Gross, Julia Christina

[["dc.bibliographiccitation.firstpage","1560"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Biomolecules"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Karuna M, Pradhipa"],["dc.contributor.author","Witte, Leonie"],["dc.contributor.author","Linnemannstoens, Karen"],["dc.contributor.author","Choezom, Dolma"],["dc.contributor.author","Danieli-Mackay, Adi"],["dc.contributor.author","Honemann-Capito, Mona"],["dc.contributor.author","Gross, Julia Christina"],["dc.date.accessioned","2021-04-14T08:31:10Z"],["dc.date.available","2021-04-14T08:31:10Z"],["dc.date.issued","2020"],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft"],["dc.identifier.doi","10.3390/biom10111560"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83502"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.publisher","MDPI"],["dc.relation.eissn","2218-273X"],["dc.rights","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Phosphorylation of Ykt6 SNARE Domain Regulates Its Membrane Recruitment and Activity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2057"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","2066"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Menck, Kerstin"],["dc.contributor.author","Klemm, Florian"],["dc.contributor.author","Gross, Julia Christina"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Wenzel, Dirk"],["dc.contributor.author","Binder, Claudia"],["dc.date.accessioned","2019-07-10T08:11:46Z"],["dc.date.available","2019-07-10T08:11:46Z"],["dc.date.issued","2013-11-01"],["dc.description.abstract","Recently, we have shown that macrophage (MΦ)-induced invasion of breast cancer cells requires upregulation of Wnt 5a in MΦ leading to activation of β-Catenin-independent Wnt signaling in the tumor cells. However, it remained unclear, how malignant cells induce Wnt 5a in MΦ and how it is transferred back to the cancer cells. Here we identify two types of extracellular particles as essential for this intercellular interaction in both directions. Plasma membrane-derived microvesicles (MV) as well as exosomes from breast cancer cells, although biologically distinct populations, both induce Wnt 5a in MΦ. In contrast, the particle-free supernatant and vesicles from benign cells, such as platelets, have no such effect. Induction is antagonized by the Wnt inhibitor Dickkopf-1. Subsequently, Wnt 5a is shuttled via responding MΦ-MV and exosomes to the tumor cells enhancing their invasion. Wnt 5a export on both vesicle fractions depends at least partially on the cargo protein Evenness interrupted (Evi). Its knockdown leads to Wnt 5a depletion of both particle populations and reduced vesicle-mediated invasion. In conclusion, MV and exosomes are critical for MΦ-induced invasion of cancer cells since they are responsible for upregulation of MΦ-Wnt 5a as well as for its delivery to the recipient cells via a reciprocal loop. Although of different biogenesis, both populations share common features regarding function and Evi-dependent secretion of non-canonical Wnts."],["dc.identifier.fs","603831"],["dc.identifier.pmid","24185202"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10760"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60794"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1949-2553"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY 3.0"],["dc.rights.uri","http://creativecommons.org/licenses/by/3.0"],["dc.title","Induction and transport of Wnt 5a during macrophage-induced malignant invasion is mediated by two types of extracellular vesicles."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","10"],["dc.bibliographiccitation.journal","Frontiers in Cardiovascular Medicine"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Gross, Julia Christina"],["dc.contributor.author","Zelarayan, Laura Cecilia"],["dc.date.accessioned","2019-07-09T11:45:10Z"],["dc.date.available","2019-07-09T11:45:10Z"],["dc.date.issued","2018"],["dc.description.abstract","Wnt signaling is an important pathway in health and disease and a key regulator of stem cell maintenance, differentiation, and proliferation. During heart development, Wnt signaling controls specification, proliferation and differentiation of cardiovascular cells. In this regard, the role of activated Wnt signaling in cardiogenesis is well defined. However, the knowledge about signaling transmission has been challenged. Recently, the packaging of hydrophobic Wnt proteins on extracellular vesicles (EVs) has emerged as a mechanism to facilitate their extracellular spreading and their functioning as morphogens. EVs spread systemically and therefore can have pleiotropic effects on very different cell types. They are heavily studied in tumor biology where they affect tumor growth and vascularization and can serve as biomarkers in liquid biopsies. In this review we will highlight recent discoveries of factors involved in the release of Wnts on EVs and its potential implications in the communication between physiological and pathological heart cells."],["dc.identifier.doi","10.3389/fcvm.2018.00010"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15048"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59172"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/299"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C07: Kardiomyozyten Wnt/β-catenin Komplex Aktivität im pathologischen Herz-Remodeling - als gewebespezifischer therapeutischer Ansatz"],["dc.relation.eissn","2297-055X"],["dc.relation.issn","2297-055X"],["dc.relation.workinggroup","RG Zelarayán-Behrend (Developmental Pharmacology)"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","The Mingle-Mangle of Wnt Signaling and Extracellular Vesicles: Functional Implications for Heart Research"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","overview_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","dev186833"],["dc.bibliographiccitation.issue","15"],["dc.bibliographiccitation.journal","Development"],["dc.bibliographiccitation.volume","147"],["dc.contributor.author","Witte, Leonie"],["dc.contributor.author","Linnemannstöns, Karen"],["dc.contributor.author","Schmidt, Kevin"],["dc.contributor.author","Honemann-Capito, Mona"],["dc.contributor.author","Grawe, Ferdinand"],["dc.contributor.author","Wodarz, Andreas"],["dc.contributor.author","Gross, Julia Christina"],["dc.date.accessioned","2021-04-14T08:23:55Z"],["dc.date.available","2021-04-14T08:23:55Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1242/dev.186833"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17518"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81096"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","1477-9129"],["dc.relation.issn","0950-1991"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","The kinesin motor Klp98A mediates apical to basal Wg transport"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0150377"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Niessner, Christine"],["dc.contributor.author","Gross, Julia Christina"],["dc.contributor.author","Denzau, Susanne"],["dc.contributor.author","Peichl, Leo"],["dc.contributor.author","Fleissner, Gerta"],["dc.contributor.author","Wiltschko, Wolfgang"],["dc.contributor.author","Wiltschko, Roswitha"],["dc.date.accessioned","2018-11-07T10:16:54Z"],["dc.date.available","2018-11-07T10:16:54Z"],["dc.date.issued","2016"],["dc.description.abstract","Cryptochromes, blue-light absorbing proteins involved in the circadian clock, have been proposed to be the receptor molecules of the avian magnetic compass. In birds, several cryptochromes occur: Cryptochrome 2, Cryptochrome 4 and two splice products of Cryptochrome 1, Cry1a and Cry1b. With an antibody not distinguishing between the two splice products, Cryptochrome 1 had been detected in the retinal ganglion cells of garden warblers during migration. A recent study located Cry1a in the outer segments of UV/V-cones in the retina of domestic chickens and European robins, another migratory species. Here we report the presence of cryptochrome 1b (eCry1b) in retinal ganglion cells and displaced ganglion cells of European Robins, Erithacus rubecula. Immuno-histochemistry at the light microscopic and electron microscopic level showed eCry1b in the cell plasma, free in the cytosol as well as bound to membranes. This is supported by immuno-blotting. However, this applies only to robins in the migratory state. After the end of the migratory phase, the amount of eCry1b was markedly reduced and hardly detectable. In robins, the amount of eCry1b in the retinal ganglion cells varies with season: it appears to be strongly expressed only during the migratory period when the birds show nocturnal migratory restlessness. Since the avian magnetic compass does not seem to be restricted to the migratory phase, this seasonal variation makes a role of eCry1b in magnetoreception rather unlikely. Rather, it could be involved in physiological processes controlling migratory restlessness and thus enabling birds to perform their nocturnal flights."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft; Alfons und Gertrud Kassel Stiftung"],["dc.identifier.doi","10.1371/journal.pone.0150377"],["dc.identifier.isi","000371991300025"],["dc.identifier.pmid","26953690"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13154"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41129"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Seasonally Changing Cryptochrome 1b Expression in the Retinal Ganglion Cells of a Migrating Passerine Bird"],["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","43"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Cancers"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Worst, Thomas Stefan"],["dc.contributor.author","Previti, Christopher"],["dc.contributor.author","Nitschke, Katja"],["dc.contributor.author","Diessl, Nicolle"],["dc.contributor.author","Gross, Julia Christina"],["dc.contributor.author","Hoffmann, Lena"],["dc.contributor.author","Frey, Lisa"],["dc.contributor.author","Thomas, Vanessa"],["dc.contributor.author","Kahlert, Christoph"],["dc.contributor.author","Bieback, Karen"],["dc.contributor.author","Torres Crigna, Adriana"],["dc.contributor.author","Fricke, Fabia"],["dc.contributor.author","Porubsky, Stefan"],["dc.contributor.author","Westhoff, Niklas"],["dc.contributor.author","von Hardenberg, Jost"],["dc.contributor.author","Nuhn, Philipp"],["dc.contributor.author","Erben, Philipp"],["dc.contributor.author","Michel, Maurice Stephan"],["dc.contributor.author","Boutros, Michael"],["dc.date.accessioned","2020-12-10T18:46:58Z"],["dc.date.available","2020-12-10T18:46:58Z"],["dc.date.issued","2020"],["dc.description.sponsorship","German Society of Urology"],["dc.identifier.doi","10.3390/cancers12010043"],["dc.identifier.eissn","2072-6694"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78598"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.publisher","MDPI"],["dc.relation.eissn","2072-6694"],["dc.rights","https://creativecommons.org/licenses/by/4.0/"],["dc.title","miR-10a-5p and miR-29b-3p as Extracellular Vesicle-Associated Prostate Cancer Detection Markers"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","1378056"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Extracellular Vesicles"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Menck, Kerstin"],["dc.contributor.author","Sönmezer, Can"],["dc.contributor.author","Worst, Thomas Stefan"],["dc.contributor.author","Schulz, Matthias"],["dc.contributor.author","Dihazi, Gry Helene"],["dc.contributor.author","Streit, Frank"],["dc.contributor.author","Erdmann, Gerrit"],["dc.contributor.author","Kling, Simon"],["dc.contributor.author","Boutros, Michael"],["dc.contributor.author","Binder, Claudia"],["dc.contributor.author","Gross, Julia Christina"],["dc.date.accessioned","2019-07-09T11:45:57Z"],["dc.date.available","2019-07-09T11:45:57Z"],["dc.date.issued","2017"],["dc.description.abstract","Extracellular vesicles (EVs) are membrane particles secreted from cells into all body fluids. Several EV populations exist differing in size and cellular origin. Using differential centrifugation EVs pelleting at 14,000 g (\"microvesicles\" (MV)) and 100,000 g (\"exosomes\") are distinguishable by protein markers. Neutral sphingomyelinase (nSMase) inhibition has been shown to inhibit exosome release from cells and has since been used to study their functional implications. How nSMases (also known as SMPD2 and SMPD3) affect the basal secretion of MVs is unclear. Here we investigated how SMPD2/3 impact both EV populations. SMPD2/3 inhibition by GW4869 or RNAi decreases secretion of exosomes, but also increases secretion of MVs from the plasma membrane. Both populations differ significantly in metabolite composition and Wnt proteins are specifically loaded onto MVs under these conditions. Taken together, our data reveal a novel regulatory function of SMPD2/3 in vesicle budding from the plasma membrane and clearly suggest that - despite the different vesicle biogenesis - the routes of vesicular export are adaptable."],["dc.identifier.doi","10.1080/20013078.2017.1378056"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15354"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59345"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2001-3078"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.subject.ddc","610"],["dc.title","Neutral sphingomyelinases control extracellular vesicles budding from the plasma membrane"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]