Lenz, Christof

[["dc.bibliographiccitation.issue","19"],["dc.bibliographiccitation.journal","Cancer Research"],["dc.bibliographiccitation.volume","74"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Stroebel, Philipp"],["dc.contributor.author","Henric-Petri, Hannah"],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Emmert, Alexander"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Strecker, Jasmin"],["dc.contributor.author","Holland, Rainer"],["dc.contributor.author","Hinterthaner, Marc"],["dc.contributor.author","Corso, Jasmin"],["dc.contributor.author","Wagner, Sebastian"],["dc.contributor.author","Kueffer, Stefan"],["dc.contributor.author","Sebastian, Martin"],["dc.contributor.author","Bergmann, Lothar"],["dc.contributor.author","Danner, Bernd"],["dc.contributor.author","Schoendube, Friedrich Albert"],["dc.contributor.author","Serve, Hubert"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Oellerich, Thomas"],["dc.date.accessioned","2018-11-07T09:33:49Z"],["dc.date.available","2018-11-07T09:33:49Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.1158/1538-7445.AM2014-2487"],["dc.identifier.isi","000349906903219"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32050"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Cancer Research"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","105th Annual Meeting of the American-Association-for-Cancer-Research (AACR)"],["dc.relation.eventlocation","San Diego, CA"],["dc.relation.issn","1538-7445"],["dc.relation.issn","0008-5472"],["dc.title","Comprehensive quantitative proteomic profiling of lung cancers reveals novel biomarkers and potential drug targets"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e99941"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","JCI Insight"],["dc.bibliographiccitation.lastpage","17"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Sekeres, Karolina"],["dc.contributor.author","Gerstenberg, Kathleen"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Henze, Sarah"],["dc.contributor.author","Stauske, Michael"],["dc.contributor.author","Salinas, Gabriela"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Guan, Kaomei"],["dc.date.accessioned","2019-02-04T14:06:58Z"],["dc.date.available","2019-02-04T14:06:58Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1172/jci.insight.99941"],["dc.identifier.pmid","29925689"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57518"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/214"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A04: Patienten-spezifische induzierte pluripotente Stammzellen zur funktionellen Untersuchung von Ryanodinrezeptor-Mutationen"],["dc.relation","SFB 1002 | D01: Erholung aus der Herzinsuffizienz – Einfluss von Fibrose und Transkriptionssignatur"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation","SFB 1002 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation.issn","0021-9738"],["dc.relation.workinggroup","RG Cyganek (Stem Cell Unit)"],["dc.relation.workinggroup","RG Guan (Application of patient-specific induced pluripotent stem cells in disease modelling)"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Lenz"],["dc.relation.workinggroup","RG Tiburcy (Stem Cell Disease Modeling)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.title","Deep phenotyping of human induced pluripotent stem cell–derived atrial and ventricular cardiomyocytes"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e52435"],["dc.bibliographiccitation.issue","96"],["dc.bibliographiccitation.journal","Journal of Visualized Experiments"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Stroebel, Philipp"],["dc.contributor.author","Mohr, Sebastian"],["dc.contributor.author","Corso, Jasmin"],["dc.contributor.author","Berg, Tobias"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Serve, Hubert"],["dc.contributor.author","Oellerich, Thomas"],["dc.date.accessioned","2018-11-07T10:01:07Z"],["dc.date.available","2018-11-07T10:01:07Z"],["dc.date.issued","2015"],["dc.description.abstract","In-depth analyses of cancer cell proteomes are needed to elucidate oncogenic pathomechanisms, as well as to identify potential drug targets and diagnostic biomarkers. However, methods for quantitative proteomic characterization of patient-derived tumors and in particular their cellular subpopulations are largely lacking. Here we describe an experimental set-up that allows quantitative analysis of proteomes of cancer cell subpopulations derived from either liquid or solid tumors. This is achieved by combining cellular enrichment strategies with quantitative Super-SILAC-based mass spectrometry followed by bioinformatic data analysis. To enrich specific cellular subsets, liquid tumors are first immunophenotyped by flow cytometry followed by FACS-sorting; for solid tumors, laser-capture microdissection is used to purify specific cellular subpopulations. In a second step, proteins are extracted from the purified cells and subsequently combined with a tumor-specific, SILAC-labeled spike-in standard that enables protein quantification. The resulting protein mixture is subjected to either gel electrophoresis or Filter Aided Sample Preparation (FASP) followed by tryptic digestion. Finally, tryptic peptides are analyzed using a hybrid quadrupole-orbitrap mass spectrometer, and the data obtained are processed with bioinformatic software suites including MaxQuant. By means of the workflow presented here, up to 8,000 proteins can be identified and quantified in patient-derived samples, and the resulting protein expression profiles can be compared among patients to identify diagnostic proteomic signatures or potential drug targets."],["dc.identifier.doi","10.3791/52435"],["dc.identifier.isi","000361533700047"],["dc.identifier.pmid","25867170"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12150"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37949"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Journal Of Visualized Experiments"],["dc.relation.issn","1940-087X"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Quantitative Mass Spectrometric Profiling of Cancer-cell Proteomes Derived From Liquid and Solid Tumors"],["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.journal","Cancer Research"],["dc.bibliographiccitation.volume","75"],["dc.contributor.author","Döbele, Carmen"],["dc.contributor.author","Corso, Jasmin"],["dc.contributor.author","Cremer, Anjali"],["dc.contributor.author","Muench, Silvia"],["dc.contributor.author","Beck, Julia"],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Wachter, Astrid"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Schuetz, Ekkehard"],["dc.contributor.author","Serve, Hubert"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Oellerich, Thomas"],["dc.date.accessioned","2018-11-07T09:53:25Z"],["dc.date.available","2018-11-07T09:53:25Z"],["dc.date.issued","2015"],["dc.identifier.doi","10.1158/1538-7445.AM2015-50"],["dc.identifier.isi","000371578500047"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36326"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Cancer Research"],["dc.publisher.place","Philadelphia"],["dc.relation.eventlocation","Philadelphia, PA"],["dc.relation.issn","1538-7445"],["dc.relation.issn","0008-5472"],["dc.title","Elucidation of B cell receptor signaling in Burkitt's lymphoma reveals novel signaling nodes with potential therapeutic relevance"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3170"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","International Journal of Cancer"],["dc.bibliographiccitation.lastpage","3183"],["dc.bibliographiccitation.volume","146"],["dc.contributor.author","Blazquez, Raquel"],["dc.contributor.author","Rietkötter, Eva"],["dc.contributor.author","Wenske, Britta"],["dc.contributor.author","Wlochowitz, Darius"],["dc.contributor.author","Sparrer, Daniela"],["dc.contributor.author","Vollmer, Elena"],["dc.contributor.author","Müller, Gunnar"],["dc.contributor.author","Seegerer, Julia"],["dc.contributor.author","Sun, Xueni"],["dc.contributor.author","Dettmer, Katja"],["dc.contributor.author","Barrantes‐Freer, Alonso"],["dc.contributor.author","Stange, Lena"],["dc.contributor.author","Utpatel, Kirsten"],["dc.contributor.author","Bleckmann, Annalen"],["dc.contributor.author","Treiber, Hannes"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Schulz, Matthias"],["dc.contributor.author","Reimelt, Christian"],["dc.contributor.author","Hackl, Christina"],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Büyüktas, Deram"],["dc.contributor.author","Siam, Laila"],["dc.contributor.author","Balkenhol, Marko"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Krahn, Michael P."],["dc.contributor.author","Proescholdt, Martin A."],["dc.contributor.author","Riemenschneider, Markus J."],["dc.contributor.author","Evert, Matthias"],["dc.contributor.author","Oefner, Peter J."],["dc.contributor.author","Klein, Chistoph A."],["dc.contributor.author","Hanisch, Uwe K."],["dc.contributor.author","Binder, Claudia"],["dc.contributor.author","Pukrop, Tobias"],["dc.date.accessioned","2019-12-09T11:26:05Z"],["dc.date.accessioned","2021-10-27T13:21:49Z"],["dc.date.available","2019-12-09T11:26:05Z"],["dc.date.available","2021-10-27T13:21:49Z"],["dc.date.issued","2020"],["dc.description.abstract","More than half of all brain metastases show infiltrating rather than displacing growth at the macro-metastasis/organ parenchyma interface (MMPI), a finding associated with shorter survival. The lymphoid enhancer-binding factor-1 (LEF1) is an epithelial-mesenchymal transition (EMT) transcription factor that is commonly overexpressed in brain-colonizing cancer cells. Here, we overexpressed LEF1 in an in vivo breast cancer brain colonization model. It shortened survival, albeit without engaging EMT at the MMPI. By differential proteome analysis, we identified a novel function of LEF1 as a regulator of the glutathione (GSH) system, the principal cellular redox buffer. LEF1 overexpression also conferred resistance against therapeutic GSH depletion during brain colonization and improved management of intracellular ROS. We conclude that besides EMT, LEF1 facilitates metastasis by improving the antioxidative capacity of epithelial breast cancer cells, in particular during colonization of the brain parenchyma."],["dc.identifier.doi","10.1002/ijc.32742"],["dc.identifier.eissn","1097-0215"],["dc.identifier.issn","0020-7136"],["dc.identifier.pmid","31626715"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16874"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92047"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.eissn","1097-0215"],["dc.relation.issn","1097-0215"],["dc.relation.issn","0020-7136"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","LEF1 supports metastatic brain colonization by regulating glutathione metabolism and increasing ROS resistance in breast cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S226"],["dc.bibliographiccitation.journal","Clinical Lymphoma Myeloma & Leukemia"],["dc.bibliographiccitation.lastpage","S227"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Oellerich, Thomas"],["dc.contributor.author","Corso, Jasmin"],["dc.contributor.author","Beck, J."],["dc.contributor.author","Döbele, Carmen"],["dc.contributor.author","Wachter, Astrid"],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Goekbuget, Nicola"],["dc.contributor.author","Schuetzatz, E."],["dc.contributor.author","Serve, Hubert"],["dc.contributor.author","Urlaub, Henning"],["dc.date.accessioned","2018-11-07T09:56:00Z"],["dc.date.available","2018-11-07T09:56:00Z"],["dc.date.issued","2015"],["dc.identifier.isi","000370676300127"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36875"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cig Media Group, Lp"],["dc.publisher.place","Dallas"],["dc.relation.issn","2152-2669"],["dc.relation.issn","2152-2650"],["dc.title","Elucidation of B cell receptor signaling in Burkitt's lymphoma reveals novel signaling nodes with potential therapeutic relevance"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","5688"],["dc.bibliographiccitation.issue","20"],["dc.bibliographiccitation.journal","PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA"],["dc.bibliographiccitation.lastpage","5693"],["dc.bibliographiccitation.volume","113"],["dc.contributor.author","Corso, Jasmin"],["dc.contributor.author","Pan, Kuan-Ting"],["dc.contributor.author","Walter, Roland"],["dc.contributor.author","Doebele, Carmen"],["dc.contributor.author","Mohr, Sebastian"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Stroebel, Philipp"],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Slabicki, Mikolaj"],["dc.contributor.author","Huellein, Jennifer"],["dc.contributor.author","Comoglio, Federico"],["dc.contributor.author","Rieger, Michael A."],["dc.contributor.author","Zenz, Thorsten"],["dc.contributor.author","Wienands, Juergen"],["dc.contributor.author","Engelke, Michael"],["dc.contributor.author","Serve, Hubert"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Oellerich, Thomas"],["dc.date.accessioned","2018-11-07T10:14:14Z"],["dc.date.available","2018-11-07T10:14:14Z"],["dc.date.issued","2016"],["dc.description.abstract","Burkitt's lymphoma (BL) is a highly proliferative B-cell neoplasm and is treated with intensive chemotherapy that, because of its toxicity, is often not suitable for the elderly or for patients with endemic BL in developing countries. BL cell survival relies on signals transduced by B-cell antigen receptors (BCRs). However, tonic as well as activated BCR signaling networks and their relevance for targeted therapies in BL remain elusive. We have systematically characterized and compared tonic and activated BCR signaling in BL by quantitative phosphoproteomics to identify novel BCR effectors and potential drug targets. We identified and quantified similar to 16,000 phospho-sites in BL cells. Among these sites, 909 were related to tonic BCR signaling, whereas 984 phospho-sites were regulated upon BCR engagement. The majority of the identified BCR signaling effectors have not been described in the context of B cells or lymphomas yet. Most of these newly identified BCR effectors are predicted to be involved in the regulation of kinases, transcription, and cytoskeleton dynamics. Although tonic and activated BCR signaling shared a considerable number of effector proteins, we identified distinct phosphorylation events in tonic BCR signaling. We investigated the functional relevance of some newly identified BCR effectors and show that ACTN4 and ARFGEF2, which have been described as regulators of membrane-trafficking and cytoskeleton-related processes, respectively, are crucial for BL cell survival. Thus, this study provides a comprehensive dataset for tonic and activated BCR signaling and identifies effector proteins that may be relevant for BL cell survival and thus may help to develop new BL treatments."],["dc.identifier.doi","10.1073/pnas.1601053113"],["dc.identifier.isi","000375977600058"],["dc.identifier.pmid","27155012"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40583"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Natl Acad Sciences"],["dc.relation.issn","0027-8424"],["dc.title","Elucidation of tonic and activated B-cell receptor signaling in Burkitt's lymphoma provides insights into regulation of cell survival"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","World Journal of Urology"],["dc.contributor.author","Fichtner, A."],["dc.contributor.author","Bohnenberger, H."],["dc.contributor.author","Elakad, O."],["dc.contributor.author","Richter, A."],["dc.contributor.author","Lenz, C."],["dc.contributor.author","Oing, C."],["dc.contributor.author","Ströbel, P."],["dc.contributor.author","Kueffer, S."],["dc.contributor.author","Nettersheim, D."],["dc.contributor.author","Bremmer, F."],["dc.date.accessioned","2022-02-01T10:31:51Z"],["dc.date.available","2022-02-01T10:31:51Z"],["dc.date.issued","2022"],["dc.description.abstract","Abstract Purpose Advanced testicular germ cell tumours (GCT) generally have a good prognosis owing to their unique sensitivity towards cisplatin-based chemotherapies. However, cisplatin-resistant GCT have a poor outcome. Further studies are mandatory to better understand resistance mechanisms and develop therapeutic strategies for refractory GCTs. Methods Protein levels in cisplatin-resistant GCT cell lines of NTERA-2, NCCIT and 2102EP were analyzed by quantitative proteomic mass spectrometry (MS) in combination with stable isotope labelling by amino acids in cell culture (SILAC). Differentially abundant protein markers of acquired cisplatin resistance were validated by Western blotting. Comprehensive bioinformatical annotation using gene set enrichment analyses (GSEA) and STRING interaction analysis were performed to identify commonly affected pathways in cisplatin resistance and the data were compared to the GCT cohort of the ‘The Cancer Genome Atlas’. Results A total of 4375 proteins were quantified by MS, 144 of which were found to be differentially abundant between isogenic resistant and sensitive cell line pairs (24 proteins for NTERA-2, 60 proteins for NCCIT, 75 proteins for 2102EP). Western blotting confirmed regulation of key resistance-associated proteins (CBS, ANXA1, LDHA, CTH, FDXR). GSEA revealed a statistically significant enrichment of DNA repair-associated proteins in all three resistant cell lines and specific additional processes for individual cell lines. Conclusion High resolution MS combined with SILAC is a powerful tool and 144 significantly deregulated proteins were found in cisplatin-resistant GCT cell lines. Our study provides the largest proteomic in vitro library for cisplatin resistance in GCT, yet, enabling further studies to develop new treatment options for patients with refractory GCT."],["dc.description.abstract","Abstract Purpose Advanced testicular germ cell tumours (GCT) generally have a good prognosis owing to their unique sensitivity towards cisplatin-based chemotherapies. However, cisplatin-resistant GCT have a poor outcome. Further studies are mandatory to better understand resistance mechanisms and develop therapeutic strategies for refractory GCTs. Methods Protein levels in cisplatin-resistant GCT cell lines of NTERA-2, NCCIT and 2102EP were analyzed by quantitative proteomic mass spectrometry (MS) in combination with stable isotope labelling by amino acids in cell culture (SILAC). Differentially abundant protein markers of acquired cisplatin resistance were validated by Western blotting. Comprehensive bioinformatical annotation using gene set enrichment analyses (GSEA) and STRING interaction analysis were performed to identify commonly affected pathways in cisplatin resistance and the data were compared to the GCT cohort of the ‘The Cancer Genome Atlas’. Results A total of 4375 proteins were quantified by MS, 144 of which were found to be differentially abundant between isogenic resistant and sensitive cell line pairs (24 proteins for NTERA-2, 60 proteins for NCCIT, 75 proteins for 2102EP). Western blotting confirmed regulation of key resistance-associated proteins (CBS, ANXA1, LDHA, CTH, FDXR). GSEA revealed a statistically significant enrichment of DNA repair-associated proteins in all three resistant cell lines and specific additional processes for individual cell lines. Conclusion High resolution MS combined with SILAC is a powerful tool and 144 significantly deregulated proteins were found in cisplatin-resistant GCT cell lines. Our study provides the largest proteomic in vitro library for cisplatin resistance in GCT, yet, enabling further studies to develop new treatment options for patients with refractory GCT."],["dc.identifier.doi","10.1007/s00345-022-03936-1"],["dc.identifier.pii","3936"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/98961"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-517"],["dc.relation.eissn","1433-8726"],["dc.relation.issn","0724-4983"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Proteomic profiling of cisplatin-resistant and cisplatin-sensitive germ cell tumour cell lines using quantitative mass spectrometry"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S226"],["dc.bibliographiccitation.journal","Clinical Lymphoma, Myeloma & Leukemia"],["dc.bibliographiccitation.lastpage","S227"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Oellerich, T."],["dc.contributor.author","Corso, J."],["dc.contributor.author","Beck, J."],["dc.contributor.author","Doebele, C."],["dc.contributor.author","Wachter, A."],["dc.contributor.author","Lenz, C."],["dc.contributor.author","Bohnenberger, H."],["dc.contributor.author","Beissbarth, Tim"],["dc.contributor.author","Gökbuget, N."],["dc.contributor.author","Schütz, E."],["dc.contributor.author","Urlaub, H."],["dc.date.accessioned","2022-06-08T07:57:48Z"],["dc.date.available","2022-06-08T07:57:48Z"],["dc.date.issued","2015"],["dc.identifier.doi","10.1016/j.clml.2015.04.106"],["dc.identifier.pii","S2152265015002645"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/110215"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-575"],["dc.relation.issn","2152-2650"],["dc.title","Elucidation of B cell receptor signaling in Burkitt’s lymphoma reveals novel signaling nodes with potential therapeutic relevance"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]