Ohlenbusch, Andreas

[["dc.bibliographiccitation.firstpage","840"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Der Nervenarzt"],["dc.bibliographiccitation.lastpage","842"],["dc.bibliographiccitation.volume","90"],["dc.contributor.author","Buggle, Florian"],["dc.contributor.author","Ciric, Elizabeta"],["dc.contributor.author","Boujan, Timan"],["dc.contributor.author","Ohlenbusch, Andreas"],["dc.contributor.author","Gärtner, Jutta"],["dc.contributor.author","Grau, Armin J."],["dc.date.accessioned","2020-12-10T14:08:38Z"],["dc.date.available","2020-12-10T14:08:38Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1007/s00115-019-0693-7"],["dc.identifier.eissn","1433-0407"],["dc.identifier.issn","0028-2804"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70502"],["dc.language.iso","de"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","„Vanishing white matter disease“ im Erwachsenenalter"],["dc.title.alternative","Vanishing white matter disease in adulthood"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","European journal of human genetics : EJHG"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Rosewich, Hendrik"],["dc.contributor.author","Waterham, Hans"],["dc.contributor.author","Poll-The, Bwee Tien"],["dc.contributor.author","Ohlenbusch, Andreas"],["dc.contributor.author","Gärtner, Jutta"],["dc.date.accessioned","2018-02-21T15:04:57Z"],["dc.date.available","2018-02-21T15:04:57Z"],["dc.date.issued","2014-08"],["dc.identifier.doi","10.1038/ejhg.2014.250"],["dc.identifier.pmid","25407003"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/12405"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1476-5438"],["dc.title","Clinical utility gene card for: Zellweger syndrome spectrum"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","869"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Inherited Metabolic Disease"],["dc.bibliographiccitation.lastpage","876"],["dc.bibliographiccitation.volume","39"],["dc.contributor.author","Rosewich, Hendrik"],["dc.contributor.author","Dechent, Peter"],["dc.contributor.author","Krause, Cindy"],["dc.contributor.author","Ohlenbusch, Andreas"],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Gärtner, Jutta"],["dc.date.accessioned","2017-09-07T11:44:32Z"],["dc.date.available","2017-09-07T11:44:32Z"],["dc.date.issued","2016"],["dc.description.abstract","Defects in the biogenesis of peroxisomes cause a clinically and genetically heterogeneous group of neurometabolic disorders, the Zellweger syndrome spectrum (ZSS). Diagnosis predominantly is based on characteristic clinical symptoms, a typical biochemical profile, as well as on identification of the molecular defect in any of the 12 known human PEX genes. The diagnostic workup can be hindered if the typical clinical symptoms are missing and predicting the clinical course of a given patient is almost unfeasible. As a safe and noninvasive method to analyze specific chemical compounds in localized brain regions, in vivo proton magnetic resonance spectroscopy (MRS) can provide an indication in this diagnostic process and may help predict the clinical course. However, to date, there are very few reports on this topic. In this study, we performed localized in vivo proton MRS without confounding contributions from T1- and T2-relaxation effects at 2 Tesla in a comparably large group of seven ZSS patients. Patients' absolute metabolite concentrations in cortical gray matter, white matter, and basal ganglia were assessed and compared with age-matched control values. Our results confirm and extend knowledge about in vivo MRS findings in ZSS patients. Besides affirmation of nonspecific reduction of N-acetylaspartate + N-acetylaspartylglutamate (tNAA) in combination with lipid accumulation as a diagnostic hint for this disease group, the amount of tNAA loss seems to reflect disease burden and may prove to be of prognostic value regarding the clinical course of an already diagnosed patient."],["dc.identifier.doi","10.1007/s10545-016-9965-6"],["dc.identifier.gro","3141599"],["dc.identifier.isi","000386383500011"],["dc.identifier.pmid","27488561"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/10"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Springer"],["dc.relation.eissn","1573-2665"],["dc.relation.issn","0141-8955"],["dc.title","Diagnostic and prognostic value of in vivo proton MR spectroscopy for Zellweger syndrome spectrum patients"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","764"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","The Lancet Neurology"],["dc.bibliographiccitation.lastpage","773"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Rosewich, Hendrik"],["dc.contributor.author","Thiele, Holger"],["dc.contributor.author","Ohlenbusch, Andreas"],["dc.contributor.author","Maschke, Ulrike"],["dc.contributor.author","Altmüller, Janine"],["dc.contributor.author","Frommolt, Peter"],["dc.contributor.author","Zim, Birgit"],["dc.contributor.author","Ebinger, Friedrich"],["dc.contributor.author","Siemes, Hartmut"],["dc.contributor.author","Nürnberg, Peter"],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Gärtner, Jutta"],["dc.date.accessioned","2017-09-07T11:48:26Z"],["dc.date.available","2017-09-07T11:48:26Z"],["dc.date.issued","2012"],["dc.description.abstract","Background Alternating hemiplegia of childhood (AHC) is a rare neurological disorder characterised by early-onset episodes of hemiplegia, dystonia, various paroxysmal symptoms, and developmental impairment. Almost all cases of AHC are sporadic but AHC concordance in monozygotic twins and dominant transmission in a family with a milder phenotype have been reported. Thus, we aimed to identify de-novo mutations associated with this disease. Methods We recruited patients with clinically characterised AHC from paediatric neurology departments in Germany and with the aid of a parental support group between Sept, 2004, and May 18, 2012. We used whole-exome sequencing of three proband-parent trios to identify a disease-associated gene and then tested whether mutations in the gene were also present in the remaining patients and their healthy parents. We analysed genotypes and characterised their associations with the phenotypic spectrum of the disease. Findings We studied 15 female and nine male patients with AHC who were aged 8-35 years. ATP1A3 emerged as the disease-associated gene in AHC. Whole-exome sequencing showed three heterozygous de-novo missense mutations. Sequencing of the 21 remaining affected individuals identified disease-associated mutations in ATP1A3 in all patients, including six de-novo missense mutations and one de-novo splice-site mutation. Because ATP1A3 is also the gene associated with rapid-onset dystonia-parkinsonism (DYT12, OMIM 128235) we compared the genotypes and phenotypes of patients with AHC in our cohort with those of patients with rapid-onset dystonia-parkinsonism reported in the scientific literature. We noted overlapping clinical features, such as abrupt onset of dystonic episodes often triggered by emotional stress, a rostrocaudal (face to arm to leg) gradient of involvement, and signs of brainstem dysfunction, as well as clearly differentiating clinical characteristics, such as episodic hemiplegia and quadriplegia. Interpretation Mutation analysis of the ATP1A3 gene in patients who met clinical criteria for AHC allows for definite genetic diagnosis and sound genetic counselling. AHC and rapid-onset dystonia-parkinsonism are allelic diseases related to mutations in ATP1A3 and form a phenotypical continuum of a dystonic movement disorder."],["dc.identifier.doi","10.1016/S1474-4422(12)70182-5"],["dc.identifier.gro","3142472"],["dc.identifier.isi","000307911700011"],["dc.identifier.pmid","22850527"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11305"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8662"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: Eva Luise and Horst Kohler Foundation for Humans with Rare Diseases"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Inc"],["dc.relation.eissn","1474-4465"],["dc.relation.issn","1474-4422"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Heterozygous de-novo mutations in ATP1A3 in patients with alternating hemiplegia of childhood: a whole-exome sequencing gene-identification study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","945"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","955"],["dc.bibliographiccitation.volume","82"],["dc.contributor.author","Rosewich, Hendrik"],["dc.contributor.author","Ohlenbusch, Andreas"],["dc.contributor.author","Huppke, Peter"],["dc.contributor.author","Schlotawa, Lars"],["dc.contributor.author","Baethmann, Martina"],["dc.contributor.author","Carrilho, Ines"],["dc.contributor.author","Fiori, Simona"],["dc.contributor.author","Lourenco, Charles Marques"],["dc.contributor.author","Sawyer, Sarah"],["dc.contributor.author","Steinfeld, Robert"],["dc.contributor.author","Gärtner, Jutta"],["dc.contributor.author","Brockmann, Knut"],["dc.date.accessioned","2017-09-07T11:46:24Z"],["dc.date.available","2017-09-07T11:46:24Z"],["dc.date.issued","2014"],["dc.description.abstract","Objective:We aimed to delineate the clinical and genetic spectrum of ATP1A3-related disorders and recognition of a potential genotype-phenotype correlation.Methods:We identified 16 new patients with alternating hemiplegia of childhood (AHC) and 3 new patients with rapid-onset dystonia-parkinsonism (RDP) and included these as well as the clinical and molecular findings of all previously reported 164 patients with mutation-positive AHC and RDP in our analyses.Results:Major clinical characteristics shared in common by AHC and RDP comprise a strikingly asymmetric, predominantly dystonic movement disorder with rostrocaudal gradient of involvement and physical, emotional, or chemical stressors as triggers. The clinical courses include an early-onset polyphasic for AHC, a later-onset mono- or biphasic for RDP, as well as intermediate forms. Meta-analysis of the 8 novel and 38 published ATP1A3 mutations shows that the ones affecting transmembrane and functional domains tend to be associated with AHC as the more severe phenotype. The majority of mutations are located in exons 8, 14, 17, and 18.Conclusion:AHC and RDP constitute clinical prototypes in a continuous phenotypic spectrum of ATP1A3-related disorders. Intermediate phenotypes combining criteria of both conditions are increasingly recognized. Efficient stepwise mutation analysis of the ATP1A3 gene may prioritize those exons where current state of knowledge indicates mutational clusters."],["dc.identifier.doi","10.1212/WNL.0000000000000212"],["dc.identifier.gro","3142165"],["dc.identifier.isi","000336262500012"],["dc.identifier.pmid","24523486"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/5255"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.eissn","1526-632X"],["dc.relation.issn","0028-3878"],["dc.title","The expanding clinical and genetic spectrum of ATP1A3-related disorders"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","136"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","American Journal of Medical Genetics"],["dc.bibliographiccitation.lastpage","138"],["dc.bibliographiccitation.volume","137A"],["dc.contributor.author","Huppke, Peter"],["dc.contributor.author","Ohlenbusch, Andreas"],["dc.contributor.author","Brendel, Cornelia"],["dc.contributor.author","Laccone, F"],["dc.contributor.author","Gärtner, Jutta"],["dc.date.accessioned","2017-09-07T11:54:18Z"],["dc.date.available","2017-09-07T11:54:18Z"],["dc.date.issued","2005"],["dc.description.abstract","Mutations in the MECP2 gene are found in only 80% of patients with Rett syndrome (RTT). Therefore other genes have to be involved in the pathogenesis of RTT. By using our defined diagnostic criteria we first re-evaluated 50 girls with possible RTT in whom the sequencing of the MECP2 gene had not revealed any mutations. Only 15 of theses patients fulfilled all criteria for RTT and could be considered to have classical RTT. In eight of these, further molecular analyses revealed large deletions of the MECP2 gene. In the remaining seven girls we then analyzed the genes HDAC1, HDAC2, and HDAC8 that encode for the histone deacetylases 1, 2, and 8 which interact with McCP2 and are essential for its function. Although these histone deacetylase genes have been considered as good candidate genes for RTT, our molecular analysis of these genes did not detect any mutations. Because recently mutations in CDKL5 were reported in patients with RTT, we included this gene in our analysis but failed to detect any mutations. We conclude that only a subgroup of girls with possible RTT and no detectable mutation in the sequencing of the MECP2 gene do really have classical RTT. In many of those large MECP2 gene deletions can be detected by further analysis. The genes HDAC1, HDAC2, and HDAC8 do not seem to play a role in the pathogenesis of RTT and at least in our subgroup no mutations in the CDKL5 gene were detected. (c) 2005 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/ajmg.a.30764"],["dc.identifier.gro","3143813"],["dc.identifier.isi","000231634600004"],["dc.identifier.pmid","16086395"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1369"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Wiley-liss"],["dc.relation.issn","1552-4825"],["dc.title","Mutation analysis of the HDAC 1, 2, 8 and CDKL5 genes in Rett syndrome patients without mutations in MECP2"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","758"],["dc.bibliographiccitation.issue","70"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","754"],["dc.contributor.author","Henneke, Marco"],["dc.contributor.author","Combes, P."],["dc.contributor.author","Diekmann, S."],["dc.contributor.author","Bertini, E."],["dc.contributor.author","Brockmann, K."],["dc.contributor.author","Burlina, A. P."],["dc.contributor.author","Kaiser, J."],["dc.contributor.author","Ohlenbusch, A."],["dc.contributor.author","Plecko, B."],["dc.contributor.author","Rodriguez, D."],["dc.contributor.author","Boespflug-Tanguy, Odile"],["dc.contributor.author","Gärtner, J."],["dc.date.accessioned","2019-07-10T08:13:34Z"],["dc.date.available","2019-07-10T08:13:34Z"],["dc.date.issued","2008"],["dc.description.abstract","Background: Pelizaeus-Merzbacher-like disease (PMLD) is a genetically heterogeneous disorder within the group of hypomyelinating leukoencephalopathies. Mutations of the gap junction protein 12 (GJA12) gene are known to cause one autosomal recessive PMLD form. Few patients with GJA12 mutated PMLD have been reported, and to date, the frequency as well as the genotypic and phenotypic spectrum of GJA12 related PMLD is unclear. Methods: We report mutation analysis of the GJA12 gene in a clinical and radiologic wellcharacterized multiethnic cohort of 193 patients with PMLD from 182 families. Results and Conclusions: Only 16 patients (8.3%) from 14 families (7.7%) carry GJA12 mutations including five families where we detected only one mutated allele. Among those, we identified 11 novel alterations. Thus, GJA12 mutations are a rather rare cause for Pelizaeus- Merzbacher-like disease. The clinical phenotype of patients with a GJA12 mutation was evaluated and is overall comparable to the clinical features seen in mild forms of proteolipid protein 1 (PLP1) related disorder but with better cognition and earlier signs of axonal degeneration."],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6318"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/61279"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.subject.ddc","610"],["dc.title","GJA12 mutations are a rare cause of Pelizaeus-Merzbacher-like disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","861"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","863"],["dc.bibliographiccitation.volume","83"],["dc.contributor.author","Rosewich, H."],["dc.contributor.author","Weise, D."],["dc.contributor.author","Ohlenbusch, A."],["dc.contributor.author","Gärtner, J."],["dc.contributor.author","Brockmann, K."],["dc.date.accessioned","2021-06-01T10:48:10Z"],["dc.date.available","2021-06-01T10:48:10Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.1212/WNL.0000000000000735"],["dc.identifier.gro","3142067"],["dc.identifier.isi","000341096100020"],["dc.identifier.pmid","25056583"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85849"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.eissn","1526-632X"],["dc.relation.issn","0028-3878"],["dc.title","Phenotypic overlap of alternating hemiplegia of childhood and CAPOS syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","133"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of the Neurological Sciences"],["dc.bibliographiccitation.lastpage","135"],["dc.bibliographiccitation.volume","341"],["dc.contributor.author","Rosewich, Hendrik"],["dc.contributor.author","Baethmann, Martina"],["dc.contributor.author","Ohlenbusch, Andreas"],["dc.contributor.author","Gärtner, Jutta"],["dc.contributor.author","Brockmann, Knut"],["dc.date.accessioned","2017-09-07T11:46:12Z"],["dc.date.available","2017-09-07T11:46:12Z"],["dc.date.issued","2014"],["dc.description.abstract","Mutations in the ATP1A3 gene are associated with rapid-onset dystonia-parkinsonism (RDP) and alternating hemiplegia of childhood (ARC) as well as RDP/AHC intermediate presentations. Phenotypic diversity is being recognized. In order to identify ATP1A3-related phenotypes not meeting the classical criteria for RDP or AHC we lowered the threshold for mutation analysis in clinical presentations resembling AHC or RDP. A novel heterozygous ATP1A3 missense mutation c.2600G > A (p.Gly867Asp, G867D) was detected in a 15-year-old girl. Her clinical phenotype is partially consistent with an intermediate presentation between alternating hemiplegia of childhood and rapid-onset dystonia-parkinsonism and comprises additional yet unreported features. With onset at 41/2 years of age recurrent paroxysmal flaccid hemiplegia alternating in laterality was triggered by watching television or playing computer games. Occlusion of both eyes reliably stopped the plegic attacks with the patient remaining awake. Our observation further widens the phenotypic spectrum associated with ATP1A3 mutations. (C) 2014 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.jns.2014.03.034"],["dc.identifier.gro","3142105"],["dc.identifier.isi","000337262200025"],["dc.identifier.pmid","24713507"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/4600"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Bv"],["dc.relation.eissn","1878-5883"],["dc.relation.issn","0022-510X"],["dc.title","A novel ATP1A3 mutation with unique clinical presentation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","26997"],["dc.bibliographiccitation.issue","37"],["dc.bibliographiccitation.journal","Journal of biological chemistry"],["dc.bibliographiccitation.lastpage","27005"],["dc.bibliographiccitation.volume","282"],["dc.contributor.author","Hillebrand, Merle"],["dc.contributor.author","Verrier, Sophie E."],["dc.contributor.author","Ohlenbusch, Andreas"],["dc.contributor.author","Schaefer, Annika"],["dc.contributor.author","Soeling, Hans-Dieter"],["dc.contributor.author","Wouters, Fred S."],["dc.contributor.author","Gärtner, Jutta"],["dc.date.accessioned","2017-09-07T11:49:24Z"],["dc.date.available","2017-09-07T11:49:24Z"],["dc.date.issued","2007"],["dc.description.abstract","The adrenoleukodystrophy protein ( ALDP) and the 70-kDa peroxisomal membrane protein (PMP70) are half-ATP-binding cassette (ABC) transporters in the mammalian peroxisome membrane. Mutations in the gene encoding ALDP result in a devastating neurodegenerative disorder, X-linked adrenoleukodystrophy (X-ALD) that is associated with elevated levels of very long chain fatty acids because of impaired peroxisomal beta-oxidation. The interactions of peroxisomal ABC transporters, their role in the peroxisomal membrane, and their functions in disease pathogenesis are poorly understood. Studies on ABC transporters revealed that half-transporters have to dimerize to gain functionality. So far, conflicting observations are described for ALDP. By the use of in vitro methods ( yeast two-hybrid and immunoprecipitation assays) on the one hand, it was shown that ALDP can form homodimers as well as heterodimers with PMP70 and ALDR, while on the other hand, it was demonstrated that ALDP and PMP70 exclusively homodimerize. To circumvent the problems of artificial interactions due to biochemical sample preparation in vitro, we investigated protein-protein interaction of ALDP in its physiological environment by FRET microscopy in intact living cells. The statistical relevance of FRET data was determined in two different ways using probability distribution shift analysis and Kolmogorov-Smirnov statistics. We demonstrate in vivo that ALDP and PMP70 form homodimers as well as ALDP/PMP70 heterodimers where ALDP homodimers predominate. Using C-terminal deletion constructs of ALDP, we demonstrate that the last 87 C-terminal amino acids harbor the most important protein domain mediating these interactions, and that the N-terminal transmembrane region of ALDP has an additional stabilization effect on ALDP homodimers. Loss of ALDP homo- or heterodimerization is highly relevant for understanding the disease mechanisms of X-ALD."],["dc.identifier.doi","10.1074/jbc.M702122200"],["dc.identifier.gro","3143437"],["dc.identifier.isi","000249304900040"],["dc.identifier.pmid","17609205"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/951"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Amer Soc Biochemistry Molecular Biology Inc"],["dc.relation.issn","0021-9258"],["dc.title","Live cell FRET microscopy - Homo-and heterodimerization of two human peroxisomal ABC transporters, the adrenoleukodystrophy protein (ALDP, ABCD1) and PMP70 (ABCD3)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]