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Albert-Ludwigs-Universität Freiburg Institut für Molekulare Medizin und Zellforschung

Overview
Works: 20 works in 20 publications in 2 languages and 71 library holdings
Roles: Contributor, isb
Publication Timeline
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Most widely held works by Albert-Ludwigs-Universität Freiburg
Signaling cascades of the Aspergillus fumigatus virulence factor Gliotoxin in mediating apoptosis and invasive aspergillosis by Florian Haun( )

1 edition published in 2016 in English and held by 17 WorldCat member libraries worldwide

Abstract: Gliotoxin (GT) ist der zentrale Virulenz Faktor des Schimmelpilzes Aspergillus fumigatus (A.f.) und verantwortlich für die Manifestation von invasiver Aspergillose (IA) in immunsupprimierten Patienten. Die Invasivität von A.f. beruht hierbei auf dem GT-induzierten Verlust der Barrierefunktion des Lungenepithels. GT-induzierte Apoptose von Epithelzellen könnte in diesem Zusammenhang eine wichtige Rolle spielen.<br>Ziel dieser Arbeit war es die GT-abhängigen, pro-apoptotischen Signal Kaskaden zu charakterisieren. GT aktiviert die GTPase RhoA, welche über die nachgeschaltete Kinase ROCK, die folgende Kinase-Kaskade stimuliert: ROCK phosphoryliert die MAPK Kinasen MKK4 und MKK7, welche wiederum JNK phosphorylieren und somit aktivieren. Diese Kaskade endet mit der JNK-abhängigen Phosphorylierung von Bim und der damit verbundenen Freisetzung von Bcl-2. Bim ist dann in der Lage mit dem Effektor Protein Bak zu interagieren, um die GT-induzierte Perforation von Mitochondrien und somit Zelltod umzusetzen. <br>In diesem Zusammenhang fungiert ROCK als eine pro-apoptotische MAPKK Kinase, zusätzlich zu seiner bekannten Funktion in der Regulation von Zellmorphologie. Dementsprechend wurde gefunden, dass Zellen resistent gegen GT induzierte Apoptose waren, wenn sie (i) mit JNK oder ROCK Inhibitoren behandelt wurden, oder (ii) ROCK oder MKK4/7 genetisch reduziert beziehungsweise ausgeschaltet waren.<br>Interessanterweise bewirkt GT das Ablösen von Zellen. Dieser Vorgang kann den programmierten Zelltod einleiten und wird dann als Anoikis bezeichnet. Wir konnten zeigen, dass GT direkt relevante cysteine in der Ligandenbindungsdomäne von Integrin [alpha]V[beta]3 modifiziert. Zusätzlich inaktiviert GT Integrine, um Anoikis zu vermitteln. Integrin Inaktivierung induziert die Inhibition der Focal Adhesion Kinase (FAK) und des nachgeschalteten Faktors p190RhoGAP, um die RhoA abhängige Signal Kaskade zu stimulieren. Somit wirkt GT als ein neuartiger und physiologischer Stimulus, um Anoikis zu induzieren und Integrin-abhängige Signaltransduktion zu studieren.<br><br>Wir zeigen, dass ROCK Inhibitoren sowohl den GT-induzierten Zelltod als auch das Ablösen von Zellen verhindern konnten und daher in der Lage waren, die Epithelzell-Morphologie zu erhalten. Da diese beiden Mechanismen ursächlich für die GT vermittelte Invasivität von A.f. sein könnten, könnte die pharmakologische Inhibition von ROCK eine interessante Strategie zur Bekämpfung von IA
Proteomic analysis of metastatic factors in breast cancer model systems: miR-200 and cysteine cathepsins by Florian Christoph Sigloch( )

1 edition published in 2017 in English and held by 11 WorldCat member libraries worldwide

Abstract: Breast cancer patients most often die of metastatic disease, in which cancer cells disseminate from the primary tumor site to invade into distant organs. While the primary tumor can often be treated, it is much harder to treat the diffuse metastatic disease. Understanding processes that lead to the formation of distant metastases is a major goal of cancer research.<br><br>This work deals with two mechanistic factors that may influence the formation of metastases in the context of breast cancer. Both mechanisms were studied on the molecular level by evaluating changes in the proteomes of cell lines or extracted lung metastases. Firstly, I studied the microRNAs miR-141 and miR-200c in the highly invasive breast cancer cell line MDA-MB-231. Secondly, I investigated the impact of the lysosomal proteases cathepsin B (CTSB) and cathepsin L (CTSL) on the secretome of cancer cell lines and on the proteome of murine lung metastases.<br><br>In the first project, I identified protein kinase A (PKA) and lim kinase 1 (LIMK1) as targets of miR-200c. Both kinases regulate the activity of the formerly known miR-200c target cofilin-2. I showed that the miR-200c simultaneously down-regulates the regulatory protein kinase a (PKA) subunit 1 alpha and the catalytic PKA subunit beta. I proved that RNAi-mediated suppression of these PKA subunits or inhibition of the PKA activity both led to reduced migration of the MDA-MB-231 cell line. The inhibition of cellular migration induced by miR-200c expression could be reversed by stimulation of the PKA activity.<br>A comparison of miR-141 and miR-200c revealed that both miRNAs induced almost identical changes in the cellular proteome. I found that both miRNAs suppress the expression of proteins linked to the cellular processes of chemotaxis, translation and glycolysis.<br><br>In the second project, I analyzed the effects of stable RNAi-mediated CTSB suppression in two human cancer cell lines. In the cellular secretome, suppression of CTSB reduced the shedding of trans-membrane proteins by the protease "A Disintegrin and Metalloprotease domain-containing protein" (ADAM10). Surprisingly, this effect was independent of the proteolytic activity of CTSB. Specific inhibition of the CTSB activity had no effect on the shedding of the ADAM10 substrate amyloid precursor protein (APP), and re-expression of inactive CTSB in a CTSB-suppressed MDA-MB-231 cell line led to normalized levels of APP shedding. The suppression of ADAM10-media
Proteomic analysis of lung metastases in a murine breast cancer model reveals divergent influence of CTSB and CTSL overexpression by Florian Christoph Sigloch( )

1 edition published in 2017 in English and held by 3 WorldCat member libraries worldwide

Abstract: Studies in the MMTV-PyMT (PyMT) breast cancer mouse model have shown a strong influence of the lysosomal cysteine cathepsins B or L on lung metastasis formation. Transgenic expression of human CTSB (tgCTSB) or CTSL (tgCTSL) both led to similar metastatic phenotypes with increased metastatic burden in the PyMT mice. However, recent studies in other tumor models proved marked differences in effects of either cathepsin on the proteome composition. We sought to analyze and compare proteome changes in the metastatic proteome of PyMT mice expressing either tgCTSB or tgCTSL to evaluate similarities and differences in those models.<br><br>Performing an explorative, quantitative proteome comparison based on LC-MS/MS, we identified up to 3,000 proteins from murine lung metastases in three independent biological replicates per genotype. In both cases, when compared to wild-type (WT) mice, we noticed a pronounced impact of transgene cathepsin expression on the metastasis proteome. Highlights include increased moesin, integrin beta 1 and vinexin levels in the tgCTSB dataset and increased saposin and granulin levels in the tgCTSL dataset. Importantly, non-supervised hierarchical clustering clearly separated tgCTSB vs. tgCTSL induced proteome changes.<br><br>In summary, tgCTSB and tgCTSL both display a strong and distinct impact on proteome composition of lung macrometastases in the PyMT model. Our observations suggest that they impact malignant behavior in distinct ways, thus further emphasizing interest into their tumor-contextual functionality
Towards simulating carcinogenesis : the hallmark concept revisited by Jenny Groten( )

1 edition published in 2018 in English and held by 3 WorldCat member libraries worldwide

<> by Ursula Kern( )

1 edition published in 2015 in English and held by 3 WorldCat member libraries worldwide

Reproducible proteomics sample preparation for single FFPE tissue slices using acid-labile surfactant and direct trypsinization by Melanie Christine Föll( )

1 edition published in 2018 in English and held by 3 WorldCat member libraries worldwide

Abstract: Background<br>Proteomic analyses of clinical specimens often rely on human tissues preserved through formalin-fixation and paraffin embedding (FFPE). Minimal sample consumption is the key to preserve the integrity of pathological archives but also to deal with minimal invasive core biopsies. This has been achieved by using the acid-labile surfactant RapiGest in combination with a direct trypsinization (DTR) strategy. A critical comparison of the DTR protocol with the most commonly used filter aided sample preparation (FASP) protocol is lacking. Furthermore, it is unknown how common histological stainings influence the outcome of the DTR protocol.<br><br>Methods<br>Four single consecutive murine kidney tissue specimens were prepared with the DTR approach or with the FASP protocol using both 10 and 30 k filter devices and analyzed by label-free, quantitative liquid chromatography-tandem mass spectrometry (LC-MS/MS). We compared the different protocols in terms of proteome coverage, relative label-free quantitation, missed cleavages, physicochemical properties and gene ontology term annotations of the proteins. Additionally, we probed compatibility of the DTR protocol for the analysis of common used histological stainings, namely hematoxylin & eosin (H&E), hematoxylin and hemalaun. These were proteomically compared to an unstained control by analyzing four human tonsil FFPE tissue specimens per condition.<br><br>Results<br>On average, the DTR protocol identified 1841 ± 22 proteins in a single, non-fractionated LC-MS/MS analysis, whereas these numbers were 1857 ± 120 and 1970 ± 28 proteins for the FASP 10 and 30 k protocol. The DTR protocol showed 15% more missed cleavages, which did not adversely affect quantitation and intersample comparability. Hematoxylin or hemalaun staining did not adversely impact the performance of the DTR protocol. A minor perturbation was observed for H&E staining, decreasing overall protein identification by 13%.<br><br>Conclusions<br>In essence, the DTR protocol can keep up with the FASP protocol in terms of qualitative and quantitative reproducibility and performed almost as well in terms of proteome coverage and missed cleavages. We highlight the suitability of the DTR protocol as a viable and straightforward alternative to the FASP protocol for proteomics-based clinical research
Network theory inspired analysis of time-resolved expression data reveals key players guiding P. patens stem cell development by Hauke Busch( )

1 edition published in 2013 in English and held by 2 WorldCat member libraries worldwide

Abstract: Transcription factors (TFs) often trigger developmental decisions, yet, their transcripts are often only moderately regulated and thus not easily detected by conventional statistics on expression data. Here we present a method that allows to determine such genes based on trajectory analysis of time-resolved transcriptome data. As a proof of principle, we have analysed apical stem cells of filamentous moss (P. patens) protonemata that develop from leaflets upon their detachment from the plant. By our novel correlation analysis of the post detachment transcriptome kinetics we predict five out of 1,058 TFs to be involved in the signaling leading to the establishment of pluripotency. Among the predicted regulators is the basic helix loop helix TF PpRSL1, which we show to be involved in the establishment of apical stem cells in P. patens. Our methodology is expected to aid analysis of key players of developmental decisions in complex plant and animal systems
CREBBP is a target of epigenetic, but not genetic, modification in juvenile myelomonocytic leukemia by Silvia Fluhr( )

1 edition published in 2016 in English and held by 2 WorldCat member libraries worldwide

Abstract: Background<br><br>Juvenile myelomonocytic leukemia (JMML) is a myeloproliferative neoplasm of childhood whose clinical heterogeneity is only poorly represented by gene sequence alterations. It was previously shown that aberrant DNA methylation of distinct target genes defines a more aggressive variant of JMML, but only few significant targets are known so far. To get a broader picture of disturbed CpG methylation patterns in JMML, we carried out a methylation screen of 34 candidate genes in 45 patients using quantitative mass spectrometry.<br>Findings<br><br>Five of 34 candidate genes analyzed showed recurrent hypermethylation in JMML. cAMP-responsive element-binding protein-binding protein (CREBBP) was the most frequent target of epigenetic modification (77 % of cases). However, no pathogenic mutations of CREBBP were identified in a genetic analysis of 64 patients. CREBBP hypermethylation correlated with clinical parameters known to predict poor outcome.<br>Conclusions<br><br>This study supports the relevance of epigenetic aberrations in JMML pathophysiology. Our data confirm that DNA hypermethylation in JMML is highly target-specific and associated with higher-risk features. These findings encourage the development of prognostic markers based on epigenetic alterations, which will be helpful in the difficult clinical management of this heterogeneous disease
Characterization of various cell lines from different ampullary cancer subtypes and cancer associated fibroblast-mediated responses by Zon Weng Lai( )

1 edition published in 2016 in English and held by 2 WorldCat member libraries worldwide

Abstract: Background<br><br>Ampullary cancer is a relatively rare form of cancer and usually treated by pancreatoduodenectomy, followed by adjuvant therapy. The intestinal subtype is associated with markedly improved prognosis after resection. At present, only few cell lines are available for in vitro studies of ampullary cancer and they have not been collectively characterized.<br><br>Methods<br><br>We characterize five ampullary cancer cell lines by subtype maker expression, epithelial-mesenchymal transition (EMT) features, growth and invasion, drug sensitivity and response to cancer-associated fibroblast conditioned medium (CAF-CM).<br><br>Results<br><br>On the basis of EMT features, subtype marker expression, growth, invasion and drug sensitivity three types of cell lines could be distinguished: mesenchymal-like, pancreatobiliary-like and intestinal-like. Heterogeneous effects from the cell lines in response to CAF-CM, such as different growth rates, induction of EMT markers as well as suppression of intestinal differentiation markers were observed. In addition, proteomic analysis showed a clear difference in intestinal-like cell line from other cell lines.<br><br>Conclusion<br><br>Most of the available AMPAC cell lines seem to reflect a poorly differentiated pancreatobiliary or mesenchymal-like phenotype, which is consistent to their origin. We suggest that the most appropriate cell line model for intestinal-like AMPAC is the SNU869, while others seem to reflect aggressive AMPAC subtypes
Acetylation of human TCF4 (TCF7L2) proteins attenuates inhibition by the HBP1 repressor and induces a conformational change in the TCF4::DNA complex by Susanne Claudia Elfert( )

1 edition published in 2013 in English and held by 2 WorldCat member libraries worldwide

Abstract: The members of the TCF/LEF family of DNA-binding proteins are components of diverse gene regulatory networks. As<br>nuclear effectors of Wnt/ß-catenin signaling they act as assembly platforms for multimeric transcription complexes that either repress or activate gene expression. Previously, it was shown that several aspects of TCF/LEF protein function are regulated by post-translational modification. The association of TCF/LEF family members with acetyltransferases and deacetylases prompted us to investigate whether vertebrate TCF/LEF proteins are subject to acetylation. Through co-expression with p300 and CBP and subsequent analyses using mass spectrometry and immunodetection with anti-acetyl-lysine antibodies we show that TCF4 can be acetylated at lysine K150 by CBP. K150<br>acetylation is restricted to TCF4E splice variants and requires the simultaneous presence of ß-catenin and the unique TCF4E C-terminus. To examine the functional consequences of K150 acetylation we substituted K150 with amino acids representing the non-acetylated and acetylated states. Reporter gene assays based on Wnt/ß-catenin-responsive promoter regions did not indicate a general role of K150<br>acetylation in transactivation by TCF4E. However, in the presence of CBP, non-acetylatable TCF4E with a K150<br>R substitution was more susceptible to inhibition by the HBP-1 repressor protein compared to wild-type TCF4E. Acetylation of K150 using a bacterial expression system or amino acid substitutions at K150 alter the electrophoretic properties of TCF4E::DNA complexes. This result suggests that K150<br>acetylation leads to a conformational change that may also represent the mechanism whereby acetylated TCF4E acquires resistance against HBP1. In summary, TCF4 not only recruits acetyltransferases but is also a substrate for these enzymes. The fact that acetylation affects only a subset of TCF4 splice variants and is mediated preferentially by CBP suggests that the conditional acetylation of TCF4E is a novel regulatory mechanism that diversifies the transcriptional output of Wnt/ß-catenin signaling in response to changing intracellular signaling milieus
Alterations of Gab2 signalling complexes in imatinib and dasatinib treated chronic myeloid leukaemia cells by Sebastian Halbach( )

1 edition published in 2013 in English and held by 2 WorldCat member libraries worldwide

Abstract: Background:<br>The Gab2 docking protein acts as an important signal amplifier downstream of various growth factor receptors and Bcr-Abl, the driver of chronic myeloid leukaemia (CML). Despite the success of Bcr-Abl tyrosine kinase inhibitors (TKI) in the therapy of CML, TKI-resistance remains an unsolved problem in the clinic. We have recently shown that Gab2 signalling counteracts the efficacy of four distinct Bcr-Abl inhibitors. In the course of that project, we noticed that two clinically relevant drugs, imatinib and dasatinib, provoke distinct alterations in the electrophoretic mobility of Gab2, its signalling output and protein interactions. As the signalling potential of the docking protein is highly modulated by its phosphorylation status, we set out to obtain more insights into the impact of TKIs on Gab2 phosphorylation.<br>Findings:<br>Using stable isotope labelling by amino acids in cell culture (SILAC)-based quantitative mass spectrometry (MS), we show now that imatinib and dasatinib provoke distinct effects on the phosphorylation status and interactome of Gab2. This study identifies several new phosphorylation sites on Gab2 and confirms many sites previously known from other experimental systems. At equimolar concentrations, dasatinib is more effective in preventing Gab2 tyrosine and serine/threonine phosphorylation than imatinib. It also affects the phosphorylation status of more residues than imatinib. In addition, we also identify novel components of the Gab2 signalling complex, such as casein kinases, stathmins and PIP1 as well as known interaction partners whose association with Gab2 is disrupted by imatinib and/or dasatinib.<br>Conclusions:<br>By using MS-based proteomics, we have identified new and confirmed known phosphorylation sites and interaction partners of Gab2, which may play an important role in the regulation of this docking protein. Given the growing importance of Gab2 in several tumour entities we expect that our results will help to understand the complex regulation of Gab2 and how this docking protein can contribute to malignancy
Quantitative proteomic analysis of formalin-fixed, paraffin-embedded clear cell renal cell carcinoma tissue using stable isotopic dimethylation of primary amines by Johannes Weisser( )

1 edition published in 2015 in English and held by 2 WorldCat member libraries worldwide

Abstract: Background<br><br>Formalin-fixed, paraffin-embedded (FFPE) tissues represent the most abundant resource of archived human specimens in pathology. Such tissue specimens are emerging as a highly valuable resource for translational proteomic studies. In quantitative proteomic analysis, reductive di-methylation of primary amines using stable isotopic formaldehyde variants is increasingly used due to its robustness and cost-effectiveness.<br><br>Results<br><br>In the present study we show for the first time that isotopic amine dimethylation can be used in a straightforward manner for the quantitative proteomic analysis of FFPE specimens without interference from formalin employed in the FFPE process. Isotopic amine dimethylation of FFPE specimens showed equal labeling efficiency as for cryopreserved specimens. For both FFPE and cryopreserved specimens, differential labeling of identical samples yielded highly similar ratio distributions within the expected range for dimethyl labeling. In an initial application, we profiled proteome changes in clear cell renal cell carcinoma (ccRCC) FFPE tissue specimens compared to adjacent non-malignant renal tissue. Our findings highlight increased levels of glyocolytic enzymes, annexins as well as ribosomal and proteasomal proteins.<br><br>Conclusion<br><br>Our study establishes isotopic amine dimethylation as a versatile tool for quantitative proteomic analysis of FFPE specimens and underlines proteome alterations in ccRCC.<br><br>Keywords<br><br>Dimethylation - Formalin-fixation - Paraffin-embedment clear cell renal cell carcinoma
Axitinib and sorafenib are potent in tyrosine kinase inhibitor resistant chronic myeloid leukemia cells by Sebastian Halbach( )

1 edition published in 2016 in English and held by 2 WorldCat member libraries worldwide

The prognostic impact of the carcinoembryonic antigen in ampullary cancer - a retrospective single center study by Hannah Füllgraf( )

1 edition published in 2017 in English and held by 2 WorldCat member libraries worldwide

Abstract: Background: <br>Carcinoembryonic antigen cell adhesion molecule (CEA) is a commonly immunohistochemically used antibody in pathological routine diagnostics with an overexpression in different cancers. We aimed to examine the immunohistochemically detectable CEA level in ampullary cancer and to correlate it with clinico-pathological data.<br>Methods: <br>Shot-gun proteomics revealed CEA in undifferentiated ampullary cancer cell lines. Next, tumor tissue of 40 ampullary cancers of a retrospective single center cohort of 40 patients<br>was stained immunohistochemically for CEA; CEA expression was determined and correlated with clinico-pathological data.<br>Results: <br>Thirty-six patient specimens were included in statistical analysis. CEA expression and lymph node ratio (LNR) were the only independent predictors of overall survival in multivariate analysis.<br>Conclusion: <br>To our knowledge, cell line and patient cohorts are the largest and characterized cohorts examined for CEA so far. Hereby, CEA expression in ampullary cancer cells permits an estimation of outcome and suggests an opportunity for individualized CEA-directed therapy. Further trials with larger cohorts are needed to verify our results and to integrate CEA<br>immunohistochemistry into clinical routine
Regulation of the Deubiquitinase CYLD in the TNFR signaling pathway by Lisa Katharina Schlicher( )

1 edition published in 2017 in English and held by 2 WorldCat member libraries worldwide

Exometabolom analysis of breast cancer cell lines: metabolic signature by Lucas Willmann( )

1 edition published in 2015 in English and held by 2 WorldCat member libraries worldwide

Abstract: Cancer cells show characteristic effects on cellular turnover and DNA/RNA modifications leading to elevated levels of excreted modified nucleosides. We investigated the molecular signature of different subtypes of breast cancer cell lines and the breast epithelial cell line MCF-10A. Prepurification of cell culture supernatants was performed by cis-diol specific affinity chromatography using boronate-derivatized polyacrylamide gel. Samples were analyzed by application of reversed phase chromatography coupled to a triple quadrupole mass spectrometer. Collectively, we determined 23 compounds from RNA metabolism, two from purine metabolism, five from polyamine/methionine cycle, one from histidine metabolism and two from nicotinate and nicotinamide metabolism. We observed major differences of metabolite excretion pattern between the breast cancer cell lines and MCF-10A, just as well as between the different breast cancer cell lines themselves. Differences in metabolite excretion resulting from cancerous metabolism can be integrated into altered processes on the cellular level. Modified nucleosides have great potential as biomarkers in due consideration of the heterogeneity of breast cancer that is reflected by the different molecular subtypes of breast cancer. Our data suggests that the metabolic signature of breast cancer cell lines might be a more subtype-specific tool to predict breast cancer, rather than a universal approach
Cell-nonautonomous signaling of FOXO/DAF-16 to the stem cells of Caenorhabditis elegans by Wenjing Qi( )

1 edition published in 2012 in English and held by 2 WorldCat member libraries worldwide

Abstract: In Caenorhabditis elegans (C. elegans), the promotion of longevity by the transcription factor DAF-16 requires reduced insulin/IGF receptor (IIR) signaling or the ablation of the germline, although the reason for the negative impact of germ cells is unknown. FOXO/DAF-16 activity inhibits germline proliferation in both daf-2 mutants and gld-1 tumors. In contrast to its function as a germline tumor suppressor, we now provide evidence that somatic DAF-16 in the presence of IIR signaling can also result in tumorigenic activity, which counteracts robust lifespan extension. In contrast to the cell-autonomous IIR signaling, which is required for larval germline proliferation, activation of DAF-16 in the hypodermis results in hyperplasia of the germline and disruption of the surrounding basement membrane. SHC-1 adaptor protein and AKT-1 kinase antagonize, whereas AKT-2 and SGK-1 kinases promote, this cell-nonautonomous DAF-16 function. Our data suggest that a functional balance of DAF-16 activities in different tissues determines longevity and reveals a novel, cell-nonautonomous role of FOXO/DAF-16 to affect stem cells
Entwicklung gentherapeutischer Ansätze auf Basis der optimierten Lipofektion gegen neue, bei Brustkrebs relevanten Onko- und Tumorsup-pressor-Genen : Bewilligungszeitraum: 03.2000 - 05.2002( )

1 edition published in 2002 in German and held by 1 WorldCat member library worldwide

Di12 Onkogen, KL1-14, lipoplexe, MDA-MB-468 Mammakarzinomzellen, Tumorhemmung in vitro und in vivo
 
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Alternative Names
Albert-Ludwigs-Universität Freiburg, Institut für Molekulare Medizin und Zellforschung

Albert-Ludwigs-Universität Freiburg Institut für Molekulare Medizin und Zellforschung Sektion Biophysik

Albert-Ludwigs-Universität Freiburg Medizinische Fakultät Institut für Molekulare Medizin und Zellforschung

Institut für Molekulare Medizin und Zellforschung

Institute of Molecular Medicine and Cell Research, Faculty of Medicine, University of Freiburg

Universität Freiburg, Breisgau Institut für Molekulare Medizin und Zellforschung

University of Freiburg Faculty of Medicine Institute of Molecular Medicine and Cell Research

University of Freiburg Institute of Molecular Medicine and Cell Research

University of Freiburg Institute of Molecular Medicine and Cell Research Department of Biophysics

Languages
English (17)

German (3)