and a target for therapy in polycystic kidney disease
Zhang C, Rehman M, Tian X, Pei S, Gu J, Bell T, Dong K, Tham M, Cai Y, Wei Z, Behrens F, Jetten A, Zhao H, Lek M, Somlo S. Glis2 is an early effector of polycystin signaling and a target for therapy in polycystic kidney disease. Nature Communications 2024, 15: 3698. PMID: 38693102, PMCID: PMC11063051, DOI: 10.1038/s41467-024-48025-6.Peer-Reviewed Original ResearchAltmetricMeSH Keywords and ConceptsConceptsMouse models of autosomal dominant polycystic kidney diseaseModel of autosomal dominant polycystic kidney diseasePolycystin signalingAutosomal dominant polycystic kidney diseasePolycystin-1Polycystic kidney diseaseTreat autosomal dominant polycystic kidney diseaseGlis2Primary ciliaKidney tubule cellsSignaling pathwayMouse modelDominant polycystic kidney diseasePotential therapeutic targetTranslatomeAntisense oligonucleotidesKidney diseasePolycystinMouse kidneyFunctional effectorsCyst formationTherapeutic targetInactivationFunctional targetPharmacological targetsA synthetic agent ameliorates polycystic kidney disease by promoting apoptosis of cystic cells through increased oxidative stress
Fedeles B, Bhardwaj R, Ishikawa Y, Khumsubdee S, Krappitz M, Gubina N, Volpe I, Andrade D, Westergerling P, Staudner T, Campolo J, Liu S, Dong K, Cai Y, Rehman M, Gallagher A, Ruchirawat S, Croy R, Essigmann J, Fedeles S, Somlo S. A synthetic agent ameliorates polycystic kidney disease by promoting apoptosis of cystic cells through increased oxidative stress. Proceedings Of The National Academy Of Sciences Of The United States Of America 2024, 121: e2317344121. PMID: 38241440, PMCID: PMC10823221, DOI: 10.1073/pnas.2317344121.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsCyst cellsAutosomal dominant polycystic kidney diseaseMouse models of autosomal dominant polycystic kidney diseasePolycystic kidney diseaseModel of autosomal dominant polycystic kidney diseaseKidney diseaseDeveloped primersMitochondrial oxidative stressPathophysiology of autosomal dominant polycystic kidney diseaseOxidative stressInduce apoptosisMitochondrial respirationCystic cellsUp-regulating aerobic glycolysisHomozygous inactivationMonogenic causeDominant polycystic kidney diseaseAerobic glycolysisRenal replacement therapyApoptosisEnd-stage kidney diseaseAnti-tumor agentsAdult mouse modelChronic kidney diseaseAlkylate DNA
2023
Dephosphorylation Facilitates Trafficking of Mutant Polycystin-2 to Cilia
Cai Y, Dong K, Spitzer M, Geiges L, Tian X, Krappitz M, Diggs L, Wei Z, Cordido A, Pei S, Fedeles S, Somlo S. Dephosphorylation Facilitates Trafficking of Mutant Polycystin-2 to Cilia. Journal Of The American Society Of Nephrology 2023, 34: 560-560. DOI: 10.1681/asn.20233411s1560b.Peer-Reviewed Original ResearchThe C-terminal tail of polycystin-1 suppresses cystic disease in a mitochondrial enzyme-dependent fashion
Onuchic L, Padovano V, Schena G, Rajendran V, Dong K, Shi X, Pandya R, Rai V, Gresko N, Ahmed O, Lam T, Wang W, Shen H, Somlo S, Caplan M. The C-terminal tail of polycystin-1 suppresses cystic disease in a mitochondrial enzyme-dependent fashion. Nature Communications 2023, 14: 1790. PMID: 36997516, PMCID: PMC10063565, DOI: 10.1038/s41467-023-37449-1.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsPolycystin-1Nicotinamide nucleotide transhydrogenaseTerminal tailCystic phenotypeAutosomal dominant polycystic kidney diseaseCyst cell proliferationC-terminal domainAmino acid residuesLethal monogenic disorderC-terminal cleavageNucleotide transhydrogenaseAcid residuesMitochondrial functionTransgenic expressionPKD1 geneRedox stateShort fragmentsCell proliferationMonogenic disordersDominant polycystic kidney diseasePolycystic kidney diseaseGene therapy strategiesProteinPhenotypeFragments
2022
Pkd2 Re-Expression Can Reverse Liver Cysts and Improve GFR in Mouse Models of Autosomal Dominant Polycystic Kidney Disease
Dong K, Tham M, Cordido A, Cai Y, Pei S, Bhardwaj R, Wei Z, Rehman M, Roy K, Tian X, Somlo S. Pkd2 Re-Expression Can Reverse Liver Cysts and Improve GFR in Mouse Models of Autosomal Dominant Polycystic Kidney Disease. Journal Of The American Society Of Nephrology 2022, 33: 418-418. DOI: 10.1681/asn.20223311s1418c.Peer-Reviewed Original Research
2021
FC 008INTERDEPENDENT REGULATION OF POLYCYSTIN EXPRESSION INFLUENCES STARVATION-INDUCED AUTOPHAGY AND CELL DEATH
Decuypere J, Van Giel D, Janssens P, Dong K, Somlo S, Cai Y, Mekahli D, Vennekens R. FC 008INTERDEPENDENT REGULATION OF POLYCYSTIN EXPRESSION INFLUENCES STARVATION-INDUCED AUTOPHAGY AND CELL DEATH. Nephrology Dialysis Transplantation 2021, 36: gfab125.001. DOI: 10.1093/ndt/gfab125.001.Peer-Reviewed Original ResearchConceptsAutosomal dominant polycystic kidney diseaseEarly-stage ADPKD patientsProximal tubular epithelial cellsProteins polycystin-1Renal stressADPKD patientsEarly-stage autosomal dominant polycystic kidney diseasePC1 levelsCell deathCyst formationTruncating PKD1 mutationsSevere disease progressionAutophagy upregulationDominant polycystic kidney diseaseTubular epithelial cellsRenal cell survivalPolycystic kidney diseasePolycystin-2Cell survivalCell death resistanceKidney diseaseDisease progressionGFP-LC3 punctaeSiRNA-mediated knockdownChronic starvation
2020
A shrinkage approach to joint estimation of multiple covariance matrices
Hu Z, Hu Z, Dong K, Tong T, Wang Y. A shrinkage approach to joint estimation of multiple covariance matrices. Metrika 2020, 84: 339-374. DOI: 10.1007/s00184-020-00781-3.Peer-Reviewed Original ResearchCitationsConceptsSample covariance matrixCovariance matrixMultiple covariance matricesPooled sample covariance matrixOptimal shrinkage parameterQuadratic loss functionShrinkage parameterJoint estimationNumber of groupsShrinkage approachShrinkage methodSimulation studyLoss functionMatrixInfinityEstimatorSample sizeEstimationFrameworkSAT-443 INTERDEPENDENT REGULATION OF POLYCYSTINS INFLUENCES AUTOPHAGY, CELL DEATH AND PROLIFERATION
Decuypere J, Janssens P, Dong K, Cai Y, Mekahli D, Vennekens R. SAT-443 INTERDEPENDENT REGULATION OF POLYCYSTINS INFLUENCES AUTOPHAGY, CELL DEATH AND PROLIFERATION. Kidney International Reports 2020, 5: s185. DOI: 10.1016/j.ekir.2020.02.470.Peer-Reviewed Original Research
2017
A Comparison of Methods for Estimating the Determinant of High-Dimensional Covariance Matrix
Hu Z, Dong K, Dai W, Tong T. A Comparison of Methods for Estimating the Determinant of High-Dimensional Covariance Matrix. The International Journal Of Biostatistics 2017, 13: 20170013. PMID: 28953454, DOI: 10.1515/ijb-2017-0013.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsConceptsHigh-dimensional covariance matricesCovariance matrixCovariance matrix estimationMatrix estimation methodExtensive simulation studyHigh-dimensional dataStatistical inferenceCovariance matrix estimation methodMatrix estimationComputational challengesInformation theoryEstimation methodSimulation studyHigh dimensionalityLoss functionStatistical testsComparison resultsReal applicationsInteresting comparison resultsComparison of methodsMatrixRecent proposalSample sizeDimensionalityTheoryIsolated polycystic liver disease genes define effectors of polycystin-1 function
Besse W, Dong K, Choi J, Punia S, Fedeles SV, Choi M, Gallagher AR, Huang EB, Gulati A, Knight J, Mane S, Tahvanainen E, Tahvanainen P, Sanna-Cherchi S, Lifton RP, Watnick T, Pei YP, Torres VE, Somlo S. Isolated polycystic liver disease genes define effectors of polycystin-1 function. Journal Of Clinical Investigation 2017, 127: 3558-3558. PMID: 28862642, PMCID: PMC5669574, DOI: 10.1172/jci96729.Peer-Reviewed Original ResearchCitationsConceptsPolycystin-1 functionPolycystin-1Protein biogenesis pathwaysGenome-wide basisPolycystic liver diseaseLoss-of-function mutationsWhole-exome sequencingHeterozygous loss-of-function mutationsBiogenesis pathwayLoss of functionAdditional genesDisease genesGene productsCell line modelsCandidate genesExome sequencingEndoplasmic reticulumCausative genesFunction mutationsGenesAutosomal dominant polycystic kidney diseaseDominant polycystic kidney diseaseSec63Defective maturationKidney cysts
Academic Achievements and Community Involvement
activity Member
Professional OrganizationsThe American Society of NephrologyDetails2001 - Presentactivity Renal plasticity revealed through reversal of polycystic kidney disease in mice
Oral PresentationPolycystic Kidney Disease Research Resource Consortium (PKD RRC) Annual SymposiumDetails10/27/2021 - PresentThe PKD RRC: a central coordinating site (University of Maryland); three research and translation core centers (The University of Alabama at Birmingham; Kansas University Medical Center; University of Maryland); and NIDDK. Develops and shares research resources to support innovation in PKD researchSponsored by PKD RRC Coordinating Site, University of Maryland School of Medicineactivity Member
Professional OrganizationsThe American Physiological SocietyDetails2001 - 2008activity Member
Professional OrganizationsThe American Physiological SocietyDetails2001 - 2008activity Member
Professional OrganizationsChinese Medical AssociationDetails1993 - 2001
Links & Media
News
- June 07, 2024
Polycystic Kidney Disease Treatment: Gene Target Identified at Yale
- May 04, 2023
Department of Internal Medicine Promotions
- October 21, 2022
Researchers Demonstrate XBP1 Reduces Severity of Polycystic Kidney Disease
- October 12, 2021
ADPKD is Reversible in Preclinical Models, Finds New Yale Study
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