2024
Identification and validation of urinary CXCL9 as a biomarker for diagnosis of acute interstitial nephritis
Moledina D, Obeid W, Smith R, Rosales I, Sise M, Moeckel G, Kashgarian M, Kuperman M, Campbell K, Lefferts S, Meliambro K, Bitzer M, Perazella M, Luciano R, Pober J, Cantley L, Colvin R, Wilson F, Parikh C. Identification and validation of urinary CXCL9 as a biomarker for diagnosis of acute interstitial nephritis. Journal Of Clinical Investigation 2024, 134: e180583. PMID: 38488004, PMCID: PMC10940080, DOI: 10.1172/jci180583.Peer-Reviewed Original Research
2023
Analysis of the human kidney transcriptome and plasma proteome identifies markers of proximal tubule maladaptation to injury
Wen Y, Su E, Xu L, Menez S, Moledina D, Obeid W, Palevsky P, Mansour S, Devarajan P, Cantley L, Cahan P, Parikh C, Project K, Injury T. Analysis of the human kidney transcriptome and plasma proteome identifies markers of proximal tubule maladaptation to injury. Science Translational Medicine 2023, 15: eade7287. PMID: 38091407, PMCID: PMC11405121, DOI: 10.1126/scitranslmed.ade7287.Peer-Reviewed Original ResearchThe ASSESS-AKI Study found urinary epidermal growth factor is associated with reduced risk of major adverse kidney events
Menez S, Wen Y, Xu L, Moledina D, Thiessen-Philbrook H, Hu D, Obeid W, Bhatraju P, Ikizler T, Siew E, Chinchilli V, Garg A, Go A, Liu K, Kaufman J, Kimmel P, Himmelfarb J, Coca S, Cantley L, Parikh C. The ASSESS-AKI Study found urinary epidermal growth factor is associated with reduced risk of major adverse kidney events. Kidney International 2023, 104: 1194-1205. PMID: 37652206, PMCID: PMC10840723, DOI: 10.1016/j.kint.2023.08.007.Peer-Reviewed Original ResearchConceptsMajor adverse kidney eventsUEGF/CrUrinary epidermal growth factorAdverse kidney eventsChronic kidney diseaseEpidermal growth factorKidney eventsKidney failureEGF expressionUrinary EGF/CrAcute Kidney Injury studyGrowth factorIschemia-reperfusion injuryProportional hazards regressionTubular healthKidney atrophyObservational cohortHospitalized participantsTubular functionClinical findingsHazards regressionKidney diseaseClinical variablesProgressive atrophyUrinary EGFIdentification and validation of urinary CXCL9 as a biomarker for diagnosis of acute interstitial nephritis
Moledina D, Obeid W, Smith R, Rosales I, Sise M, Moeckel G, Kashgarian M, Kuperman M, Campbell K, Lefferts S, Meliambro K, Bitzer M, Perazella M, Luciano R, Pober J, Cantley L, Colvin R, Wilson F, Parikh C. Identification and validation of urinary CXCL9 as a biomarker for diagnosis of acute interstitial nephritis. Journal Of Clinical Investigation 2023, 133: e168950. PMID: 37395276, PMCID: PMC10313360, DOI: 10.1172/jci168950.Peer-Reviewed Original ResearchConceptsUrinary CXCL9External validation cohortValidation cohortControl groupAIN diagnosisDiscovery cohortKidney tissueDiagnostic biomarkersAcute interstitial nephritisCXCL9 mRNA expressionAcute kidney injuryBiopsy-confirmed diagnosisAvailable clinical testsNational InstituteKidney injuryTubulointerstitial nephritisInterstitial nephritisKidney biopsyHistological confirmationHistological diagnosisTreatment optionsLymphocyte chemotaxisCXCL9MRNA expression differencesPatientsThe Lymphatic System in Kidney Disease
Baker M, Cantley L. The Lymphatic System in Kidney Disease. Kidney360 2023, 4: e841-e850. PMID: 37019177, PMCID: PMC10371377, DOI: 10.34067/kid.0000000000000120.Peer-Reviewed Original ResearchConceptsKidney diseaseLymphatic systemSetting of AKIKidney allograft rejectionNormal kidney functionImmune response modulationAllograft rejectionLymph nodesInflammatory infiltrateKidney functionImmune cellsTissue edemaNovel therapiesImmune surveillanceNumerous disease statesSystemic circulationFluid removalKidney tissueResident cellsTherapeutic potentialSurveillance cellsAKIDisease statesKidneyResponse modulationThe ion transporter Na+-K+-ATPase enables pathological B cell survival in the kidney microenvironment of lupus nephritis
Chernova I, Song W, Steach H, Hafez O, Al Souz J, Chen P, Chandra N, Cantley L, Veselits M, Clark M, Craft J. The ion transporter Na+-K+-ATPase enables pathological B cell survival in the kidney microenvironment of lupus nephritis. Science Advances 2023, 9: eadf8156. PMID: 36724234, PMCID: PMC9891690, DOI: 10.1126/sciadv.adf8156.Peer-Reviewed Original ResearchConceptsB cellsAutoimmune diseasesAmelioration of proteinuriaLupus nephritis biopsiesB cell infiltrationSodium-potassium adenosine triphosphataseB cell survivalPotassium adenosine triphosphataseLupus nephritisCell infiltrationKidney microenvironmentTissue injuryTherapeutic targetPharmacological inhibitionElevated sodium concentrationLupusHostile microenvironmentHigh expressionKidneySodium concentrationGenetic knockoutCell survivalDiseaseCellsAdenosine triphosphatase
2022
Multi-Scalar Data Integration Links Glomerular Angiopoietin-Tie Signaling Pathway Activation With Progression of Diabetic Kidney Disease
Liu J, Nair V, Zhao Y, Chang D, Limonte C, Bansal N, Fermin D, Eichinger F, Tanner E, Bellovich K, Steigerwalt S, Bhat Z, Hawkins J, Subramanian L, Rosas S, Sedor J, Vasquez M, Waikar S, Bitzer M, Pennathur S, Brosius F, De Boer I, Chen M, Kretzler M, Ju W, Group F, Knight R, Lecker S, Stillman I, Bogen S, Amodu A, Ilori T, Maikhor S, Schmidt I, Beck L, Henderson J, Onul I, Verma A, Waikar S, McMahon G, Valerius M, Waikar S, Weins A, Colona M, Greka A, Hacohen N, Hoover P, Marshall J, Aulisio M, Chen Y, Janowczyk A, Jayapandian C, Viswanathan V, Bush W, Crawford D, Madabhushi A, Bush L, Cooperman L, Gonzalez-Vicente A, Herlitz L, Jolly S, Nguyen J, O’toole J, Palmer E, Poggio E, Sedor J, Sendrey D, Spates-Harden K, Taliercio J, Bjornstad P, Pyle L, Vinovskis C, Appelbaum P, Barasch J, Bomback A, Canetta P, D’Agati V, Kiryluk K, Kudose S, Mehl K, Shang N, Balderes O, Bansal S, Alexandrov T, Rennke H, El-Achkar T, Barwinska D, Bledsoe S, Borner K, Bueckle A, Cheng Y, Dagher P, Dunn K, Eadon M, Ferkowicz M, Herr B, Kelly K, Ferreira R, Quardokus E, Record E, Rivera M, Su J, Sutton T, Williams J, Winfree S, Menez S, Parikh C, Rosenberg A, Corona-Villalobos C, Wen Y, Johansen C, Rosas S, Roy N, Sun J, Williams M, Azeloglu E, Hansen J, He C, Iyengar R, Xiong Y, Prasad P, Srivastava A, Madhavan S, Parikh S, Rovin B, Shapiro J, Anderton C, Lukowski J, Pasa-Tolic L, Velickovic D, Oliver G, Ardayfio J, Bebiak J, Brown K, Campbell T, Campbell C, Hayashi L, Jefferson N, Roberts G, Saul J, Shpigel A, Stutzke C, Koewler R, Pinkeney R, Sealfon R, Troyanskaya O, Wong A, Tuttle K, Pollack A, Goltsev Y, Lucarelli N, Sarder P, Lake B, Zhang K, Boada P, Laszik Z, Nolan G, Anjani K, Sarwal M, Mukatash T, Sigdel T, Alloway R, Burg A, Lee P, Rike A, Shi T, Woodle E, Balis U, Blanc V, Conser N, Eddy S, Frey R, He Y, Hodgin J, Kretzler M, Lienczewski C, Luo J, Mariani L, Menon R, Otto E, Schaub J, Steck B, Elder M, Gilliam M, Hall D, Murugan R, Palevsky P, Randhawa P, Rosengart M, Tublin M, Vita T, Kellum J, Winters J, Alpers C, Berglund A, Blank K, Carson J, Daniel S, De Boer I, Dighe A, Dowd F, Grewenow S, Himmelfarb J, Hoofnagle A, Limonte C, McClelland R, Mooney S, Rezaei K, Shankland S, Snyder J, Wang R, Wilcox A, Williams K, Park C, Bansal S, Montellano R, Pamreddy A, Sharma K, Venkatachalam M, Ye H, Zhang G, Hedayati S, Kermani A, Lee S, Lu C, Miller R, Moe O, Patel J, Pillai A, Sambandam K, Torrealba J, Toto R, Vazquez M, Wang N, Wen N, Zhang D, Park H, Caprioli R, Patterson N, Sharman K, Spraggins J, Van de Plas R, Basta J, Diettman S, Gaut J, Jain S, Rauchman M, Vijayan A, Cantley L, Kakade V, Moledina D, Shaw M, Ugwuowo U, Wilson F, Arora T, Bitzer M, Brosius F, Gadegbeku C, Gipson D, Hawkins J, Kretzler M, Lienczewski C, Pennathur S, Troost J, Gadegbeku C, Bellovich K, Bhat Z, Massengill S, Perumal K. Multi-Scalar Data Integration Links Glomerular Angiopoietin-Tie Signaling Pathway Activation With Progression of Diabetic Kidney Disease. Diabetes 2022, 71: 2664-2676. PMID: 36331122, PMCID: PMC9750948, DOI: 10.2337/db22-0169.Peer-Reviewed Original ResearchConceptsEnd-stage kidney diseaseDiabetic kidney diseaseKidney diseaseAngiopoietin-2ANGPT2 levelsChinese cohort studyChronic kidney diseaseGlomerular filtration rateCardiovascular Health StudyPlasma angiopoietin-2High receptor expressionStandard clinical parametersSignaling Pathway ActivationPathway scoresThree-marker panelKidney outcomesCohort studyComposite outcomeClinical parametersEndothelial biomarkersFiltration rateReceptor expressionPrognostic biomarkerClinical phenotypingHealth StudyMortality after acute kidney injury and acute interstitial nephritis in patients prescribed immune checkpoint inhibitor therapy
Baker ML, Yamamoto Y, Perazella MA, Dizman N, Shirali AC, Hafez N, Weinstein J, Simonov M, Testani JM, Kluger HM, Cantley LG, Parikh CR, Wilson FP, Moledina DG. Mortality after acute kidney injury and acute interstitial nephritis in patients prescribed immune checkpoint inhibitor therapy. Journal For ImmunoTherapy Of Cancer 2022, 10: e004421. PMID: 35354588, PMCID: PMC8968986, DOI: 10.1136/jitc-2021-004421.Peer-Reviewed Original ResearchConceptsAcute interstitial nephritisAcute kidney injuryImmune checkpoint inhibitor therapyCheckpoint inhibitor therapyICI therapyKidney injuryInhibitor therapyInterstitial nephritisTime-varying Cox proportional hazards modelsHigher peak serum creatinineSevere acute kidney injuryCancer typesCox proportional hazards modelAssociations of biopsyBaseline laboratory valuesObservational cohort studyPeak serum creatinineFavorable treatment responseProportional hazards modelAKI patientsTherapy initiationCohort studySerum creatinineUnivariable analysisImmune activationCharacterization of temporospatial distribution of renal tubular casts by nephron tracking after ischemia-reperfusion injury
Shin NS, Marlier A, Xu L, Lam T, Cantley LG, Guo JK. Characterization of temporospatial distribution of renal tubular casts by nephron tracking after ischemia-reperfusion injury. American Journal Of Physiology. Renal Physiology 2022, 322: f322-f334. PMID: 35100823, PMCID: PMC8897010, DOI: 10.1152/ajprenal.00284.2021.Peer-Reviewed Original ResearchConceptsIschemia-reperfusion injuryCast formationGlomerular filtration rateTubular cast formationUrine 24 hDetached epithelial cellsDead cell debrisRenal recoveryRenal functionFiltration rateS3 tubulesTubular castsTubular cellsTubular nucleiKidney sectionsOuter medullaTrypsin levelsEntire nephronRenal tubular castsFuture interventionsInjurySelective lossTubule segmentsEpithelial cellsKidney
2021
Development and external validation of a diagnostic model for biopsy-proven acute interstitial nephritis using electronic health record data
Moledina DG, Eadon MT, Calderon F, Yamamoto Y, Shaw M, Perazella MA, Simonov M, Luciano R, Schwantes-An TH, Moeckel G, Kashgarian M, Kuperman M, Obeid W, Cantley LG, Parikh CR, Wilson FP. Development and external validation of a diagnostic model for biopsy-proven acute interstitial nephritis using electronic health record data. Nephrology Dialysis Transplantation 2021, 37: 2214-2222. PMID: 34865148, PMCID: PMC9755995, DOI: 10.1093/ndt/gfab346.Peer-Reviewed Original ResearchConceptsAcute interstitial nephritisInterstitial nephritisUrine biomarkersBiopsy-proven acute interstitial nephritisElectronic health record dataExternal validation cohortTypical clinical featuresBlood urea nitrogenTumor necrosis factorCharacteristic curve analysisHealth record dataExternal validationElectronic health recordsAIN diagnosisModest AUCsSerum creatinineCreatinine ratioKidney biopsyClinical featuresValidation cohortNecrosis factorUnrecognized casesInterleukin-9PatientsUrea nitrogenCadherin-11, Sparc-related modular calcium binding protein-2, and Pigment epithelium-derived factor are promising non-invasive biomarkers of kidney fibrosis
Schmidt I, Colona M, Kestenbaum B, Alexopoulos L, Palsson R, Srivastava A, Liu J, Stillman I, Rennke H, Vaidya V, Wu H, Humphreys B, Waikar S, Knight R, Lecker S, Stillman I, Bogen S, Amodu A, Ilori T, Maikhor S, Schmidt I, Beck L, Henderson J, Onul I, Verma A, McMahon G, Valerius M, Waikar S, Weins A, Colona M, Greka A, Hacohen N, Hoover P, Marshall J, Aulisio M, Chen Y, Janowczyk A, Jayapandian C, Viswanathan V, Bush W, Crawford D, Madabhushi A, Bush L, Cooperman L, Gonzalez-Vicente A, Herlitz L, Jolly S, Nguyen J, O’toole J, Palmer E, Poggio E, Sedor J, Sendrey D, Spates-Harden K, Taliercio J, Bjornstad P, Pyle L, Vinovskis C, Appelbaum P, Balderes O, Barasch J, Bomback A, Canetta P, D’Agati V, Kiryluk K, Kudose S, Mehl K, Shang N, Bansal S, Alexandrov T, Rennke H, El-Achkar T, Barwinska D, Bledso S, Borner K, Bueckle A, Cheng Y, Dagher P, Dunn K, Eadon M, Ferkowicz M, Herr B, Kelly K, Ferreira R, Quardokus E, Record E, Rivera M, Su J, Sutton T, Williams J, Winfree S, Jain Y, Menez S, Parikh C, Rosenberg A, Corona-Villalobos C, Wen Y, Johansen C, Rosas S, Roy N, Sun J, Williams M, Azeloglu E, Hansen J, He C, Iyengar R, Xiong Y, Prasad P, Srivastava A, Madhavan S, Parikh S, Rovin B, Shapiro J, Anderton C, Lukowski J, Pasa-Tolic L, Velickovic D, Oliver G, Ardayfio J, Bebiak J, Brown K, Campbell T, Campbell C, Hayashi L, Jefferson N, Roberts G, Saul J, Shpigel A, Stutzke C, Koewler R, Pinkeney R, Sealfon R, Troyanskaya O, Wong A, Tuttle K, Pollack A, Goltsev Y, Ginley B, Lucarelli N, Lutnick B, Sarder P, Lake B, Zhang K, Boada P, Laszik Z, Nolan G, Anjani K, Sarwal M, Mukatash T, Sigdel T, Alloway R, Burg A, Lee P, Rike A, Shi T, Woodle E, Ascani H, Balis U, Blanc V, Conser N, Eddy S, Frey R, He Y, Hodgin J, Kretzler M, Lienczewski C, Luo J, Mariani L, Menon R, Otto E, Schaub J, Steck B, Elder M, Gilliam M, Hall D, Murugan R, Palevsky P, Randhawa P, Rosengart M, Tublin M, Vita T, Winters J, Kellum J, Alpers C, Berglund A, Berry B, Blank K, Carson J, Daniel S, De Boer I, Dighe A, Dowd F, Grewenow S, Himmelfarb J, Hoofnagle A, Limonte C, McClelland R, Mooney S, Rezaei K, Shankland S, Snyder J, Wang R, Wilcox A, Williams K, Park C, Bansal S, Montellano R, Pamreddy A, Sharma K, Venkatachalam M, Ye H, Zhang G, Basit M, Hedayati S, Kermani A, Lee S, Lu C, Miller R, Moe O, Patel J, Pillai A, Sambandam K, Torrealba J, Toto R, Vazquez M, Wang N, Wen N, Zhang D, Park H, Caprioli R, Patterson N, Sharman K, Spraggins J, Van de Plas R, Basta J, Diettman S, Gaut J, Jain S, Rauchman M, Vijayan A, Cantley L, Kakade V, Moledina D, Shaw M, Ugwuowo U, Wilson F, Arora T. Cadherin-11, Sparc-related modular calcium binding protein-2, and Pigment epithelium-derived factor are promising non-invasive biomarkers of kidney fibrosis. Kidney International 2021, 100: 672-683. PMID: 34051265, PMCID: PMC8384690, DOI: 10.1016/j.kint.2021.04.037.Peer-Reviewed Original ResearchConceptsPigment epithelium-derived factorBoston Kidney Biopsy CohortEnd-stage kidney diseaseChronic kidney diseaseModular calcium binding protein-2Seattle Kidney StudyKidney fibrosisKidney diseaseEpithelium-derived factorNon-invasive biomarkersBiopsy cohortTubular atrophyInterstitial fibrosisKidney StudyBinding protein 2Cox proportional hazards regression modelHuman chronic kidney diseaseProportional hazards regression modelsUrine biomarker levelsCohort of patientsHazards regression modelsPromising non-invasive biomarkerIndependent prospective cohortsAssociation of biomarkersNon-invasive assessment
2020
Polycystin 2 is increased in disease to protect against stress-induced cell death
Brill AL, Fischer TT, Walters JM, Marlier A, Sewanan LR, Wilson PC, Johnson EK, Moeckel G, Cantley LG, Campbell SG, Nerbonne JM, Chung HJ, Robert ME, Ehrlich BE. Polycystin 2 is increased in disease to protect against stress-induced cell death. Scientific Reports 2020, 10: 386. PMID: 31941974, PMCID: PMC6962458, DOI: 10.1038/s41598-019-57286-x.Peer-Reviewed Original ResearchConceptsPolycystin-2General cellular homeostasisCell deathStress-induced cell deathPathological cell deathAutosomal dominant polycystic kidney diseaseEndoplasmic reticulum membraneCellular homeostasisCellular stressPrimary ciliaUbiquitous expressionExpression changesCell stressReticulum membraneTransient receptor potential cation channelHuman diseasesMultiple tissuesEndogenous roleDominant polycystic kidney diseaseTissue typesCation channelsPolycystic kidney diseaseDifferent pathological statesMultiple diseasesKidney disease
2019
Development of a 2-dimensional atlas of the human kidney with imaging mass cytometry
Singh N, Avigan ZM, Kliegel JA, Shuch BM, Montgomery RR, Moeckel GW, Cantley LG. Development of a 2-dimensional atlas of the human kidney with imaging mass cytometry. JCI Insight 2019, 4: e129477. PMID: 31217358, PMCID: PMC6629112, DOI: 10.1172/jci.insight.129477.Peer-Reviewed Original ResearchConceptsCell typesIndividual cell typesCritical baseline dataRenal cell typesMass cytometryQuantitative atlasNormal human samplesHuman kidneyRelative abundanceDevelopment of therapiesHuman kidney diseaseKidney diseaseMetal-conjugated antibodiesQuantitative interrogationScarce samplesMachine-learning pipelineDiscovery purposesFuture quantitative analysisNovel abnormalityNormal human kidneySingle tissue sectionHuman samplesRenal biopsyImmune cellsCellsUrine TNF-α and IL-9 for clinical diagnosis of acute interstitial nephritis
Moledina DG, Wilson FP, Pober JS, Perazella MA, Singh N, Luciano RL, Obeid W, Lin H, Kuperman M, Moeckel GW, Kashgarian M, Cantley LG, Parikh CR. Urine TNF-α and IL-9 for clinical diagnosis of acute interstitial nephritis. JCI Insight 2019, 4: e127456. PMID: 31092735, PMCID: PMC6542610, DOI: 10.1172/jci.insight.127456.Peer-Reviewed Original ResearchConceptsAcute interstitial nephritisAcute kidney diseasePrebiopsy diagnosisKidney biopsyKidney diseaseIL-9AIN diagnosisUrine TNFInterstitial nephritisSpecific T cell subsetsAcute tubular injuryDiabetic kidney diseaseIL-9 levelsTNF-α levelsT cell subsetsAddition of biomarkersPlasma cytokinesCytokine levelsTubular injuryHighest quartileMultivariable analysisCell subsetsUrinary TNFBlood eosinophilsGlomerular disease
2018
Mcp1 Promotes Macrophage-Dependent Cyst Expansion in Autosomal Dominant Polycystic Kidney Disease
Cassini MF, Kakade VR, Kurtz E, Sulkowski P, Glazer P, Torres R, Somlo S, Cantley LG. Mcp1 Promotes Macrophage-Dependent Cyst Expansion in Autosomal Dominant Polycystic Kidney Disease. Journal Of The American Society Of Nephrology 2018, 29: 2471-2481. PMID: 30209078, PMCID: PMC6171277, DOI: 10.1681/asn.2018050518.Peer-Reviewed Original ResearchConceptsAutosomal dominant polycystic kidney diseaseSingle knockout miceTubular cell injuryDominant polycystic kidney diseaseCyst growthPolycystic kidney diseaseKidney diseaseCell injuryMonocyte chemoattractant protein-1Alternative activation phenotypeChemoattractant protein-1Double knockout miceOrthologous mouse modelCell proliferative rateRenal functionMacrophage accumulationMacrophage infiltrationReceptor CCR2Cystic dilationMacrophage numbersFunctional improvementOxidative DNA damageMouse modelActivation phenotypeCyst expansion
2015
Development of a Targeted Urine Proteome Assay for kidney diseases
Cantley LG, Colangelo CM, Stone KL, Chung L, Belcher J, Abbott T, Cantley JL, Williams KR, Parikh CR. Development of a Targeted Urine Proteome Assay for kidney diseases. Proteomics Clinical Applications 2015, 10: 58-74. PMID: 26220717, PMCID: PMC5003777, DOI: 10.1002/prca.201500020.Peer-Reviewed Original ResearchConceptsKidney diseaseUrinary proteinGraft functionImmediate graft functionDelayed graft functionKidney transplant patientsMultiple kidney diseasesTransplant patientsKidney transplantClinical relevancePotential biomarkersUrine proteomeDiseaseAvailable biofluidBiomarkersPatientsProtein biomarkersAssaysSingle assayProteome changesHuman urineQuantifiable proteinsTransplantProteinPeptides
2014
Casein kinase 2 prevents mesenchymal transformation by maintaining Foxc2 in the cytoplasm
Golden D, Cantley LG. Casein kinase 2 prevents mesenchymal transformation by maintaining Foxc2 in the cytoplasm. Oncogene 2014, 34: 4702-4712. PMID: 25486430, PMCID: PMC4459945, DOI: 10.1038/onc.2014.395.Peer-Reviewed Original ResearchConceptsCK2β regulatory subunitSerine 124Epithelial-mesenchymal transitionRegulatory subunitNuclear localizationCytoplasmic localizationCasein kinase 2 phosphorylation sitesDevelopmental epithelial-mesenchymal transitionMesenchymal transformationCell migrationEpithelial cellsDe novo accumulationCK2 associatesTranscriptional regulatorsMalignant breast cancer cellsPhosphorylation sitesCK2β expressionKinase subunitMesenchymal genesBreast epithelial cellsProper targetingAmino terminusNormal breast epithelial cellsNormal epithelial cellsLeucine promotesHepatocyte Growth Factor (Hgf) Stimulates Low Density Lipoprotein Receptor-related Protein (Lrp) 5/6 Phosphorylation and Promotes Canonical Wnt Signaling*
Koraishy FM, Silva C, Mason S, Wu D, Cantley LG. Hepatocyte Growth Factor (Hgf) Stimulates Low Density Lipoprotein Receptor-related Protein (Lrp) 5/6 Phosphorylation and Promotes Canonical Wnt Signaling*. Journal Of Biological Chemistry 2014, 289: 14341-14350. PMID: 24692544, PMCID: PMC4022900, DOI: 10.1074/jbc.m114.563213.Peer-Reviewed Original ResearchConceptsΒ-catenin stabilizationRenal ischemic injuryLRP5/6 phosphorylationEpithelial cell responsesRenal proximal tubulesEpithelial cell apoptosisHepatocyte growth factorCanonical WntActive GSK3Ischemic injuryRenal epithelial cellsProximal tubulesCell responsesCanonical Wnt signalingHGF treatmentGrowth factorCell apoptosisEpithelial cellsHGFMet receptorImportant transactivatorWnt signalingInjuryLRP5/6MetS
2013
Chitinase 3-like 1 Regulates Cellular and Tissue Responses via IL-13 Receptor α2
He CH, Lee CG, Dela Cruz CS, Lee CM, Zhou Y, Ahangari F, Ma B, Herzog EL, Rosenberg SA, Li Y, Nour AM, Parikh CR, Schmidt I, Modis Y, Cantley L, Elias JA. Chitinase 3-like 1 Regulates Cellular and Tissue Responses via IL-13 Receptor α2. Cell Reports 2013, 4: 830-841. PMID: 23972995, PMCID: PMC3988532, DOI: 10.1016/j.celrep.2013.07.032.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisChitinase-3-Like Protein 1GlycoproteinsHumansInflammasomesInterleukin-13Interleukin-13 Receptor alpha2 SubunitLung NeoplasmsMacrophagesMAP Kinase Signaling SystemMelanomaMiceMice, Inbred C57BLOxidative StressProtein BindingTransforming Growth Factor betaWnt Signaling PathwayConceptsProtein kinase B/AktWnt/β-catenin signalingΒ-catenin signalingCritical roleGene familyMultimeric complexesProtein kinaseMacrophage mitogenDisease toleranceCell deathAntibacterial responseReceptor α2Antipathogen responsesChitinase 3IL-13Rα2IL-13 receptor α2Inflammasome activationBacterial killingKinaseOxidant injuryReceptorsMelanoma metastasesCHI3L1SignalingAktChitinase-Like Protein Brp-39/YKL-40 Modulates the Renal Response to Ischemic Injury and Predicts Delayed Allograft Function
Schmidt IM, Hall IE, Kale S, Lee S, He CH, Lee Y, Chupp GL, Moeckel GW, Lee CG, Elias JA, Parikh CR, Cantley LG. Chitinase-Like Protein Brp-39/YKL-40 Modulates the Renal Response to Ischemic Injury and Predicts Delayed Allograft Function. Journal Of The American Society Of Nephrology 2013, 24: 309-319. PMID: 23291472, PMCID: PMC3559482, DOI: 10.1681/asn.2012060579.Peer-Reviewed Original ResearchMeSH KeywordsAdipokinesAnimalsApoptosisBiomarkersCells, CulturedChitinase-3-Like Protein 1Delayed Graft FunctionDisease Models, AnimalEpithelial CellsGlycoproteinsHumansKidneyKidney TransplantationLectinsMacrophagesMaleMiceMice, Inbred C57BLPhosphatidylinositol 3-KinasesPredictive Value of TestsProto-Oncogene Proteins c-aktReperfusion InjurySignal TransductionTransplantation, HomologousConceptsBRP-39/YKLGraft functionKidney injuryYKL-40Reparative responseDeceased donor kidney transplantationKidney ischemia/reperfusionHours of transplantImmediate graft functionDelayed graft functionTubular cell deathIschemia/reperfusionDegree of injuryAllograft functionCell apoptotic deathKidney hypoperfusionKidney transplantationSystemic hypotensionRenal failureIschemic injuryRenal ischemiaRenal responseUrinary levelsBRP-39Activation of Akt