Wolf, Katrin

[["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Cytogenetic and Genome Research"],["dc.bibliographiccitation.volume","125"],["dc.contributor.author","Grzmil, Pawel"],["dc.contributor.author","Konietzko, J."],["dc.contributor.author","Boehm, D."],["dc.contributor.author","Hoelter, Sabine M."],["dc.contributor.author","Aguilar-Pimentel, Juan Antonio"],["dc.contributor.author","Javaheri, A."],["dc.contributor.author","Kalaydjiev, S."],["dc.contributor.author","Adler, Thure"],["dc.contributor.author","Bolle, I."],["dc.contributor.author","Adham, Ibrahim M."],["dc.contributor.author","Dixkens, C."],["dc.contributor.author","Wolf, S."],["dc.contributor.author","Fuchs, H."],["dc.contributor.author","Gailus-Durner, Valerie"],["dc.contributor.author","Wurst, Wolfgang"],["dc.contributor.author","Ollert, Markus W."],["dc.contributor.author","Busch, D. H."],["dc.contributor.author","Schulz, H."],["dc.contributor.author","de Angelis, Martin Hrabe"],["dc.contributor.author","Burfeind, Peter"],["dc.date.accessioned","2018-11-07T08:34:19Z"],["dc.date.available","2018-11-07T08:34:19Z"],["dc.date.issued","2009"],["dc.format.extent","285"],["dc.identifier.doi","10.1159/000254152"],["dc.identifier.isi","000271321600007"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17784"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","1424-8581"],["dc.title","Targeted Disruption of the Mouse Npal3 Gene Leads to Deficits in Behavior, Increased IgE Levels, and Impaired Lung Function (vol 125, pg 186, 2009)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","232"],["dc.bibliographiccitation.issue","3-4"],["dc.bibliographiccitation.journal","Cytogenetic and Genome Research"],["dc.bibliographiccitation.lastpage","244"],["dc.bibliographiccitation.volume","121"],["dc.contributor.author","Rzymski, T."],["dc.contributor.author","Grzmil, Pawel"],["dc.contributor.author","Meinhardt, Andreas"],["dc.contributor.author","Wolf, S."],["dc.contributor.author","Burfeind, Peter"],["dc.date.accessioned","2018-11-07T11:19:47Z"],["dc.date.available","2018-11-07T11:19:47Z"],["dc.date.issued","2008"],["dc.description.abstract","PHF5A is a highly conserved protein from yeast to man, and based on studies in yeast, it was suggested that the homologous protein RDS3P in S. cerevisiae takes part in the organization of U2 snRNP particles. By using the yeast two-hybrid assay we could demonstrate that PHF5A interacted both with ATP-dependent helicases EP400 and DDX1 and with arginine-serine (RS)-rich domains of splicing factors U2AF1 and SFRS5 in mouse. Furthermore, domain interaction studies revealed that PHF5A interaction with EP400 and DDX1 is restricted to the N-terminal part of PHF5A, whereas the C-terminal region of PHF5A was found to be responsible for the association with U2AF1 and SFRS5. By using the yeast three-hybrid assay, we could further show that both EP400 and DDX1 interacted only indirectly with U2AF1 and SFRS5 proteins via the bridge protein PHF5A. The subcellular localization of a PHF5A-GFP fusion protein was predominantly observed in the nucleus and, in addition, PHF5A co-localized with both U2AF1 and SFRS5 proteins in nuclear speckles of NIH3T3 cells. Moreover, expression analyses demonstrated that PHF5A and U2AF1 gene expression coincided in spermatocytes during murine spermatogenesis and interaction between these proteins was also detectable in the spermatocyte-specific cell line GC-4spc by using in vivo co-immunoprecipitation studies. Taken together, our results indicate that PHF5A resembles a protein which interacts with splicing factors U2AF1 and SFRS5 and helicases EP400 and DDX1 and functions as a bridge protein between these proteins. Copyright (c) 2008 S. Karger AG, Basel."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft [SFB 271]"],["dc.identifier.doi","10.1159/000138890"],["dc.identifier.isi","000259032000010"],["dc.identifier.pmid","18758164"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9352"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55369"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","1424-8581"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","PHF5A represents a bridge protein between splicing proteins and ATP-dependent helicases and is differentially expressed during mouse spermatogenesis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3971"],["dc.bibliographiccitation.issue","45"],["dc.bibliographiccitation.journal","Oncogene"],["dc.bibliographiccitation.lastpage","3982"],["dc.bibliographiccitation.volume","28"],["dc.contributor.author","Kaulfuss, Silke"],["dc.contributor.author","von Hardenberg, Sandra"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Herr, Anna-Maria"],["dc.contributor.author","Laccone, Franco A."],["dc.contributor.author","Wolf, S."],["dc.contributor.author","Burfeind, Peter"],["dc.date.accessioned","2018-11-07T11:22:09Z"],["dc.date.available","2018-11-07T11:22:09Z"],["dc.date.issued","2009"],["dc.description.abstract","Recently, we could show that the focal adhesion protein leupaxin (LPXN) is expressed in human prostate carcinomas (PCa) and induces invasiveness of androgen-independent PCa cells. In this study we show that LPXN enhanced the progression of existing PCa in vivo by breeding transgenic mice with prostate-specific LPXN expression and TRAMP mice (transgenic adenocarcinoma of mouse prostate). Double transgenic LPXN/TRAMP mice showed a significant increase in poorly differentiated PCa and distant metastases as compared with control TRAMP mice. Additional studies on primary PCa cells generated from both transgenic backgrounds confirmed the connection regarding LPXN overexpression and increased motility and invasiveness of PCa cells. One mediator of LPXN-induced invasion was found to be the cell-cell adhesion protein p120catenin (p120CTN). Both in vitro and in vivo experiments revealed that p120CTN expression negatively correlates with LPXN expression, followed by a redistribution of beta-catenin. Downregulation of LPXN using small interfering RNAs (siRNAs) resulted in a membranous localization of beta-catenin, whereas strong nuclear accumulation of beta-catenin was observed in p120CTN knockdown cells leading to enhanced transcription of the beta-catenin target gene matrix metalloprotease-7. In conclusion, the present results indicate that LPXN enhances the progression of PCa through downregulation of p120CTN expression and that LPXN could function as a marker for aggressive PCa in the future. Oncogene (2009) 28, 3971-3982; doi:10.1038/onc.2009.254; published online 24 August 2009"],["dc.identifier.doi","10.1038/onc.2009.254"],["dc.identifier.isi","000272560300003"],["dc.identifier.pmid","19701244"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55931"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0950-9232"],["dc.title","Leupaxin acts as a mediator in prostate carcinoma progression through deregulation of p120catenin expression"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","186"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Cytogenetic and Genome Research"],["dc.bibliographiccitation.lastpage","200"],["dc.bibliographiccitation.volume","125"],["dc.contributor.author","Grzmil, Pawel"],["dc.contributor.author","Konietzko, J."],["dc.contributor.author","Boehm, D."],["dc.contributor.author","Hoelter, Sabine M."],["dc.contributor.author","Aguilar, A."],["dc.contributor.author","Javaheri, A."],["dc.contributor.author","Kalaydjiev, S."],["dc.contributor.author","Adler, Thure"],["dc.contributor.author","Bolle, I."],["dc.contributor.author","Adham, Ibrahim M."],["dc.contributor.author","Dixkens, C."],["dc.contributor.author","Wolf, S."],["dc.contributor.author","Fuchs, H."],["dc.contributor.author","Gailus-Durne, V."],["dc.contributor.author","Wurst, Wolfgang"],["dc.contributor.author","Ollert, Markus W."],["dc.contributor.author","Busch, D."],["dc.contributor.author","Schulz, H."],["dc.contributor.author","de Angelis, Martin Hrabe"],["dc.contributor.author","Burfeind, Peter"],["dc.date.accessioned","2018-11-07T08:34:19Z"],["dc.date.available","2018-11-07T08:34:19Z"],["dc.date.issued","2009"],["dc.description.abstract","The non-imprinted in Prader-Willi/Angelman syndrome (NIPA) proteins are highly conserved receptors or transporters. Translocation of NIPA genes were found in patients with Prader-Willi syndrome, and loss-of-function of the NIPA1 gene was identified in hereditary spastic paraplegia. The family of NIPA-like domain containing (NPAL) proteins is closely related to the NIPA proteins, but to date nothing is known about their function. Here, we could demonstrate that both human NPAL3 and mouse Npal3 are ubiquitously expressed and encode highly conserved proteins. To further elucidate the function of the Npal3 gene, knockout (Npal3(-/-)) mice were generated. Intensive phenotypic analyses revealed that disruption of the Npal3 gene results in a pleiotropic phenotype. The function of the nervous system was impaired in both mutant males and females which could be demonstrated in behavioral tests. In addition, in Npal3 mutants the number of NK cells was decreased and changes in IgM, IgG(2), and IgA were observed, indicating that the immune system is also affected. Interestingly, increased IgE levels as well as impaired lung functions were observed in mutant males but not in mutant females. It should be noted that the human NPAL3 gene is located at 1p36.12 -> p35.1, and atopic diseases were previously linked to this genomic region. Thus, the Npal3(-/-) mice could serve as a valuable model system for studying atopic diseases. Copyright (C) 2009 S. Karger AG, Basel"],["dc.identifier.doi","10.1159/000230003"],["dc.identifier.isi","000269572100003"],["dc.identifier.pmid","19738379"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9315"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17783"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","1424-8581"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Targeted Disruption of the Mouse Npal3 Gene Leads to Deficits in Behavior, Increased IgE Levels, and Impaired Lung Function"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","74"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Cytogenetic and Genome Research"],["dc.bibliographiccitation.lastpage","82"],["dc.bibliographiccitation.volume","119"],["dc.contributor.author","Grzmil, Pawel"],["dc.contributor.author","Burfeind, C."],["dc.contributor.author","Preuss, Thomas"],["dc.contributor.author","Dixkens, C."],["dc.contributor.author","Wolf, S."],["dc.contributor.author","Engel, Wolfgang"],["dc.contributor.author","Burfeind, Peter"],["dc.date.accessioned","2018-11-07T11:06:22Z"],["dc.date.available","2018-11-07T11:06:22Z"],["dc.date.issued","2007"],["dc.description.abstract","Genes reported to be crucial for spermatogenesis are often exclusively expressed in the testis. We have identified a novel male germ cell-specific expressed gene named peroxisomal testis specific 1 (Pxt1) with expression starting at the spermatocyte stage during mouse spermatogenesis. The putative amino acid sequence encoded by the cDNA of the Pxt1 gene contains a conserved Asn-His-Leu (NHL)-motif at its C-terminal end, which is characteristic for peroxisomal proteins. Pxt1-EGFP fusion protein is co-localized with known peroxisomal marker proteins in transfected NIH3T3 cells. In addition, we could demonstrate that the peroxisomal targeting signal NHL is functional and responsible for the correct subcellular localization of the Pxt1-EGFP fusion protein. In male germ cells peroxisomes were reported only in spermatogonia. The Pxt1 gene is so far the first gene coding for a putative peroxisomal protein which is expressed in later steps of spermatogenesis, namely in pachytene spermatocytes. Copyright (C) 2007 S. Karger AG, Basel."],["dc.identifier.doi","10.1159/000109622"],["dc.identifier.isi","000251909600013"],["dc.identifier.pmid","18160785"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52294"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","1424-8581"],["dc.title","The putative peroxisomal gene Pxt1 is exclusively expressed in the testis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]