Pukrop, Tobias

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Clinical & Experimental Metastasis"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.date.accessioned","2018-11-07T10:00:14Z"],["dc.date.available","2018-11-07T10:00:14Z"],["dc.date.issued","2015"],["dc.format.extent","231"],["dc.identifier.isi","000351601900150"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37755"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Dordrecht"],["dc.relation.issn","1573-7276"],["dc.relation.issn","0262-0898"],["dc.title","The crucial impact of the unique organ-specific defense system during colonization and outgrowth of brain metastasis"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","841"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","MEDIZINISCHE KLINIK"],["dc.bibliographiccitation.lastpage","845"],["dc.bibliographiccitation.volume","104"],["dc.contributor.author","Raupach, Tobias"],["dc.contributor.author","Spering, Christopher"],["dc.contributor.author","Baeumler, Christine"],["dc.contributor.author","Burckhardt, Gerhard"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Pukrop, Tobias"],["dc.date.accessioned","2018-11-07T11:22:58Z"],["dc.date.available","2018-11-07T11:22:58Z"],["dc.date.issued","2009"],["dc.description.abstract","In addition to patient care and research activity, physicians working in medical school hospitals serve as teachers in undergraduate medical education. However, teaching qualifications of German university hospital physicians have not been studied in great detail. In January 2009, medical students as well as physicians involved in medical teaching at Gottingen Medical School, Germany, were invited to complete an online survey addressing their views on clinical teachers' educational skills. In addition, physicians' motivation to engage in pedagogical training was assessed. During a 12-day period, 359 students and 126 physicians involved in undergraduate medical education completed the survey. The latter did not feel well prepared for their teaching activities. At the same time, they expressed the willingness to improve their teaching skills. Students felt that, across all instructional methods, teachers would benefit from teacher training programs. In order to improve undergraduate education for future physicians, politicians and local representatives alike must set the scene for the implementation of faculty development measures in German medical schools."],["dc.identifier.doi","10.1007/s00063-009-1180-x"],["dc.identifier.isi","000271851200002"],["dc.identifier.pmid","19916073"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56090"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Urban & Vogel"],["dc.relation.conference","115th Annual Meeting of the Deutschen-Gesellschaft-fur-Innere-Medizin"],["dc.relation.eventlocation","Wiesbaden, GERMANY"],["dc.relation.issn","0723-5003"],["dc.title","A Contribution to the Needs Assessment of Faculty Development Measures in Medical Schools"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","285"],["dc.bibliographiccitation.journal","Oncology Research and Treatment"],["dc.bibliographiccitation.lastpage","286"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Menck, Kerstin"],["dc.contributor.author","Bleckmann, Annalen"],["dc.contributor.author","Scharf, Christian"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Dyck, Lydia"],["dc.contributor.author","Klemm, Florian"],["dc.contributor.author","Binder, Claudia"],["dc.date.accessioned","2018-11-07T09:34:18Z"],["dc.date.available","2018-11-07T09:34:18Z"],["dc.date.issued","2014"],["dc.identifier.isi","000343816900702"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32144"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.publisher.place","Basel"],["dc.relation.issn","2296-5262"],["dc.relation.issn","2296-5270"],["dc.title","EMMPRIN/CD147-positive tumor cell microvesicles are pro-invasive and detectable in the blood of cancer patients with metastasis"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1587"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Cancer Immunology Immunotherapy"],["dc.bibliographiccitation.lastpage","1597"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Koenig, Simone"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","Dittmann, Kai"],["dc.contributor.author","Engelke, Michael"],["dc.contributor.author","Wienands, Juergen"],["dc.contributor.author","Schwendener, Reto"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Hahn, Heidi"],["dc.date.accessioned","2018-11-07T09:19:32Z"],["dc.date.available","2018-11-07T09:19:32Z"],["dc.date.issued","2013"],["dc.description.abstract","Liposomes are frequently used in cancer therapy to encapsulate and apply anticancer drugs. Here, we show that a systemic treatment of mice bearing skin tumors with empty phosphatidylcholine liposomes (PCL) resulted in inhibition of tumor growth, which was similar to that observed with the synthetic bacterial lipoprotein and TLR1/2 agonist Pam(3)CSK(4) (BLP). Both compounds led to a substantial decrease of macrophages in spleen and in the tumor-bearing skin. Furthermore, both treatments induced the expression of typical macrophage markers in the tumor-bearing tissue. As expected, BLP induced the expression of the M1 marker genes Cxcl10 and iNOS, whereas PCL, besides inducing iNOS, also increased the M2 marker genes Arg1 and Trem2. In vitro experiments demonstrated that neither PCL nor BLP influenced proliferation or survival of tumor cells, whereas both compounds inhibited proliferation and survival and increased the migratory capacity of bone marrow-derived macrophages (BMDM). However, in contrast to BLP, PCL did not activate cytokine secretion and induced a different BMDM phenotype. Together, the data suggest that similar to BLP, PCL induce an antitumor response by influencing the tumor microenvironment, in particular by functional alterations of macrophages, however, in a distinct manner from those induced by BLP."],["dc.description.sponsorship","DFG [FOR942 HA 2197/5-2]"],["dc.identifier.doi","10.1007/s00262-013-1444-4"],["dc.identifier.isi","000325008800005"],["dc.identifier.pmid","23917775"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28662"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0340-7004"],["dc.title","Empty liposomes induce antitumoral effects associated with macrophage responses distinct from those of the TLR1/2 agonist Pam(3)CSK(4) (BLP)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1083"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","1099"],["dc.bibliographiccitation.volume","63"],["dc.contributor.author","Menzfeld, Christiane"],["dc.contributor.author","John, Michael"],["dc.contributor.author","van Rossum, Denise"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","Scheffel, Joerg"],["dc.contributor.author","Janova, Hana"],["dc.contributor.author","Goetz, Alexander A."],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Nau, Roland"],["dc.contributor.author","Borisch, Angela"],["dc.contributor.author","Boutin, Philippe"],["dc.contributor.author","Neumann, Konstantin"],["dc.contributor.author","Bremes, Vanessa"],["dc.contributor.author","Wienands, Juergen"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Tischner, Denise"],["dc.contributor.author","Waetzig, Vicky"],["dc.contributor.author","Herdegen, Thomas"],["dc.contributor.author","Teismann, Peter"],["dc.contributor.author","Greig, Iain"],["dc.contributor.author","Mueller, Michael"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Mildner, Alexander"],["dc.contributor.author","Kettenmann, Helmut"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Prinz, Marco R."],["dc.contributor.author","Rotshenker, Shlomo"],["dc.contributor.author","Weber, Martin S."],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.date.accessioned","2018-11-07T09:56:53Z"],["dc.date.available","2018-11-07T09:56:53Z"],["dc.date.issued","2015"],["dc.description.abstract","The putative protein tyrosine kinase (PTK) inhibitor tyrphostin AG126 has proven beneficial in various models of inflammatory disease. Yet molecular targets and cellular mechanisms remained enigmatic. We demonstrate here that AG126 treatment has beneficial effects in experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis. AG126 alleviates the clinical symptoms, diminishes encephalitogenic Th17 differentiation, reduces inflammatory CNS infiltration as well as microglia activation and attenuates myelin damage. We show that AG126 directly inhibits Bruton's tyrosine kinase (BTK), a PTK associated with B cell receptor and Toll-like receptor (TLR) signaling. However, BTK inhibition cannot account for the entire activity spectrum. Effects on TLR-induced proinflammatory cytokine expression in microglia involve AG126 hydrolysis and conversion of its dinitrile side chain to malononitrile (MN). Notably, while liberated MN can subsequently mediate critical AG126 features, full protection in EAE still requires delivery of intact AG126. Its anti-inflammatory potential and especially interference with TLR signaling thus rely on a dual mechanism encompassing BTK and a novel MN-sensitive target. Both principles bear great potential for the therapeutic management of disturbed innate and adaptive immune functions. GLIA 2015;63:1083-1099"],["dc.identifier.doi","10.1002/glia.22803"],["dc.identifier.isi","000353244400011"],["dc.identifier.pmid","25731696"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37056"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1098-1136"],["dc.relation.issn","0894-1491"],["dc.title","Tyrphostin AG126 Exerts Neuroprotection in CNS Inflammation by a Dual Mechanism"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Onkologie"],["dc.bibliographiccitation.volume","34"],["dc.contributor.author","Bleckmann, Annalen"],["dc.contributor.author","Siam, Laila"],["dc.contributor.author","Klemm, Florian"],["dc.contributor.author","Rietkoetter, Eva"],["dc.contributor.author","Binder, Claudia"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Pukrop, Tobias"],["dc.date.accessioned","2018-11-07T08:52:16Z"],["dc.date.available","2018-11-07T08:52:16Z"],["dc.date.issued","2011"],["dc.format.extent","151"],["dc.identifier.isi","000295160600393"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22130"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.publisher.place","Basel"],["dc.relation.issn","0378-584X"],["dc.title","LEF1 identifies a prognostically unfavourable subgroup of lung adenocarcinoma brain metastases"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","UNSP e50881"],["dc.bibliographiccitation.issue","80"],["dc.bibliographiccitation.journal","Journal of Visualized Experiments"],["dc.contributor.author","Chuang, Han-Ning"],["dc.contributor.author","Lohaus, Raphaela"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Binder, Claudia"],["dc.contributor.author","Dehghani, Faramarz"],["dc.contributor.author","Pukrop, Tobias"],["dc.date.accessioned","2018-11-07T09:19:40Z"],["dc.date.available","2018-11-07T09:19:40Z"],["dc.date.issued","2013"],["dc.description.abstract","Patients with cerebral metastasis of carcinomas have a poor prognosis. However, the process at the metastatic site has barely been investigated, in particular the role of the resident (stromal) cells. Studies in primary carcinomas demonstrate the influence of the microenvironment on metastasis, even on prognosis(1,2). Especially the tumor associated macrophages (TAM) support migration, invasion and proliferation(3). Interestingly, the major target sites of metastasis possess tissue-specific macrophages, such as Kupffer cells in the liver or microglia in the CNS. Moreover, the metastatic sites also possess other tissue-specific cells, like astrocytes. Recently, astrocytes were demonstrated to foster proliferation and persistence of cancer cells(4,5). Therefore, functions of these tissue-specific cell types seem to be very important in the process of brain metastasis(6,7). Despite these observations, however, up to now there is no suitable in vivo/in vitro model available to directly visualize glial reactions during cerebral metastasis formation, in particular by bright field microscopy. Recent in vivo live imaging of carcinoma cells demonstrated their cerebral colonization behavior(8). However, this method is very laborious, costly and technically complex. In addition, these kinds of animal experiments are restricted to small series and come with a substantial stress for the animals (by implantation of the glass plate, injection of tumor cells, repetitive anaesthesia and long-term fixation). Furthermore, in vivo imaging is thus far limited to the visualization of the carcinoma cells, whereas interactions with resident cells have not yet been illustrated. Finally, investigations of human carcinoma cells within immunocompetent animals are impossible(8). For these reasons, we established a coculture system consisting of an organotypic mouse brain slice and epithelial cells embedded in matrigel (3D cell sphere). The 3D carcinoma cell spheres were placed directly next to the brain slice edge in order to investigate the invasion of the neighboring brain tissue. This enables us to visualize morphological changes and interactions between the glial cells and carcinoma cells by fluorescence and even by bright field microscopy. After the coculture experiment, the brain tissue or the 3D cell spheroids can be collected and used for further molecular analyses (e.g. qRT-PCR, IHC, or immunoblot) as well as for investigations by confocal microscopy. This method can be applied to monitor the events within a living brain tissue for days without deleterious effects to the brain slices. The model also allows selective suppression and replacement of resident cells by cells from a donor tissue to determine the distinct impact of a given genotype. Finally, the coculture model is a practicable alternative to in vivo approaches when testing targeted pharmacological manipulations."],["dc.identifier.doi","10.3791/50881"],["dc.identifier.isi","000209228800045"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28693"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Journal Of Visualized Experiments"],["dc.relation.issn","1940-087X"],["dc.title","Coculture System with an Organotypic Brain Slice and 3D Spheroid of Carcinoma Cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","4359"],["dc.bibliographiccitation.issue","15"],["dc.bibliographiccitation.journal","Cancer Research"],["dc.bibliographiccitation.lastpage","4371"],["dc.bibliographiccitation.volume","76"],["dc.contributor.author","Schwartz, H."],["dc.contributor.author","Blacher, E."],["dc.contributor.author","Amer, M."],["dc.contributor.author","Livneh, N."],["dc.contributor.author","Abramovitz, L."],["dc.contributor.author","Klein, A."],["dc.contributor.author","Ben-Shushan, D."],["dc.contributor.author","Soffer, S."],["dc.contributor.author","Blazquez, R."],["dc.contributor.author","Barrantes-Freer, A."],["dc.contributor.author","Mu ller, M."],["dc.contributor.author","Mu ller-Decker, K."],["dc.contributor.author","Stein, R."],["dc.contributor.author","Tsarfaty, G."],["dc.contributor.author","Satchi-Fainaro, R."],["dc.contributor.author","Umansky, V."],["dc.contributor.author","Pukrop, T."],["dc.contributor.author","Erez, N."],["dc.date.accessioned","2020-12-10T18:37:43Z"],["dc.date.available","2020-12-10T18:37:43Z"],["dc.date.issued","2016"],["dc.description.abstract","Malignant melanoma is the deadliest of skin cancers. Melanoma frequently metastasizes to the brain, resulting in dismal survival. Nevertheless, mechanisms that govern early metastatic growth and the interactions of disseminated metastatic cells with the brain microenvironment are largely unknown. To study the hallmarks of brain metastatic niche formation, we established a transplantable model of spontaneous melanoma brain metastasis in immunocompetent mice and developed molecular tools for quantitative detection of brain micrometastases. Here we demonstrate that micrometastases are associated with instigation of astrogliosis, neuroinflammation, and hyperpermeability of the blood-brain barrier. Furthermore, we show a functional role for astrocytes in facilitating initial growth of melanoma cells. Our findings suggest that astrogliosis, physiologically instigated as a brain tissue damage response, is hijacked by tumor cells to support metastatic growth. Studying spontaneous melanoma brain metastasis in a clinically relevant setting is the key to developing therapeutic approaches that may prevent brain metastatic relapse. (C) 2016 AACR."],["dc.identifier.doi","10.1158/0008-5472.CAN-16-0485"],["dc.identifier.eissn","1538-7445"],["dc.identifier.isi","000382295300008"],["dc.identifier.issn","0008-5472"],["dc.identifier.pmid","27261506"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77077"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Cancer Research"],["dc.relation.issn","1538-7445"],["dc.relation.issn","0008-5472"],["dc.title","Incipient Melanoma Brain Metastases Instigate Astrogliosis and Neuroinflammation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1136"],["dc.bibliographiccitation.issue","7-8"],["dc.bibliographiccitation.journal","TISSUE ENGINEERING"],["dc.bibliographiccitation.lastpage","1147"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Wulf, Gerald G."],["dc.contributor.author","Viereck, Volker"],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Haase, Detlef"],["dc.contributor.author","Vehmeyer, K."],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Glass, Bertram"],["dc.contributor.author","Emons, G."],["dc.contributor.author","Truemper, Lorenz H."],["dc.date.accessioned","2018-11-07T10:47:58Z"],["dc.date.available","2018-11-07T10:47:58Z"],["dc.date.issued","2004"],["dc.description.abstract","Progenitor cells with differentiation capacity along multiple mesengenic lineages are attractive tools for numerous purposes in regenerative medicine. Such mesengenic progenitor cells have been isolated from adult mammalian bone marrow, and we here report placental tissue as an alternative source for these cells. By means of dissection/proteinase digestion techniques, high numbers of viable mononuclear cells were harvested from human placenta at term, and a mesenchymal cell population with characteristic expression of CD9, CD29, and CD73 was obtained in culture. The in vitro growth behavior of such placenta-derived mesengenic cells was similar to that of human bone marrow mesengenic progenitor cells. After in vitro propagation for more than three passages the cells were exclusively of maternal origin. Differentiation experiments showed differentiation potential along osteogenic, chondrogenic, adipogenic, and myogenic lineages. In conclusion, we propose human term placenta as an easily accessible, ample source of multipotent mesengenic progenitor cells."],["dc.identifier.doi","10.1089/ten.2004.10.1136"],["dc.identifier.isi","000223851200017"],["dc.identifier.pmid","15363170"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48088"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Mary Ann Liebert Inc"],["dc.relation.issn","1076-3279"],["dc.title","Mesengenic progenitor cells derived from human placenta"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","61"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Mechanisms of Development"],["dc.bibliographiccitation.lastpage","76"],["dc.bibliographiccitation.volume","106"],["dc.contributor.author","Kuhl, M."],["dc.contributor.author","Geis, K."],["dc.contributor.author","Sheldahl, L. C."],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Moon, R. T."],["dc.contributor.author","Wedlich, D."],["dc.date.accessioned","2018-11-07T08:49:53Z"],["dc.date.available","2018-11-07T08:49:53Z"],["dc.date.issued","2001"],["dc.description.abstract","Convergent extension movements are the main driving force of Xenopus gastrulation. A fine-tuned regulation of cadherin-mediated cell-cell adhesion is thought to be required for this process. Members of the Wnt family of extracellular glycoproteins have been shown to modulate cadherin-mediated cell-cell adhesion, convergent extension movements, and cell differentiation. Here we show that endogenous Wnt/beta -catenin signaling activity is essential for convergent extension movements due to its effect on gene expression rather than on cadherins. Our data also suggest that XLEF-1 rather than XTCF-3 is required for convergent extension movements and that XLEF-1 functions in this context in the Wnt/beta -catenin pathway to regulate Xnr-3. In contrast, activation of the Wnt/Ca2+, pathway blocks convergent extension movements, with potential regulation of the Wnt/beta -catenin pathway at two different levels. PKC, activated by the Wnt/Ca2+ pathway, blocks the Wnt/beta -catenin pathway upstream of beta -catenin and phosphorylates Dishevelled. CamKII, also activated by the Wnt/Ca2+ pathway, inhibits the Wnt/beta -catenin signaling cascade downstream of beta -catenin. Thus, an opposing cross-talk of two distinct Wnt signaling cascades regulates convergent extension movements in Xenopus. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved."],["dc.identifier.doi","10.1016/S0925-4773(01)00416-6"],["dc.identifier.isi","000170370900005"],["dc.identifier.pmid","11472835"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21565"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0925-4773"],["dc.title","Antagonistic regulation of convergent extension movements in Xenopus by Wnt/beta-catenin and Wnt/Ca2+ signaling"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]