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","e202000855"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Life Science Alliance"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Lin, Yu-Chih"],["dc.contributor.author","Haas, Alexander"],["dc.contributor.author","Bufe, Anja"],["dc.contributor.author","Parbin, Sabnam"],["dc.contributor.author","Hennecke, Magdalena"],["dc.contributor.author","Voloshanenko, Oksana"],["dc.contributor.author","Gross, Julia"],["dc.contributor.author","Boutros, Michael"],["dc.contributor.author","Acebron, Sergio P"],["dc.contributor.author","Bastians, Holger"],["dc.date.accessioned","2021-04-14T08:29:53Z"],["dc.date.available","2021-04-14T08:29:53Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.26508/lsa.202000855"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83017"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","2575-1077"],["dc.title","Wnt10b-GSK3β–dependent Wnt/STOP signaling prevents aneuploidy in human somatic cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","844441"],["dc.bibliographiccitation.journal","Frontiers in Cardiovascular Medicine"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Jakobi, Tobias"],["dc.contributor.author","Groß, Julia"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Doroudgar, Shirin"],["dc.date.accessioned","2022-07-01T07:35:28Z"],["dc.date.available","2022-07-01T07:35:28Z"],["dc.date.issued","2022"],["dc.description.abstract","Introduction Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) disease (COVID-19) has emerged as a major cause of morbidity and mortality worldwide, placing unprecedented pressure on healthcare. Cardiomyopathy is described in patients with severe COVID-19 and increasing evidence suggests that cardiovascular involvement portends a high mortality. To facilitate fast development of antiviral interventions, drugs initially developed to treat other diseases are currently being repurposed as COVID-19 treatments. While it has been shown that SARS-CoV-2 invades cells through the angiotensin-converting enzyme 2 receptor (ACE2), the effect of drugs currently repurposed to treat COVID-19 on the heart requires further investigation. Methods Human induced pluripotent stem cell-derived cardiac myocytes (hiPSC-CMs) were treated with five repurposed drugs (remdesivir, lopinavir/ritonavir, lopinavir/ritonavir/interferon beta (INF-β), hydroxychloroquine, and chloroquine) and compared with DMSO controls. Transcriptional profiling was performed to identify global changes in gene expression programs. Results RNA sequencing of hiPSC-CMs revealed significant changes in gene programs related to calcium handling and the endoplasmic reticulum stress response, most prominently for lopinavir/ritonavir and lopinavir/ritonavir/interferon-beta. The results of the differential gene expression analysis are available for interactive access at https://covid19drugs.jakobilab.org . Conclusion Transcriptional profiling in hiPSC-CMs treated with COVID-19 drugs identified unfavorable changes with lopinavir/ritonavir and lopinavir/ritonavir/INF-β in key cardiac gene programs that may negatively affect heart function."],["dc.identifier.doi","10.3389/fcvm.2022.844441"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112179"],["dc.notes.intern","DOI-Import GROB-581"],["dc.relation.eissn","2297-055X"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Transcriptional Effects of Candidate COVID-19 Treatments on Cardiac Myocytes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","dev185421"],["dc.bibliographiccitation.issue","15"],["dc.bibliographiccitation.journal","Development"],["dc.bibliographiccitation.volume","147"],["dc.contributor.author","Linnemannstöns, Karen"],["dc.contributor.author","Witte, Leonie"],["dc.contributor.author","Karuna M, Pradhipa"],["dc.contributor.author","Kittel, Jeanette Clarissa"],["dc.contributor.author","Danieli, Adi"],["dc.contributor.author","Müller, Denise"],["dc.contributor.author","Nitsch, Lena"],["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.185421"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81097"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1477-9129"],["dc.relation.issn","0950-1991"],["dc.title","Ykt6-dependent endosomal recycling is required for Wnt secretion in the Drosophila wing epithelium"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","6"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Circulation Research"],["dc.bibliographiccitation.lastpage","24"],["dc.bibliographiccitation.volume","126"],["dc.contributor.author","Schoger, Eric"],["dc.contributor.author","Carroll, Kelli J."],["dc.contributor.author","Iyer, Lavanya M."],["dc.contributor.author","McAnally, John R."],["dc.contributor.author","Tan, Wei"],["dc.contributor.author","Liu, Ning"],["dc.contributor.author","Noack, Claudia"],["dc.contributor.author","Shomroni, Orr"],["dc.contributor.author","Salinas, Gabriela"],["dc.contributor.author","Groß, Julia"],["dc.contributor.author","Herzog, Nicole"],["dc.contributor.author","Doroudgar, Shirin"],["dc.contributor.author","Bassel-Duby, Rhonda"],["dc.contributor.author","Zimmermann, Wolfram-H."],["dc.contributor.author","Zelarayán, Laura C."],["dc.date.accessioned","2020-12-10T18:38:00Z"],["dc.date.available","2020-12-10T18:38:00Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1161/CIRCRESAHA.118.314522"],["dc.identifier.pmid","31730408"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77162"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/332"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation","SFB 1002 | C07: Kardiomyozyten Wnt/β-catenin Komplex Aktivität im pathologischen Herz-Remodeling - als gewebespezifischer therapeutischer Ansatz"],["dc.relation","SFB 1002 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation.workinggroup","RG Zelarayán-Behrend (Developmental Pharmacology)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.title","CRISPR-Mediated Activation of Endogenous Gene Expression in the Postnatal Heart"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["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.journal","Journal of Cell Science"],["dc.contributor.author","Choezom, Dolma"],["dc.contributor.author","Gross, Julia Christina"],["dc.date.accessioned","2022-02-01T10:31:33Z"],["dc.date.available","2022-02-01T10:31:33Z"],["dc.date.issued","2022"],["dc.description.abstract","During endosome maturation, neutral sphingomyelinase 2 (nSMase2) is involved in intraluminal vesicles (ILVs) budding into late endosomes or multivesicular bodies (MVBs). Fusion of these with the plasma membrane results in exosomes or small extracellular vesicles (sEV) secretion. Here, we describe nSMase2 activity to control sEV secretion through modulation of V-ATPase activity. Specifically, we show that nSMase2 inhibition induces V-ATPase complex assembly that drives MVB lumen acidification and consequently reduces sEV secretion. Conversely, we further demonstrate that stimulating nSMase2 activity with the inflammatory cytokine TNFα decreases acidification and increases sEV secretion. Thus, we find that nSMase2 activity affects MVB membrane lipid composition to counteract V-ATPase-mediated endosome acidification, thereby shifting MVB fate towards sEV secretion."],["dc.description.abstract","During endosome maturation, neutral sphingomyelinase 2 (nSMase2) is involved in intraluminal vesicles (ILVs) budding into late endosomes or multivesicular bodies (MVBs). Fusion of these with the plasma membrane results in exosomes or small extracellular vesicles (sEV) secretion. Here, we describe nSMase2 activity to control sEV secretion through modulation of V-ATPase activity. Specifically, we show that nSMase2 inhibition induces V-ATPase complex assembly that drives MVB lumen acidification and consequently reduces sEV secretion. Conversely, we further demonstrate that stimulating nSMase2 activity with the inflammatory cytokine TNFα decreases acidification and increases sEV secretion. Thus, we find that nSMase2 activity affects MVB membrane lipid composition to counteract V-ATPase-mediated endosome acidification, thereby shifting MVB fate towards sEV secretion."],["dc.identifier.doi","10.1242/jcs.259324"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/98888"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-517"],["dc.relation.eissn","1477-9137"],["dc.relation.issn","0021-9533"],["dc.title","Neutral Sphingomyelinase 2 controls exosomes secretion via counteracting V-ATPase-mediated endosome acidification"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["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"]]