Kornak, Uwe

[["dc.bibliographiccitation.firstpage","325"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Human Genetics"],["dc.bibliographiccitation.lastpage","328"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Al-Bughaili, Mohammed"],["dc.contributor.author","Neuhann, Teresa M"],["dc.contributor.author","Flöttmann, Ricarda"],["dc.contributor.author","Mundlos, Stefan"],["dc.contributor.author","Spielmann, Malte"],["dc.contributor.author","Kornak, Uwe"],["dc.contributor.author","Fischer-Zirnsak, Björn"],["dc.date.accessioned","2020-06-23T14:53:14Z"],["dc.date.available","2020-06-23T14:53:14Z"],["dc.date.issued","2017-02"],["dc.description.abstract","Gerodermia osteodysplastica is a recessive segmental progeroid disorder mainly characterized by wrinkled skin, generalized connective tissue weakness, infantile onset osteoporosis and normal intelligence. Coding mutations in GORAB, localized on chromosome 1q24.2, are the cause of this disease. 1q24 deletions underlie a spectrum of disorders with intellectual disability and ear abnormalities as phenotypic hallmarks. Here we report on an individual from Azerbaijan originating from a non-consanguineous couple showing short stature, cutis laxa, frequent fractures, facial dysmorphism, cup-shaped ears and intellectual disability. Sanger sequencing of GORAB revealed the seemingly homozygous missense mutation p.Ser175Phe. This mutation was detected in a heterozygous state in the clinically unaffected mother, but was absent in the healthy father. We performed copy-number investigations by high-resolution array-CGH and PCR approaches and found an ~6 Mb de novo deletion spanning 1q23.3-q24.2 in the affected boy. This novel combination of genetic defects very well explains the phenotype that goes beyond the usual presentation of gerodermia osteodysplastica. Our data provide new insight into the phenotypic spectrum of 1q23-q25 deletions and shows that the combination with another pathogenic allele can lead to more severe clinical manifestations."],["dc.identifier.doi","10.1038/jhg.2016.111"],["dc.identifier.pmid","27604556"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/66682"],["dc.language.iso","en"],["dc.relation.eissn","1435-232X"],["dc.relation.issn","1434-5161"],["dc.title","A de novo 1q23.3-q24.2 deletion combined with a GORAB missense mutation causes a distinctive phenotype with cutis laxa"],["dc.type","journal_article"],["dc.type.internalPublication","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2149"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Human Molecular Genetics"],["dc.bibliographiccitation.lastpage","2165"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Hucthagowder, Vishwanathan"],["dc.contributor.author","Morava, Eva"],["dc.contributor.author","Kornak, Uwe"],["dc.contributor.author","Lefeber, Dirk J"],["dc.contributor.author","Fischer, Björn"],["dc.contributor.author","Dimopoulou, Aikaterini"],["dc.contributor.author","Aldinger, Annika"],["dc.contributor.author","Choi, Jiwon"],["dc.contributor.author","Davis, Elaine C"],["dc.contributor.author","Abuelo, Dianne N"],["dc.contributor.author","Adamowicz, Maciej"],["dc.contributor.author","Al-Aama, Jumana"],["dc.contributor.author","Basel-Vanagaite, Lina"],["dc.contributor.author","Fernandez, Bridget"],["dc.contributor.author","Greally, Marie T"],["dc.contributor.author","Gillessen-Kaesbach, Gabriele"],["dc.contributor.author","Kayserili, Hulya"],["dc.contributor.author","Lemyre, Emmanuelle"],["dc.contributor.author","Tekin, Mustafa"],["dc.contributor.author","Türkmen, Seval"],["dc.contributor.author","Tuysuz, Beyhan"],["dc.contributor.author","Yüksel-Konuk, Berrin"],["dc.contributor.author","Mundlos, Stefan"],["dc.contributor.author","Van Maldergem, Lionel"],["dc.contributor.author","Wevers, Ron A"],["dc.contributor.author","Urban, Zsolt"],["dc.date.accessioned","2020-06-24T12:24:09Z"],["dc.date.available","2020-06-24T12:24:09Z"],["dc.date.issued","2009-06-15"],["dc.description.abstract","Autosomal recessive cutis laxa type 2 (ARCL2), a syndrome of growth and developmental delay and redundant, inelastic skin, is caused by mutations in the a2 subunit of the vesicular ATPase H+-pump (ATP6V0A2). The goal of this study was to define the disease mechanisms that lead to connective tissue lesions in ARCL2. In a new cohort of 17 patients, DNA sequencing of ATP6V0A2 detected either homozygous or compound heterozygous mutations. Considerable allelic and phenotypic heterogeneity was observed, with a missense mutation of a moderately conserved residue p.P87L leading to unusually mild disease. Abnormal N- and/or mucin type O-glycosylation was observed in all patients tested. Premature stop codon mutations led to decreased ATP6V0A2 mRNA levels by destabilizing the mutant mRNA via the nonsense-mediated decay pathway. Loss of ATP6V0A2 either by siRNA knockdown or in ARCL2 cells resulted in distended Golgi cisternae, accumulation of abnormal lysosomes and multivesicular bodies. Immunostaining of ARCL2 cells showed the accumulation of tropoelastin (TE) in the Golgi and in large, abnormal intracellular and extracellular aggregates. Pulse-chase studies confirmed impaired secretion and increased intracellular retention of TE, and insoluble elastin assays showed significantly reduced extracellular deposition of mature elastin. Fibrillin-1 microfibril assembly and secreted lysyl oxidase activity were normal in ARCL2 cells. TUNEL staining demonstrated increased rates of apoptosis in ARCL2 cell cultures. We conclude that loss-of-function mutations in ATP6V0A2 lead to TE aggregation in the Golgi, impaired clearance of TE aggregates and increased apoptosis of elastogenic cells."],["dc.identifier.doi","10.1093/hmg/ddp148"],["dc.identifier.pmid","19321599"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/66712"],["dc.language.iso","en"],["dc.relation.eissn","1460-2083"],["dc.relation.issn","0964-6906"],["dc.title","Loss-of-function mutations in ATP6V0A2 impair vesicular trafficking, tropoelastin secretion and cell survival"],["dc.type","journal_article"],["dc.type.internalPublication","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","310"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Molecular Genetics and Metabolism"],["dc.bibliographiccitation.lastpage","316"],["dc.bibliographiccitation.volume","112"],["dc.contributor.author","Fischer, Björn"],["dc.contributor.author","Callewaert, Bert"],["dc.contributor.author","Schröter, Phillipe"],["dc.contributor.author","Coucke, Paul J"],["dc.contributor.author","Schlack, Claire"],["dc.contributor.author","Ott, Claus-Eric"],["dc.contributor.author","Morroni, Manrico"],["dc.contributor.author","Homann, Wolfgang"],["dc.contributor.author","Mundlos, Stefan"],["dc.contributor.author","Morava, Eva"],["dc.contributor.author","Ficcadenti, Anna"],["dc.contributor.author","Kornak, Uwe"],["dc.date.accessioned","2020-06-23T14:52:27Z"],["dc.date.available","2020-06-23T14:52:27Z"],["dc.date.issued","2014-08"],["dc.description.abstract","Autosomal recessive cutis laxa (ARCL) type 2 constitutes a heterogeneous group of diseases mainly characterized by lax and wrinkled skin, skeletal anomalies, and a variable degree of intellectual disability. ALDH18A1-related ARCL is the most severe form within this disease spectrum. Here we report on the clinical and molecular findings of two affected individuals from two unrelated families. The patients presented with typical features of de Barsy syndrome and an overall progeroid appearance. However, the phenotype was highly variable including cardiovascular involvement in the more severe case. Investigation of a skin biopsy of one patient revealed not only the typical alterations of elastic fibers, but also an altered structure of mitochondria in cutaneous fibroblasts. Using conventional sequencing and copy number analysis we identified a frameshift deletion of one nucleotide and a microdeletion affecting the ALDH18A1 gene, respectively, in a homozygous state in both patients. Expression analysis in dermal fibroblasts from the patient carrying the microdeletion showed an almost complete absence of the ALDH18A1 mRNA resulting in an absence of the ALDH18A1 protein. So far, only 13 affected individuals from seven unrelated families suffering from ALDH18A1-related cutis laxa have been described in literature. Our findings provide new insights into the clinical spectrum and show that beside point mutations microdeletions are a possible cause of ALDH18A1-ARCL."],["dc.identifier.doi","10.1016/j.ymgme.2014.05.003"],["dc.identifier.pmid","24913064"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/66672"],["dc.language.iso","en"],["dc.relation.eissn","1096-7206"],["dc.relation.issn","1096-7192"],["dc.title","Severe congenital cutis laxa with cardiovascular manifestations due to homozygous deletions in ALDH18A1"],["dc.type","journal_article"],["dc.type.internalPublication","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S80"],["dc.bibliographiccitation.journal","Calcified Tissue International"],["dc.bibliographiccitation.volume","80"],["dc.contributor.author","Kühnisch, Jirko"],["dc.contributor.author","Kolanczyk, Mateusz"],["dc.contributor.author","Stumpp, S."],["dc.contributor.author","Kossler, N."],["dc.contributor.author","Inderchand, Manjubala"],["dc.contributor.author","Sporle, R."],["dc.contributor.author","Herrman, B."],["dc.contributor.author","Fatzl, P."],["dc.contributor.author","Mundlos, Stefan"],["dc.contributor.author","Kornak, Uwe"],["dc.date.accessioned","2020-06-19T09:36:31Z"],["dc.date.available","2020-06-19T09:36:31Z"],["dc.date.issued","2007"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/66537"],["dc.title","Growth defect, reduced mineralization and tibial bowing in a mouse model for neurofibromatosis type 1"],["dc.type","journal_article"],["dc.type.internalPublication","no"],["dspace.entity.type","Publication"]]

[["dc.contributor.author","Kornak, Uwe"],["dc.contributor.author","Oheim, Ralf"],["dc.contributor.author","Krawitz, Peter"],["dc.contributor.author","Zemojtel, Tomasz"],["dc.contributor.author","Amling, Michael"],["dc.contributor.author","Mundlos, Stefan"],["dc.contributor.author","Robinson, Peter"],["dc.date.accessioned","2020-06-19T09:54:53Z"],["dc.date.available","2020-06-19T09:54:53Z"],["dc.date.issued","2014"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/66546"],["dc.title","Gene Panel Diagnostics for Disorders with Abnormal Bone Mass: Results From 50 Patients"],["dc.type","report"],["dc.type.internalPublication","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","e2014481118"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences"],["dc.bibliographiccitation.volume","118"],["dc.contributor.author","Rodríguez de los Santos, Miguel"],["dc.contributor.author","Rivalan, Marion"],["dc.contributor.author","David, Friederike S."],["dc.contributor.author","Stumpf, Alexander"],["dc.contributor.author","Pitsch, Julika"],["dc.contributor.author","Tsortouktzidis, Despina"],["dc.contributor.author","Velasquez, Laura Moreno"],["dc.contributor.author","Voigt, Anne"],["dc.contributor.author","Schilling, Karl"],["dc.contributor.author","Mattei, Daniele"],["dc.contributor.author","Long, Melissa"],["dc.contributor.author","Vogt, Guido"],["dc.contributor.author","Knaus, Alexej"],["dc.contributor.author","Fischer-Zirnsak, Björn"],["dc.contributor.author","Wittler, Lars"],["dc.contributor.author","Timmermann, Bernd"],["dc.contributor.author","Robinson, Peter N."],["dc.contributor.author","Horn, Denise"],["dc.contributor.author","Mundlos, Stefan"],["dc.contributor.author","Kornak, Uwe"],["dc.contributor.author","Becker, Albert J."],["dc.contributor.author","Schmitz, Dietmar"],["dc.contributor.author","Winter, York"],["dc.contributor.author","Krawitz, Peter M."],["dc.date.accessioned","2021-04-14T08:30:13Z"],["dc.date.available","2021-04-14T08:30:13Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1073/pnas.2014481118"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83155"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1091-6490"],["dc.relation.issn","0027-8424"],["dc.title","A CRISPR-Cas9–engineered mouse model for GPI-anchor deficiency mirrors human phenotypes and exhibits hippocampal synaptic dysfunctions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","32"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Genetics"],["dc.bibliographiccitation.lastpage","34"],["dc.bibliographiccitation.volume","40"],["dc.contributor.author","Kornak, Uwe"],["dc.contributor.author","Reynders, Ellen"],["dc.contributor.author","Dimopoulou, Aikaterini"],["dc.contributor.author","van Reeuwijk, Jeroen"],["dc.contributor.author","Fischer, Bjoern"],["dc.contributor.author","Rajab, Anna"],["dc.contributor.author","Budde, Birgit"],["dc.contributor.author","Nürnberg, Peter"],["dc.contributor.author","Foulquier, Francois"],["dc.contributor.author","Lefeber, Dirk"],["dc.contributor.author","Urban, Zsolt"],["dc.contributor.author","Gruenewald, Stephanie"],["dc.contributor.author","Annaert, Wim"],["dc.contributor.author","Brunner, Han G"],["dc.contributor.author","van Bokhoven, Hans"],["dc.contributor.author","Wevers, Ron"],["dc.contributor.author","Morava, Eva"],["dc.contributor.author","Matthijs, Gert"],["dc.contributor.author","Van Maldergem, Lionel"],["dc.contributor.author","Mundlos, Stefan"],["dc.date.accessioned","2020-06-23T14:53:28Z"],["dc.date.available","2020-06-23T14:53:28Z"],["dc.date.issued","2008-01"],["dc.description.abstract","We identified loss-of-function mutations in ATP6V0A2, encoding the a2 subunit of the V-type H+ ATPase, in several families with autosomal recessive cutis laxa type II or wrinkly skin syndrome. The mutations result in abnormal glycosylation of serum proteins (CDG-II) and cause an impairment of Golgi trafficking in fibroblasts from affected individuals. These results indicate that the a2 subunit of the proton pump has an important role in Golgi function."],["dc.identifier.doi","10.1038/ng.2007.45"],["dc.identifier.pmid","18157129"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/66685"],["dc.language.iso","en"],["dc.relation.eissn","1546-1718"],["dc.relation.issn","1061-4036"],["dc.title","Impaired glycosylation and cutis laxa caused by mutations in the vesicular H+-ATPase subunit ATP6V0A2"],["dc.type","journal_article"],["dc.type.internalPublication","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1410"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Nature Genetics"],["dc.bibliographiccitation.lastpage","1412"],["dc.bibliographiccitation.volume","40"],["dc.contributor.author","Hennies, Hans Christian"],["dc.contributor.author","Kornak, Uwe"],["dc.contributor.author","Zhang, Haikuo"],["dc.contributor.author","Egerer, Johannes"],["dc.contributor.author","Zhang, Xin"],["dc.contributor.author","Seifert, Wenke"],["dc.contributor.author","Kühnisch, Jirko"],["dc.contributor.author","Budde, Birgit"],["dc.contributor.author","Nätebus, Marc"],["dc.contributor.author","Brancati, Francesco"],["dc.contributor.author","Wilcox, William R"],["dc.contributor.author","Müller, Dietmar"],["dc.contributor.author","Kaplan, Paige B"],["dc.contributor.author","Rajab, Anna"],["dc.contributor.author","Zampino, Giuseppe"],["dc.contributor.author","Fodale, Valentina"],["dc.contributor.author","Dallapiccola, Bruno"],["dc.contributor.author","Newman, William"],["dc.contributor.author","Metcalfe, Kay"],["dc.contributor.author","Clayton-Smith, Jill"],["dc.contributor.author","Tassabehji, May"],["dc.contributor.author","Steinmann, Beat"],["dc.contributor.author","Barr, Francis A"],["dc.contributor.author","Nürnberg, Peter"],["dc.contributor.author","Wieacker, Peter"],["dc.contributor.author","Mundlos, Stefan"],["dc.date.accessioned","2020-06-23T14:53:24Z"],["dc.date.available","2020-06-23T14:53:24Z"],["dc.date.issued","2008-12"],["dc.description.abstract","Gerodermia osteodysplastica is an autosomal recessive disorder characterized by wrinkly skin and osteoporosis. Here we demonstrate that gerodermia osteodysplastica is caused by loss-of-function mutations in SCYL1BP1, which is highly expressed in skin and osteoblasts. The protein localizes to the Golgi apparatus and interacts with Rab6, identifying SCYL1BP1 as a golgin. These results associate abnormalities of the secretory pathway with age-related changes in connective tissues."],["dc.identifier.doi","10.1038/ng.252"],["dc.identifier.pmid","18997784"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/66684"],["dc.language.iso","en"],["dc.relation.eissn","1546-1718"],["dc.relation.issn","1061-4036"],["dc.title","Gerodermia osteodysplastica is caused by mutations in SCYL1BP1, a Rab-6 interacting golgin"],["dc.type","journal_article"],["dc.type.internalPublication","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","352"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Molecular Genetics and Metabolism"],["dc.bibliographiccitation.lastpage","361"],["dc.bibliographiccitation.volume","110"],["dc.contributor.author","Dimopoulou, Aikaterini"],["dc.contributor.author","Fischer, Björn"],["dc.contributor.author","Gardeitchik, Thatjana"],["dc.contributor.author","Schroeter, Phillipe"],["dc.contributor.author","Kayserili, Hülya"],["dc.contributor.author","Schlack, Claire"],["dc.contributor.author","Li, Yun"],["dc.contributor.author","Brum, Jaime Moritz"],["dc.contributor.author","Barisic, Ingeborg"],["dc.contributor.author","Castori, Marco"],["dc.contributor.author","Spaich, Christiane"],["dc.contributor.author","Fletcher, Elaine"],["dc.contributor.author","Mahayri, Zeina"],["dc.contributor.author","Bhat, Meenakshi"],["dc.contributor.author","Girisha, Katta M."],["dc.contributor.author","Lachlan, Katherine"],["dc.contributor.author","Johnson, Diana"],["dc.contributor.author","Phadke, Shubha"],["dc.contributor.author","Gupta, Neerja"],["dc.contributor.author","Simandlova, Martina"],["dc.contributor.author","Kabra, Madhulika"],["dc.contributor.author","David, Albert"],["dc.contributor.author","Nijtmans, Leo"],["dc.contributor.author","Chitayat, David"],["dc.contributor.author","Tuysuz, Beyhan"],["dc.contributor.author","Brancati, Francesco"],["dc.contributor.author","Mundlos, Stefan"],["dc.contributor.author","Van Maldergem, Lionel"],["dc.contributor.author","Morava, Eva"],["dc.contributor.author","Wollnik, Bernd"],["dc.contributor.author","Kornak, Uwe"],["dc.date.accessioned","2017-09-07T11:47:04Z"],["dc.date.available","2017-09-07T11:47:04Z"],["dc.date.issued","2013"],["dc.description.abstract","Autosomal recessive cutis laxa type 2B (ARCL2B; OMIM # 612940) is a segmental progeroid disorder caused by mutations in PYCR1 encoding pyrroline-5-carboxylate reductase 1, which is part of the conserved proline de novo synthesis pathway. Here we describe 33 patients with PYCR1-related ARCL from 27 families with initial diagnoses varying between wrinkly skin syndrome, gerodermia osteodysplastica, De Barsy syndrome or more severe progeria syndromes. Given the difficult differential diagnosis of ARCL syndromes we performed a systematic comparison of clinical features of PYCR1-related ARCL. Intrauterine growth retardation, a characteristic triangular facial gestalt, psychomotor retardation, and hypotonia were the most relevant distinctive hallmarks of ARCL due to proline de novo synthesis defects. Corneal clouding or cataracts, athetoid movements, and finger contractures were rather rare features, but had a high predictive value. In our cohort we identified 20 different PYCR1 mutations of which seven were novel. Most of the mutations accumulated in exons 4 to 6. Missense alterations of highly conserved residues were most frequent followed by splice site changes and a single nonsense mutation. Analysis of genotype phenotype correlation revealed that patients with mutations in the first two exons had lower average clinical scores and absent or only mild intellectual disability. Structural analyses predicted interference with PYCR1 multimerization for a subset of missense mutations. These findings have implications for the clinics as well as the pathomechanism of PYCR1-related ARCL. (C) 2013 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.ymgme.2013.08.009"],["dc.identifier.gro","3142262"],["dc.identifier.isi","000326058000025"],["dc.identifier.pmid","24035636"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/6331"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Academic Press Inc Elsevier Science"],["dc.relation.eissn","1096-7206"],["dc.relation.issn","1096-7192"],["dc.title","Genotype phenotype spectrum of PYCR1-related autosomal recessive cutis laxa"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.contributor.author","Kolanczyk, Mateusz"],["dc.contributor.author","Pech, Markus"],["dc.contributor.author","Zemojtel, Tomasz"],["dc.contributor.author","Yamamoto, Hiroshi"],["dc.contributor.author","Mikula, Ivan"],["dc.contributor.author","Calvaruso, Maria-Antonietta"],["dc.contributor.author","Richter-Dennerlein, Ricarda"],["dc.contributor.author","Fischer-Zirnsak, Björn"],["dc.contributor.author","Ritz, Anita"],["dc.contributor.author","Kossler, Nadine"],["dc.contributor.author","Martasek, Pavel"],["dc.contributor.author","Spoerle, Ralf"],["dc.contributor.author","Smeitink, Jan"],["dc.contributor.author","Kornak, Uwe"],["dc.contributor.author","Vingron, Martin"],["dc.contributor.author","Nijtmans, Leo"],["dc.contributor.author","Nierhaus, Knud"],["dc.contributor.author","Lightowlers, Robert"],["dc.contributor.author","Schuelke, Markus"],["dc.contributor.author","Mundlos, Stefan"],["dc.date.accessioned","2020-06-19T09:54:57Z"],["dc.date.available","2020-06-19T09:54:57Z"],["dc.date.issued","2011"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/66547"],["dc.title","Trophoblast Development Is Compromised By The Mitochondrial Dysfunction"],["dc.type","report"],["dc.type.internalPublication","no"],["dspace.entity.type","Publication"]]