Schulz, Matthias

[["dc.bibliographiccitation.artnumber","e2122476119"],["dc.bibliographiccitation.issue","30"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences"],["dc.bibliographiccitation.volume","119"],["dc.contributor.author","Schubert, Antonia"],["dc.contributor.author","Voloshanenko, Oksana"],["dc.contributor.author","Ragaller, Franziska"],["dc.contributor.author","Gmach, Philipp"],["dc.contributor.author","Kranz, Dominique"],["dc.contributor.author","Scheeder, Christian"],["dc.contributor.author","Miersch, Thilo"],["dc.contributor.author","Schulz, Matthias"],["dc.contributor.author","Trümper, Lorenz"],["dc.contributor.author","Binder, Claudia"],["dc.contributor.author","Boutros, Michael"],["dc.date.accessioned","2022-09-01T09:50:22Z"],["dc.date.available","2022-09-01T09:50:22Z"],["dc.date.issued","2022"],["dc.description.abstract","During organismal development, homeostasis, and disease, Dishevelled (Dvl) proteins act as key signaling factors in beta-catenin–dependent and beta-catenin–independent Wnt pathways. While their importance for signal transmission has been genetically demonstrated in many organisms, our mechanistic understanding is still limited. Previous studies using overexpressed proteins showed Dvl localization to large, punctate-like cytoplasmic structures that are dependent on its DIX domain. To study Dvl’s role in Wnt signaling, we genome engineered an endogenously expressed Dvl2 protein tagged with an mEos3.2 fluorescent protein for superresolution imaging. First, we demonstrate the functionality and specificity of the fusion protein in beta-catenin–dependent and beta-catenin–independent signaling using multiple independent assays. We performed live-cell imaging of Dvl2 to analyze the dynamic formation of the supramolecular cytoplasmic Dvl2_mEos3.2 condensates. While overexpression of Dvl2_mEos3.2 mimics the previously reported formation of abundant large “puncta,” supramolecular condensate formation at physiological protein levels is only observed in a subset of cells with approximately one per cell. We show that, in these condensates, Dvl2 colocalizes with Wnt pathway components at gamma-tubulin and CEP164-positive centrosomal structures and that the localization of Dvl2 to these condensates is Wnt dependent. Single-molecule localization microscopy using photoactivated localization microscopy (PALM) of mEos3.2 in combination with DNA-PAINT demonstrates the organization and repetitive patterns of these condensates in a cell cycle–dependent manner. Our results indicate that the localization of Dvl2 in supramolecular condensates is coordinated dynamically and dependent on cell state and Wnt signaling levels. Our study highlights the formation of endogenous and physiologically regulated biomolecular condensates in the Wnt pathways at single-molecule resolution."],["dc.description.sponsorship"," Deutsche Forschungsgemeinschaft 501100001659"],["dc.identifier.doi","10.1073/pnas.2122476119"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/113689"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-597"],["dc.relation.eissn","1091-6490"],["dc.relation.issn","0027-8424"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0/"],["dc.title","Superresolution microscopy localizes endogenous Dvl2 to Wnt signaling-responsive biomolecular condensates"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Onkologie"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Menck, Kerstin"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Schulz, M."],["dc.contributor.author","Dyck, Lydia"],["dc.contributor.author","Binder, Claudia"],["dc.contributor.author","Klemm, Florian"],["dc.date.accessioned","2018-11-07T09:04:54Z"],["dc.date.available","2018-11-07T09:04:54Z"],["dc.date.issued","2012"],["dc.format.extent","195"],["dc.identifier.isi","000310766700508"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25205"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.publisher.place","Basel"],["dc.relation.issn","0378-584X"],["dc.title","Breast cancer invasion mediated by plasma membrane-derived microvesicles is EMMPRIN-dependent"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3259"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","3273"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Draeger, Julia"],["dc.contributor.author","Simon-Keller, Katja"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Klemm, Florian"],["dc.contributor.author","Wilting, Joerg"],["dc.contributor.author","Sticht, Carsten"],["dc.contributor.author","Dittmann, Kai"],["dc.contributor.author","Schulz, Matthias"],["dc.contributor.author","Leuschner, Ivo"],["dc.contributor.author","Marx, Alexander"],["dc.contributor.author","Hahn, Heidi"],["dc.date.accessioned","2018-11-07T10:28:26Z"],["dc.date.available","2018-11-07T10:28:26Z"],["dc.date.issued","2017"],["dc.description.abstract","Rhabdomyosarcoma (RMS) is the most common soft tissue sarcoma in children and show characteristics of skeletal muscle differentiation. The two major RMS subtypes in children are alveolar (ARMS) and embryonal RMS (ERMS). We demonstrate that approximately 50% of ARMS and ERMS overexpress the LEF1/TCF transcription factor LEF1 when compared to normal skeletal muscle and that LEF1 can restrain aggressiveness especially of ARMS cells. LEF1 knockdown experiments in cell lines reveal that depending on the cellular context, LEF1 can induce pro-apoptotic signals. LEF1 can also suppress proliferation, migration and invasiveness of RMS cells both in vitro and in vivo. Furthermore, LEF1 can induce myodifferentiation of the tumor cells. This may involve regulation of other LEF1/TCF factors i.e. TCF1, whereas beta-catenin activity plays a subordinate role. Together these data suggest that LEF1 rather has tumor suppressive functions and attenuates aggressiveness in a subset of RMS."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2016"],["dc.identifier.doi","10.18632/oncotarget.13887"],["dc.identifier.isi","000391506300114"],["dc.identifier.pmid","27965462"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14022"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43418"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Impact Journals Llc"],["dc.relation.issn","1949-2553"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","LEF1 reduces tumor progression and induces myodifferentiation in a subset of rhabdomyosarcoma"],["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","Onkologie"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Klemm, Florian"],["dc.contributor.author","Menck, Kerstin"],["dc.contributor.author","Schulz, M."],["dc.contributor.author","Binder, Claudia"],["dc.date.accessioned","2018-11-07T08:38:50Z"],["dc.date.available","2018-11-07T08:38:50Z"],["dc.date.issued","2010"],["dc.format.extent","199"],["dc.identifier.isi","000282988401115"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18852"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.publisher.place","Basel"],["dc.relation.issn","0378-584X"],["dc.title","Tumor-Microparticles mediate invasiveness and elicit a M2-response in macrophages"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1331"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","1346"],["dc.bibliographiccitation.volume","61"],["dc.contributor.author","Chuang, Han-Ning"],["dc.contributor.author","van Rossum, Denise"],["dc.contributor.author","Sieger, Dirk"],["dc.contributor.author","Siam, Laila"],["dc.contributor.author","Klemm, Florian"],["dc.contributor.author","Bleckmann, Annalen"],["dc.contributor.author","Bayerlova, Michaela"],["dc.contributor.author","Farhat, Katja"],["dc.contributor.author","Scheffel, Joerg"],["dc.contributor.author","Schulz, Matthias"],["dc.contributor.author","Dehghani, Faramarz"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Binder, Claudia"],["dc.contributor.author","Pukrop, Tobias"],["dc.date.accessioned","2018-11-07T09:21:57Z"],["dc.date.available","2018-11-07T09:21:57Z"],["dc.date.issued","2013"],["dc.description.abstract","The metastatic colonization of the brain by carcinoma cells is still barely understood, in particular when considering interactions with the host tissue. The colonization comes with a substantial destruction of the surrounding host tissue. This leads to activation of damage responses by resident innate immune cells to protect, repair, and organize the wound healing, but may distract from tumoricidal actions. We recently demonstrated that microglia, innate immune cells of the CNS, assist carcinoma cell invasion. Here we report that this is a fatal side effect of a physiological damage response of the brain tissue. In a brain slice coculture model, contact with both benign and malignant epithelial cells induced a response by microglia and astrocytes comparable to that seen at the interface of human cerebral metastases. While the glial damage response intended to protect the brain from intrusion of benign epithelial cells by inducing apoptosis, it proved ineffective against various malignant cell types. They did not undergo apoptosis and actually exploited the local tissue reaction to invade instead. Gene expression and functional analyses revealed that the C-X-C chemokine receptor type 4 (CXCR4) and WNT signaling were involved in this process. Furthermore, CXCR4-regulated microglia were recruited to sites of brain injury in a zebrafish model and CXCR4 was expressed in human stroke patients, suggesting a conserved role in damage responses to various types of brain injuries. Together, our findings point to a detrimental misuse of the glial damage response program by carcinoma cells resistant to glia-induced apoptosis. GLIA 2013;61:1331-1346"],["dc.identifier.doi","10.1002/glia.22518"],["dc.identifier.isi","000321983400011"],["dc.identifier.pmid","23832647"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10955"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29226"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0894-1491"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","Carcinoma cells misuse the host tissue damage response to invade the brain"],["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","2452"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Molecular Cancer Therapeutics"],["dc.bibliographiccitation.lastpage","2460"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Binder, Claudia"],["dc.contributor.author","Hagemann, Thorsten"],["dc.contributor.author","Sperling, Swetlana"],["dc.contributor.author","Schulz, Matthias"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Grimshaw, Matthew J."],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:45:47Z"],["dc.date.available","2017-09-07T11:45:47Z"],["dc.date.issued","2009"],["dc.description.abstract","The endothelin (ET) axis, often deregulated in cancers, is a promising target for anticancer strategies. Whereas previous investigations have focused mostly on ET action in malignant cells, we chose a model allowing separate assessment of the effects of ETs and their receptors ETAR and ETBR in the tumor cells and the stromal compartment, which is increasingly recognized as a key player in cancer progression. In homozygous spotting lethal rats (sl/sl), a model of constitutive ETBR deficiency, we showed significant reduction of growth and metastasis of MAT B III rat mammary adenocarcinoma cells overexpressing ETAR and ET-1 but negative for ETBR. Lack of stromal ETBR expression did not influence angiogenesis. However, it was correlated with diminished infiltration by tumor-associated macrophages and with reduced production of tumor necrosis factor-α, both known as powerful promoters of tumor progression. These effects were almost completely abolished in transgenic sl/sl rats, wherein ETBR function is restored by expression of an intact ETBR transgene. This shows that tumor growth and metastasis are critically dependent on ETBR function in cells of the microenvironment and suggests that successful ETR antagonist therapy should also target the stromal component of ET signaling."],["dc.identifier.doi","10.1158/1535-7163.MCT-09-0032"],["dc.identifier.gro","3150445"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7210"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.title","Stromal endothelin B receptor-deficiency inhibits breast cancer growth and metastasis"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","227"],["dc.bibliographiccitation.issue","No. 2"],["dc.bibliographiccitation.journal","Library Hi Tech"],["dc.bibliographiccitation.lastpage","230"],["dc.bibliographiccitation.volume","Vol. 22"],["dc.contributor.author","Mittler, Elmar"],["dc.contributor.author","Schulz, Matthias"],["dc.date.accessioned","2020-04-15T08:40:26Z"],["dc.date.available","2020-04-15T08:40:26Z"],["dc.date.issued","2004"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17266"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/64119"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.issn","0737-8831"],["dc.rights.access","openAccess"],["dc.title","ProPrint world-wide print-on-demand services for study and research"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","434"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Carcinogenesis"],["dc.bibliographiccitation.lastpage","442"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Klemm, Florian"],["dc.contributor.author","Bleckmann, Annalen"],["dc.contributor.author","Siam, Laila"],["dc.contributor.author","Chuang, Han-Ning"],["dc.contributor.author","Rietkoetter, Eva"],["dc.contributor.author","Behme, Daniel"],["dc.contributor.author","Schulz, M."],["dc.contributor.author","Schaffrinski, Meike"],["dc.contributor.author","Schindler, Stefanie"],["dc.contributor.author","Trümper, Lorenz H."],["dc.contributor.author","Kramer, Franz-Josef"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Stadelmann, C."],["dc.contributor.author","Binder, Claudia"],["dc.contributor.author","Pukrop, Tobias"],["dc.date.accessioned","2018-11-07T08:59:01Z"],["dc.date.available","2018-11-07T08:59:01Z"],["dc.date.issued","2011"],["dc.description.abstract","A role of WNT signaling for primary breast cancers of the basal-like subtype and as a predictor of brain metastasis has been described. However, a responsible WNT ligand has not been identified. To further clarify this question, we comparatively investigated 22 human breast cancer brain metastases as well as the highly invasive human breast cancer cell line MDA-MB-231 and the weakly motile MCF-7 as models for the basal-like and the luminal A subtype. WNT5A and B were found overexpressed in MDA-MB-231 cells as compared with MCF-7. This corresponded to reduction of MDA-MB-231 invasiveness by WNT inhibitors, whereas MCF-7 invasion was enhanced by recombinant WNT5B and abolished by WNT and Jun-N-terminal kinase antagonists. Expression and subcellular distribution of beta-catenin remained uninfluenced. Consistently, beta-catenin was not localized in the nuclei of brain metastases while there was strong nuclear c-Jun staining. Similar to MDA-MB-231, metastases showed expression of WNT5A/B and the alternative WNT receptors ROR1 and 2. These findings were validated using external gene expression datasets (Gene Expression Omnibus) of different breast cancer subtypes and brain metastases. Hierarchical cluster analysis yielded a close relation between basal-like cancers and brain metastases. Gene set enrichment analyses confirmed WNT pathway enrichment not only in basal-like primaries but also in cerebral metastases of all subtypes. In conclusion, WNT signaling seems highly relevant for basal-like and other subtypes of breast cancers metastasizing into the brain. beta-catenin-independent WNT signaling, presumably via ROR1-2, plays a major role in this context."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft [FOR 942]"],["dc.identifier.doi","10.1093/carcin/bgq269"],["dc.identifier.isi","000288027800025"],["dc.identifier.pmid","21173432"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23785"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0143-3334"],["dc.title","beta-catenin-independent WNT signaling in basal-like breast cancer and brain metastasis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","723"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Advanced Engineering Materials"],["dc.bibliographiccitation.lastpage","731"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Borchers, Christine"],["dc.contributor.author","Stoltenhoff, Thorsten"],["dc.contributor.author","Hahn, Matthias"],["dc.contributor.author","Schulze, Matthias"],["dc.contributor.author","Assadi, Hamid"],["dc.contributor.author","Suryanarayana, Challapalli"],["dc.contributor.author","Gaertner, Frank"],["dc.contributor.author","Klassen, Thomas"],["dc.date.accessioned","2018-11-07T09:57:45Z"],["dc.date.available","2018-11-07T09:57:45Z"],["dc.date.issued","2015"],["dc.description.abstract","There is an increasing interest in cold spraying, which is commonly characterized as a solid-state deposition process offering minimal structural changes. The present paper refutes this common perception by examining the structural changes in MCrAlY as induced by cold spraying (CS). The cold-sprayed coatings were characterized for phase composition and microstructural features using X-ray diffraction, scanning electron microscopy (SEM), and transmission electron microscopy (TEM) techniques. These results are compared with those obtained from the feedstock powder, as well as those obtained from ball-milled powder. An extensive phase transition from bcc to fcc is observed after both CS and after ball milling. In CS, in addition, there is evidence for substantial grain refinement, which is not observed after ball milling."],["dc.identifier.doi","10.1002/adem.201400174"],["dc.identifier.isi","000354417300019"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37231"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1527-2648"],["dc.relation.issn","1438-1656"],["dc.relation.orgunit","Institut für Materialphysik"],["dc.title","Strain-Induced Phase Transformation of MCrAlY"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","719614"],["dc.bibliographiccitation.journal","Frontiers in Bioengineering and Biotechnology"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Graf, A."],["dc.contributor.author","Lemke, J."],["dc.contributor.author","Schulze, M."],["dc.contributor.author","Soeldner, R."],["dc.contributor.author","Rebner, K."],["dc.contributor.author","Hoehse, M."],["dc.contributor.author","Matuszczyk, J."],["dc.date.accessioned","2022-06-01T09:39:50Z"],["dc.date.available","2022-06-01T09:39:50Z"],["dc.date.issued","2022"],["dc.description.abstract","Continuous manufacturing is becoming more important in the biopharmaceutical industry. This processing strategy is favorable, as it is more efficient, flexible, and has the potential to produce higher and more consistent product quality. At the same time, it faces some challenges, especially in cell culture. As a steady state has to be maintained over a prolonged time, it is unavoidable to implement advanced process analytical technologies to control the relevant process parameters in a fast and precise manner. One such analytical technology is Raman spectroscopy, which has proven its advantages for process monitoring and control mostly in (fed-) batch cultivations. In this study, an in-line flow cell for Raman spectroscopy is included in the cell-free harvest stream of a perfusion process. Quantitative models for glucose and lactate were generated based on five cultivations originating from varying bioreactor scales. After successfully validating the glucose model (Root Mean Square Error of Prediction (RMSEP) of ∼0.2 g/L), it was employed for control of an external glucose feed in cultivation with a glucose-free perfusion medium. The generated model was successfully applied to perform process control at 4 g/L and 1.5 g/L glucose over several days, respectively, with variability of ±0.4 g/L. The results demonstrate the high potential of Raman spectroscopy for advanced process monitoring and control of a perfusion process with a bioreactor and scale-independent measurement method."],["dc.identifier.doi","10.3389/fbioe.2022.719614"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/108576"],["dc.notes.intern","DOI-Import GROB-572"],["dc.relation.eissn","2296-4185"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","A Novel Approach for Non-Invasive Continuous In-Line Control of Perfusion Cell Cultivations by Raman Spectroscopy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]