Kratzin, Hartmut Dieter

[["dc.bibliographiccitation.firstpage","261"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Proteomics"],["dc.bibliographiccitation.lastpage","269"],["dc.contributor.author","Sussulini, Alessandra"],["dc.contributor.author","Dihazi, Hassan"],["dc.contributor.author","Muller Banzato, Claudio Eduardo"],["dc.contributor.author","Zezzi Arruda, Marco Aurelio"],["dc.contributor.author","Stühmer, Walter"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Jahn, Olaf"],["dc.contributor.author","Kratzin, Hartmut D."],["dc.date.accessioned","2017-09-07T11:46:27Z"],["dc.date.available","2017-09-07T11:46:27Z"],["dc.date.issued","2011"],["dc.description.abstract","The molecular basis of bipolar disorder (BD) is still unknown as is the mechanism through which lithium, the therapy of choice, exerts its effects in treatment of BD. So far, no biomarkers exist to facilitate diagnosis of BD or treatment evaluation. To investigate whether BD and its treatment with lithium leaves a characteristic signature in the serum proteome, we used SELDI-TOF MS to analyze individual serum samples from BD patients treated with lithium (BD-plus-Li, n=15) or other drugs (BD-minus-Li, n=10) and from healthy controls (n=15). Interestingly, features of 28 kDa (one peak) and 14 kDa (three peaks) showed a decreased level in the BD-minus-Li group and a level restored to that of the control group in the BD-plus-Li group. To reveal the identity of these features, we subjected pooled serum samples from both BD groups to the 2-D DIGE technology and identified 28 kDa apolipoprotein A-I (apo A-I) and three 14 kDa fragments thereof as upregulated in the BD-plus-Li group. Immunoturbidimetry, a routine clinical assay, verified the characteristic apo A-I signature in individual serum samples. In conclusion, we propose apo A-I as a candidate marker that can visualize response to lithium treatment at the serum protein level."],["dc.identifier.doi","10.1002/pmic.201000371"],["dc.identifier.gro","3150515"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7288"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.title","Apolipoprotein A-I as a candidate serum marker for the response to lithium treatment in bipolar disorder"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1339"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Molecular and Cellular Biology"],["dc.bibliographiccitation.lastpage","1346"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Schwarz, P."],["dc.contributor.author","Reim, K."],["dc.contributor.author","Brechlin, P."],["dc.contributor.author","Jahn, O."],["dc.contributor.author","Kratzin, H."],["dc.contributor.author","Aitken, A."],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Aguzzi, A."],["dc.contributor.author","Bahn, E."],["dc.contributor.author","Baxter, Helen C."],["dc.contributor.author","Brose, N."],["dc.contributor.author","Otto, M."],["dc.date.accessioned","2017-09-07T11:43:02Z"],["dc.date.available","2017-09-07T11:43:02Z"],["dc.date.issued","2005"],["dc.description.abstract","The diagnosis of sporadic Creutzfeldt-Jakob disease (CJD) is based on typical clinical findings and is supported by a positive 14-3-3 Western blot of cerebrospinal fluid. However, it is not clear whether 14-3-3 indicates general neuronal damage or is of pathophysiological relevance in CJD. The fact that the 14-3-3 isoform spectrum in cerebrospinal fluid does not correspond to that found in the brain points to a regulated process. To investigate a possible role of 14-3-3 proteins in transmissible spongiform diseases, we generated a 14-3-3gamma-deficient mutant mouse line by using a classical knockout strategy. The anatomy and cage behavior of the mutant mice were normal. Western blot analyses of brain homogenates revealed no changes in the protein expression of other 14-3-3 isoforms (epsilon, beta, zeta, and eta). Proteomic analyses of mouse brains by two-dimensional differential gel electrophoresis showed that several proteins, including growth hormone, 1-Cys peroxiredoxin, CCT-zeta, glucose-6-phosphate isomerase, GRP170 precursor, and et-SNAP, were differentially expressed. Mutant and wild-type mice were inoculated either intracerebrally or intraperitoneally with the Rocky Mountain Laboratory strain of scrapie, but no differences were detected in the postinoculation survival rates. These results indicate that 14-3-3gamma is unlikely to play a causal role in CJD and related diseases."],["dc.identifier.doi","10.1128/MCB.25.4.1339-1346.2005"],["dc.identifier.gro","3143900"],["dc.identifier.isi","000226908000010"],["dc.identifier.pmid","15684385"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1465"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1098-5549"],["dc.relation.issn","0270-7306"],["dc.title","Unchanged survival rates of 14-3-3 gamma knockout mice after inoculation with pathological prion protein"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","4357"],["dc.bibliographiccitation.issue","20"],["dc.bibliographiccitation.journal","Proteomics"],["dc.bibliographiccitation.lastpage","4366"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Brechlin, Peter"],["dc.contributor.author","Jahn, Olaf"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Cepek, Lukas"],["dc.contributor.author","Kratzin, Hartmut"],["dc.contributor.author","Lehnert, Stefan"],["dc.contributor.author","Jesse, Sarah"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2018-11-07T11:10:48Z"],["dc.date.available","2018-11-07T11:10:48Z"],["dc.date.issued","2008"],["dc.description.abstract","So far only the detection of 14-3-3 proteins in cerebrospinal fluid (CSF) is included in the diagnostic criteria for sporadic Creutzfeldt-jakob disease (sCJD). However, this assay cannot be used for screening because of the high rate of false positive results in sCJD, and often negative results in variant CJD. To facilitate the differential diagnosis of CJD, we applied 2-D differential gel-electrophoresis (2-D DIGE) as a quantitative proteomic screening system for CSF proteins. We compared 36 patients suffering from sCJD with 30 patients suffering from other neurodegenerative diseases. Sample preparation was optimized in consideration of the fact that CSF is composed of blood- and brain-derived proteins, and an improved 2-D DIGE protocol was established. Using this method in combination with protein identification by MALDI-TOF-MS, several known surrogate markers of sCJD like 14-3-3 protein, neuron-specific enolase, and lactate dehydrogenase were readily identified. Moreover, a not yet identified protein with an approximate molecular mass of 85 kDa was found as marker for sCJD with high diagnostic specificity and sensitivity. We conclude that our proteomic approach is useful to differentiate CJD from other neurodegenerative diseases and expect that CSF-optimized 2-D DIGE will find broad application in the search for other brain derived proteins in CSF."],["dc.identifier.doi","10.1002/pmic.200800375"],["dc.identifier.isi","000260717300021"],["dc.identifier.pmid","18814332"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53290"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-Blackwell"],["dc.relation.issn","1615-9861"],["dc.relation.issn","1615-9853"],["dc.title","Cerebrospinal fluid-optimized two-dimensional difference gel electrophoresis (2-D DIGE) facilitates the differential diagnosis of Creutzfeldt-Jakob disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]