Embryonic arrest at midgestation and disruption of Notch signaling produced by the absence of both epsin 1 and epsin 2 in mice
Chen H, Ko G, Zatti A, Di Giacomo G, Liu L, Raiteri E, Perucco E, Collesi C, Min W, Zeiss C, De Camilli P, Cremona O. Embryonic arrest at midgestation and disruption of Notch signaling produced by the absence of both epsin 1 and epsin 2 in mice. Proceedings Of The National Academy Of Sciences Of The United States Of America 2009, 106: 13838-13843. PMID: 19666558, PMCID: PMC2728981, DOI: 10.1073/pnas.0907008106.Peer-Reviewed Original ResearchConceptsEndocytic adaptorsRole of epsinsClathrin-mediated endocytosisSpecific membrane proteinsDouble knockout embryosPrimary target genesBeginning of organogenesisActivation of NotchEmbryonic lethalityPutative functionsKnockout embryosEmbryonic arrestMembrane proteinsGenetic approachesTarget genesDKO embryosNotch activationNotch signalingEndocytic functionDevelopmental defectsGenesEpsinEmbryosInactivation resultsEndocytosis