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 metastasesCHI3L1SignalingAkt
2011
Role of Chitin and Chitinase/Chitinase-Like Proteins in Inflammation, Tissue Remodeling, and Injury
Lee CG, Da Silva CA, Dela Cruz CS, Ahangari F, Ma B, Kang MJ, He CH, Takyar S, Elias JA. Role of Chitin and Chitinase/Chitinase-Like Proteins in Inflammation, Tissue Remodeling, and Injury. Annual Review Of Physiology 2011, 73: 479-501. PMID: 21054166, PMCID: PMC3864643, DOI: 10.1146/annurev-physiol-012110-142250.Peer-Reviewed Original ResearchConceptsBRP-39/YKLAdaptive Th2 immunityTissue remodelingChitinase-like proteinsAlternative macrophage activationTh2 inflammationInnate inflammationLung injuryTh2 immunityAcidic mammalian chitinaseAncient gene familyIL-13YKL-40Tissue injuryNumber of chitinasesEffector functionsMacrophage activationFamily of chitinasesInflammationDisease severityInjuryRole of chitinMammalian chitinaseGene familyEndogenous chitin
2001
Atm knock-in mice harboring an in-frame deletion corresponding to the human ATM 7636del9 common mutation exhibit a variant phenotype.
Spring K, Cross S, Li C, Watters D, Ben-Senior L, Waring P, Ahangari F, Lu SL, Chen P, Misko I, Paterson C, Kay G, Smorodinsky NI, Shiloh Y, Lavin MF. Atm knock-in mice harboring an in-frame deletion corresponding to the human ATM 7636del9 common mutation exhibit a variant phenotype. Cancer Research 2001, 61: 4561-8. PMID: 11389091.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisAtaxia TelangiectasiaAtaxia Telangiectasia Mutated ProteinsBase SequenceCell Cycle ProteinsCrosses, GeneticDNADNA-Binding ProteinsFemaleHumansLymphomaMaleMiceMice, Inbred C57BLMice, KnockoutMice, Mutant StrainsMutagenesis, Site-DirectedPhenotypeProtein Serine-Threonine KinasesSequence DeletionThymus NeoplasmsTumor Suppressor ProteinsUp-RegulationConceptsAtaxia telangiectasiaFrame deletionDisorder ataxia-telangiectasiaProtein kinase activityCell cycle checkpointsAmino acid residuesSelectable marker cassetteDetectable ATM proteinMutant proteinsATM proteinCycle checkpointsHomologous recombinationKinase activityAcid residuesMarker cassetteCommon deletion mutationsDeletion mutationsDeletion resultsCre-loxPATM geneThymic lymphomasExtensive apoptosisVariant phenotypesDifferent phenotypesFas ligand