2023
Novel epigenetic molecular therapies for imprinting disorders
Wang S, Jiang Y. Novel epigenetic molecular therapies for imprinting disorders. Molecular Psychiatry 2023, 28: 3182-3193. PMID: 37626134, PMCID: PMC10618104, DOI: 10.1038/s41380-023-02208-7.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsActive alleleImprinting disordersMolecular mechanismsGenome editing approachesEpigenetic-based therapiesUnique molecular mechanismGenomic imprinting disordersImprinted genesGenome editingMolecular approachesEditing approachesInactive allelesNew therapeutic strategiesAllelesSmall moleculesMolecular therapyTherapeutic strategies
2019
Epigenetic therapy of Prader–Willi syndrome
Kim Y, Wang SE, Jiang YH. Epigenetic therapy of Prader–Willi syndrome. Translational Research 2019, 208: 105-118. PMID: 30904443, PMCID: PMC6527448, DOI: 10.1016/j.trsl.2019.02.012.Peer-Reviewed Original ResearchConceptsPWS mouse modelEpigenetic-based therapiesMaternal chromosomesImprinted gene regulationEHMT2/G9aLysine 9 methyltransferasePatient-derived fibroblastsPrader-Willi syndromeGene regulationMethyltransferase SETDB1Epigenetic mechanismsSmall molecule librariesPWS genesHigh-content screeningSame genePerinatal lethalityEpigenetic therapyFusion proteinMolecular mechanismsG9a inhibitorChromosomesSNORD116 clusterGenesMolecular defectsPatient iPSC
2018
CRISPR/Cas9-induced shank3b mutant zebrafish display autism-like behaviors
Liu CX, Li CY, Hu CC, Wang Y, Lin J, Jiang YH, Li Q, Xu X. CRISPR/Cas9-induced shank3b mutant zebrafish display autism-like behaviors. Molecular Autism 2018, 9: 23. PMID: 29619162, PMCID: PMC5879542, DOI: 10.1186/s13229-018-0204-x.Peer-Reviewed Original ResearchConceptsMutant zebrafishMutant zebrafish modelGenome editing techniquesGene editing approachesZebrafish genomeOrthologous genesAttractive organismGenomic studiesCRISPR/Cas9 gene editing approachGenetic manipulationZebrafish modelCRISPR/ZebrafishMolecular mechanismsEditing approachesAdult stageFunction mutationsMolecular analysisEditing techniquesMolecular changesAutism-like behaviorsEarly developmentSwimming behaviorPresynaptic synaptophysinMorphological measurements
2013
The Angelman Syndrome Protein Ube3a Is Required for Polarized Dendrite Morphogenesis in Pyramidal Neurons
Miao S, Chen R, Ye J, Tan G, Li S, Zhang J, Jiang Y, Xiong Z. The Angelman Syndrome Protein Ube3a Is Required for Polarized Dendrite Morphogenesis in Pyramidal Neurons. Journal Of Neuroscience 2013, 33: 327-333. PMID: 23283345, PMCID: PMC6618628, DOI: 10.1523/jneurosci.2509-12.2013.Peer-Reviewed Original ResearchConceptsPyramidal neuronsApical dendritesLong apical dendritesNeuron dendritic arborsDendrite outgrowthUbiquitin protein ligase E3ANovel pathological mechanismBasal dendritesCorticospinal tractDendritic arborsMouse modelPathological mechanismsMammalian prefrontal cortexExcitatory cellsPrefrontal cortexNeuronsDendrite morphogenesisCellular mechanismsDendritic morphologySelective inhibitionUBE3AMiceDendritesMolecular mechanismsDownregulation