Saftig, Paul

[["dc.bibliographiccitation.firstpage","3599"],["dc.bibliographiccitation.issue","15"],["dc.bibliographiccitation.journal","The EMBO Journal"],["dc.bibliographiccitation.lastpage","3608"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Saftig, Paul"],["dc.contributor.author","Hetmann, Michal"],["dc.contributor.author","Schmahl, Wolfgang"],["dc.contributor.author","Weber, Karin"],["dc.contributor.author","Heine, Lutz"],["dc.contributor.author","Mossmann, Horst"],["dc.contributor.author","Köster, Anja"],["dc.contributor.author","Hess, Barbara"],["dc.contributor.author","Evers, Meike"],["dc.contributor.author","Figura, Kurt von"],["dc.contributor.author","Peters, Christoph"],["dc.date.accessioned","2019-07-10T08:12:47Z"],["dc.date.available","2019-07-10T08:12:47Z"],["dc.date.issued","1995"],["dc.description.abstract","Mice deficient for the major lysosomal aspartic proteinase cathepsin D, generated by gene targeting, develop normally during the first 2 weeks, stop thriving in the third week and die in a state of anorexia at day 26 +- 1."],["dc.format.mimetype","application/pdf"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/3449"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/61037"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0261-4189"],["dc.rights","Goescholar"],["dc.rights.access","openAccess"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject","cathepsin; gene targeting; intestinal atrophy; lymphoid destruction; proteolysis"],["dc.subject.ddc","610"],["dc.title","Mice deficient for the lysosomal proteinase cathepsin D exhibit progressive atrophy of the intestinal mucosa and profound destruction of lyphoid cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","902"],["dc.bibliographiccitation.journal","Nature"],["dc.bibliographiccitation.lastpage","906"],["dc.bibliographiccitation.volume","406"],["dc.contributor.author","Tanaka, Yoshitaka"],["dc.contributor.author","Guhde, Gundula"],["dc.contributor.author","Suter, Anke"],["dc.contributor.author","Eskelinen, Eeva-Liisa"],["dc.contributor.author","Hartmann, Dieter"],["dc.contributor.author","Lüllmann-Rauch, Renate"],["dc.contributor.author","Blanz, Judith"],["dc.contributor.author","Figura, Kurt von"],["dc.contributor.author","Saftig, Paul"],["dc.contributor.author","Janssen, Paul M. L."],["dc.date.accessioned","2019-07-10T08:12:47Z"],["dc.date.available","2019-07-10T08:12:47Z"],["dc.date.issued","2000"],["dc.description.abstract","Lysosome-associated membrane protein-2 (LAMP-2) is a highly glycosylated protein and an important constituent of the lysosomal membrane1–7. Here we show that LAMP-2 deficiency in mice increases mortality between 20 and 40 days of age. The surviving mice are fertile and have an almost normal life span. Ultrastructurally, there is extensive accumulation of autophagic vacuoles in many tissues including liver, pancreas, spleen, kidney and skeletal and heart muscle. In hepatocytes, the autophagic degradation of long-lived proteins is severely impaired. Cardiac myocytes are ultrastructurally abnormal and heart contractility is severely reduced. These findings indicate that LAMP-2 is critical for autophagy. This theory is further substantiated by the finding that human LAMP-2 deficiency8 causing Danon’s disease is associated with the accumulation of autophagic material in striated myocytes."],["dc.format.mimetype","application/pdf"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/3447"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/61036"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.notes.status","zu prüfen"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0028-0836"],["dc.rights","Goescholar"],["dc.rights.access","openAccess"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject","autophagic vacuoles; cardiomyopathy; LAMP-2-deficient mice"],["dc.subject.ddc","610"],["dc.title","Accumulation of autophagic vacuoles and cardiomyopathy in LAMP-2-deficient mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]