Gross, Julia Christina

[["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.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.firstpage","17"],["dc.bibliographiccitation.lastpage","28"],["dc.bibliographiccitation.seriesnr","1481"],["dc.contributor.author","Glaeser, Kathrin"],["dc.contributor.author","Boutros, Michael"],["dc.contributor.author","Gross, Julia Christina"],["dc.contributor.editor","Barrett, Quinn"],["dc.contributor.editor","Lum, Lawrence"],["dc.date.accessioned","2021-06-02T10:44:25Z"],["dc.date.available","2021-06-02T10:44:25Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.1007/978-1-4939-6393-5_3"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/87029"],["dc.notes.intern","DOI-Import GROB-425"],["dc.publisher","Springer New York"],["dc.publisher.place","New York, NY"],["dc.relation.crisseries","Methods in Molecular Biology"],["dc.relation.eisbn","978-1-4939-6393-5"],["dc.relation.isbn","978-1-4939-6391-1"],["dc.relation.ispartof","Methods in Molecular Biology"],["dc.relation.ispartof","Wnt Signaling"],["dc.relation.ispartofseries","Methods in Molecular Biology; 1481"],["dc.title","Biochemical Methods to Analyze Wnt Protein Secretion"],["dc.type","book_chapter"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","8759"],["dc.bibliographiccitation.issue","26"],["dc.bibliographiccitation.journal","Journal of Biological Chemistry"],["dc.bibliographiccitation.lastpage","8774"],["dc.bibliographiccitation.volume","295"],["dc.contributor.author","Wesslowski, Janine"],["dc.contributor.author","Kozielewicz, Pawel"],["dc.contributor.author","Wang, Xianxian"],["dc.contributor.author","Cui, Haijun"],["dc.contributor.author","Schihada, Hannes"],["dc.contributor.author","Kranz, Dominique"],["dc.contributor.author","Karuna M, Pradhipa"],["dc.contributor.author","Levkin, Pavel"],["dc.contributor.author","Gross, Julia Christina"],["dc.contributor.author","Boutros, Michael"],["dc.contributor.author","Schulte, Gunnar"],["dc.contributor.author","Davidson, Gary"],["dc.date.accessioned","2021-04-14T08:25:37Z"],["dc.date.available","2021-04-14T08:25:37Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1074/jbc.RA120.012892"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81688"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.issn","0021-9258"],["dc.title","eGFP-tagged Wnt-3a enables functional analysis of Wnt trafficking and signaling and kinetic assessment of Wnt binding to full-length Frizzled"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","12263"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Journal of Extracellular Vesicles"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Linnemannstöns, Karen"],["dc.contributor.author","Karuna M, Pradhipa"],["dc.contributor.author","Witte, Leonie"],["dc.contributor.author","Choezom, Dolma"],["dc.contributor.author","Honemann‐Capito, Mona"],["dc.contributor.author","Lagurin, Alex Simon"],["dc.contributor.author","Schmidt, Chantal Vanessa"],["dc.contributor.author","Shrikhande, Shreya"],["dc.contributor.author","Steinmetz, Lara‐Kristin"],["dc.contributor.author","Wiebke, Möbius"],["dc.contributor.author","Gross, Julia Christina"],["dc.date.accessioned","2022-10-04T10:21:23Z"],["dc.date.available","2022-10-04T10:21:23Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1002/jev2.12263"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/114397"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-600"],["dc.relation.eissn","2001-3078"],["dc.relation.issn","2001-3078"],["dc.title","Microscopic and biochemical monitoring of endosomal trafficking and extracellular vesicle secretion in an endogenous in vivo model"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","UNSP M117.068577"],["dc.bibliographiccitation.firstpage","998"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Molecular & Cellular Proteomics"],["dc.bibliographiccitation.lastpage","1008"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Worst, Thomas Stefan"],["dc.contributor.author","von Hardenberg, Jost"],["dc.contributor.author","Gross, Julia Christina"],["dc.contributor.author","Erben, Philipp"],["dc.contributor.author","Schnoelzer, Martina"],["dc.contributor.author","Hausser, Ingrid"],["dc.contributor.author","Bugert, Peter"],["dc.contributor.author","Michel, Maurice Stephan"],["dc.contributor.author","Boutros, Michael"],["dc.date.accessioned","2018-11-07T10:23:18Z"],["dc.date.available","2018-11-07T10:23:18Z"],["dc.date.issued","2017"],["dc.description.abstract","In prostate cancer and other malignancies sensitive and robust biomarkers are lacking or have relevant limitations. Prostate specific antigen (PSA), the only biomarker widely used in prostate cancer, is suffering from low specificity. Exosomes offer new perspectives in the discovery of blood-based biomarkers. Here we present a proof-of principle study for a proteomics-based identification pipeline, implementing existing data sources, to exemplarily identify exosome-based biomarker candidates in prostate cancer. Exosomes from malignant PC3 and benign PNT1A cells and from FBS-containing medium were isolated using sequential ultracentrifugation. Exosome and control samples were analyzed on an LTQ-Orbitrap XL mass spectrometer. Proteomic data is available via Proteom-eXchange with identifier PXD003651. We developed a scoring scheme to rank 64 proteins exclusively found in PC3 exosomes, integrating data from four public databases and published mass spectrometry data sets. Among the top candidates, we focused on the tight junction protein claudin 3. Retests under serum-free conditions using immunoblotting and immunogold labeling confirmed the presence of claudin 3 on PC3 exosomes. Claudin 3 levels were determined in the blood plasma of patients with localized (n = 58; 42 with Gleason score 6-7, 16 with Gleason score >= 8) and metastatic prostate cancer (n = 11) compared with patients with benign prostatic hyperplasia (n = 15) and healthy individuals (n = 15) using ELISA, without prior laborious exosome isolation. ANOVA showed different CLDN3 plasma levels in these groups (p = 0.004). CLDN3 levels were higher in patients with Gleason >= 8 tumors compared with patients with benign prostatic hyperplasia (p = 0.012) and Gleason 6-7 tumors (p = 0.029). In patients with localized tumors CLDN3 levels predicted a Gleason score >= 8 (AUC = 0.705; p = 0.016) and did not correlate with serum PSA. By using the described workflow claudin 3 was identified and validated as a potential blood-based biomarker in prostate cancer. Furthermore this workflow could serve as a template to be used in other cancer entities."],["dc.identifier.doi","10.1074/mcp.M117.068577"],["dc.identifier.isi","000402576600003"],["dc.identifier.pmid","28396511"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42432"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Amer Soc Biochemistry Molecular Biology Inc"],["dc.relation.issn","1535-9484"],["dc.relation.issn","1535-9476"],["dc.title","Database-augmented Mass Spectrometry Analysis of Exosomes Identifies Claudin 3 as a Putative Prostate Cancer Biomarker"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]