Dissertations / Theses on the topic 'Genetische Mausmodelle'
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Micklich, Kateryna. "Genetische und phänotypische Charakterisierung eines Mausmodells für erbliche Polycythämie." Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-150198.
Kess, Daniel. "Genetische und zelluläre Analyse der Pathogenese des psoriasiformen Phänotyps im CD18-hypomorphen Mausmodell." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=972710949.
Amtsfeld, Linda [Verfasser]. "Etablierung und Charakterisierung eines genetisch induzierten Mausmodells des kolorektalen Karzinoms / Linda Amtsfeld." Gießen : Universitätsbibliothek, 2017. http://d-nb.info/1148264280/34.
Micklich, Kateryna [Verfasser], and Eckhard [Akademischer Betreuer] Wolf. "Genetische und phänotypische Charakterisierung eines Mausmodells für erbliche Polycythämie / Kateryna Micklich. Betreuer: Eckhard Wolf." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2012. http://d-nb.info/102819174X/34.
Myszczyszyn, Adam. "Studying normal and cancer stem cells in the kidney using 3D organoids and genetic mouse models." Doctoral thesis, Humboldt-Universität zu Berlin, 2021. http://dx.doi.org/10.18452/23127.
Adult mouse organoids are promising models for kidney research. However, their characterization has not been pushed forward to a satisfying level. Here, I have generated and characterized a long-term 3D mouse organoid (tubuloid) model, which recapitulates renewal and repair, and the architecture and functionality of the adult tubular epithelia. In the future, the model will allow detailed investigations of trajectories of self-renewing cells towards both the partial recreation and malignant transformation of the kidney. Clear cell renal cell carcinoma (ccRCC) is the most common and aggressive kidney cancer. Inactivation of the Von Hippel-Lindau (VHL) tumor suppressor gene is the major driver of ccRCC. Earlier, we identified the upregulation of Wnt and Notch signaling in CXCR4+MET+CD44+ cancer stem cells (CSCs) from primary human ccRCCs. Blocking Wnt and Notch in patient-derived xenografts, organoids and non-adherent spheres using small-molecule inhibitors impaired self-renewal of CSCs and tumor growth. To mimic CSC-governed human ccRCC in genetic mouse models, I started from the generation of two double mouse mutants; β-catenin-GOF; Notch-GOF and Vhl-LOF; β-catenin-GOF. Surprizingly, I observed neither tumors or tumor precursor lesions nor higher cell proliferation rates in the mutant kidneys. Further analyses revealed that the mutant mice displayed features of chronic kidney disease (CKD). Thus, β-catenin-GOF; Notch-GOF and Vhl-LOF; β-catenin-GOF mouse mutants did not develop kidney tumors under the given experimental conditions.
Sedelis, Marco. "Suszeptibilitätsunterschiede im MPTP-Mausmodell für Morbus Parkinson Untersuchung genetischer Einflussfaktoren anhand von Stammvergleichen /." [S.l.] : [s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=961802324.
Sander, Karoline [Verfasser], Uwe Alexander [Akademischer Betreuer] Wittel, Gabriel [Forscher] Seifert, and Cornelia Sabine [Forscher] Richter. "Einfluss des genetischen Hintergrundes auf den Verlauf der akuten nekrotisierenden Pankreatitis am Mausmodell." Freiburg : Universität, 2015. http://d-nb.info/112259352X/34.
Herzig, Catherine [Verfasser], and Sebastian [Akademischer Betreuer] Schölch. "Optimierung eines genetisch induzierten Mausmodells des kolorektalen Karzinoms / Catherine Herzig ; Betreuer: Sebastian Schölch." Heidelberg : Universitätsbibliothek Heidelberg, 2020. http://d-nb.info/1223623076/34.
Gerstenberger, Julia. "Sensomotorische Phänotypisierung von Mausmodellen für zentralnervöse Bewegungsstörungen." Doctoral thesis, Universitätsbibliothek Leipzig, 2017. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-225084.
Rohde, Franziska. "Die Rolle von onkogenem Beta-Catenin bei der Entstehung von Kolorektalkarzinomen : Analyse genetisch definierter Mausmodelle." kostenfrei, 2008. http://mediatum2.ub.tum.de/doc/645763/645763.pdf.
Wehner, Maina [Verfasser]. "Untersuchung zum Einfluss von Apoprotein A5 auf Glukose- und Fettsäurestoffwechsel im genetisch manipulierten Mausmodell / Maina Wehner." Hannover : Bibliothek der Tierärztlichen Hochschule Hannover, 2011. http://d-nb.info/1013481011/34.
Fischer, Johanna [Verfasser]. "Generierung eines induzierbaren genetischen Mausmodells zur Analyse der Funktionen von Bcl11b in der adulten Neurogenese / Johanna Fischer." Ulm : Universität Ulm, 2016. http://d-nb.info/1103026674/34.
Gertsen, Mila [Verfasser], and Corinna [Akademischer Betreuer] Grasemann. "Untersuchungen zur genetischen Grundlage des metabolischen Phänotyps von Nachkommen hyperglykämischer Elterntiere im Mausmodell / Mila Gertsen ; Betreuer: Corinna Grasemann." Duisburg, 2019. http://d-nb.info/1200352831/34.
Böhm, Ramona. "Kombination der Rekombinationssysteme Cre/loxP und Dre/rox für den genetischen rescue in knockout-Mausmodellen am Beispiel der mitochondrialen Thioredoxinreduktase." Diss., Ludwig-Maximilians-Universität München, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-156600.
The mitochondrial thioredoxin reductase (Txnrd2) is an ubiquitously expressed selenoprotein and an important oxidoreductase regulating oxidative stress. Ubiquitous deletion of Txnrd2 turned out to be embryonic lethal at day E13.0, while its pancreas-specific knockout caused spontaneous pancreas disease starting at week four post partum that developed into an exocrine fibrotic pancreas hypotrophy within one year. This pancreas-specific model, generated by breeding a Ptf1a-Cre transgenic line and a mouse line in which Txnrd2 is flanked by loxP sites is thoroughly examined at the moment. The present study aimed at the generation and testing of two targeting vectors for the establishment of a mouse model that allows the overexpression of the murine Txnrd2 in different organ systems. This took place in view of the generation of a genetic rescue of the Txnrd2 phenotype within the existing pancreas-specific knockout model, in order to clarify the question if it is possible to observe changes or the reversibility of the phenotype by Txnrd2-knockin. For the establishment of the rescue a conditional complementation strategy using the recombination systems Cre/loxP and Dre/rox was chosen. Two targeting constructs pROSA-roxSTOProx-Txnrd2-IresLacZ and pHprt-CAGGs-loxSTOPlox-DreERT2 were cloned. When combining those two constructs within the above mentioned pancreas-specific knockout, Cre catalyzes the recombination of the floxed Txnrd2 allele and at the same time of the loxSTOPlox cassette in front of DreERT2 in the pancreas during embryonic development. So that at the same time when the knockout is induced, DreERT2 is also expressed. However DreERT2 is only activated after Tamoxifen administration. The activated Dre recombines the roxSTOProx-cassette in front of the Txnrd2-IresLacZ sequence within the ROSA26 locus and thus enables the expression of transgenic Txnrd2 at a given time point. After the successful generation of both targeting vectors their singular modules were tested in vitro before integrating them into the murine germline. In cell culture experiments Txnrd2-expression by Tamoxifen-induced Dre was confirmed. Protein expression of transgenic TXNRD2 at the same time was proven in Western Blot. As the full functionality of both constructs was confirmed they were electroporated in IDG3.2 ES cells. For the following integration by homologous recombination the gene loci ROSA26 and Hprt of the mouse genome were chosen, as it is well-known that they can be targeted with high efficiency and that they are expressed ubiquitously. In order to increase the recombination efficiency a gene trap mutagenesis (ROSA26) and a complementation strategy (Hprt) were used. Following this, screening for correct integration was done by PCR and quantitative real-time PCR (ROSA26) or alternatively by Southern Blot (Hprt). Heterozygous transgenic cell clones of the ROSA26 line were injected into BDF1-blastocysts and transferred in pseudopregnant CD1 recipients. By backcrossing with C57BL/6N wild-type mice chimeras were tested for germline transmission. The resulting heterozygous transgenic F1 offspring was crossed with a so called Dre-deleter mouse ubiquitously expressing Dre-recombinase. Thereby the ubiquitous expression of LacZ was proven in E14.5 old embryos which confirmed the in vivo functionality of the generated pROSA-roxSTOProx-Txnrd2-IresLacZ-line. The generation of Hprt chimeras remains to be done. This model offers the opportunity of the genetic rescue of a Txnrd2-knockout by expressing the transgenic Txnrd2. This system is not restricted to the pancreas, as different organ systems can be targeted by the variable application of diverse tissue specific Cre-transgenic lines. Furthermore the transgenic model can be used for all other conditional knockout-systems under the influence of any tissue specific promoter. The application of the Hprt mouse line remains unchanged, all that has to be done is the exchange of the mitochondrial thioredoxin reductase by the gene of interest via cloning and the generation of the respective mouse line. The combination of the recombination systems FLP/Frt, Cre/loxP and Dre/rox enables further studies in which different genes can be induced at the same time or one by one in a tissue-specific knockout. This strategy enables to investigate the influence of gene expression on a knockout phenotype in different organ systems and also the possibly occurring potentiation of the expression of two different genes. This thesis adds one further very useful tool to the toolbox for genetic modeling of murine disease models.
Böhm, Ramona [Verfasser], and Bernhard [Akademischer Betreuer] Aigner. "Kombination der Rekombinationssysteme Cre/loxP und Dre/rox für den genetischen rescue in knockout-Mausmodellen am Beispiel der mitochondrialen Thioredoxinreduktase / Ramona Böhm. Betreuer: Bernhard Aigner." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2013. http://d-nb.info/1035626195/34.
Wanner, Laura [Verfasser], Mert [Akademischer Betreuer] Erkan, Helmut [Gutachter] Friess, and Mert [Gutachter] Erkan. "Vergleichende Analyse des Tumorstromas beim pankreatischen duktalen Adenokarzinom beim Menschen und bei genetisch modifizierten Mausmodellen / Laura Wanner ; Gutachter: Helmut Friess, Mert Erkan ; Betreuer: Mert Erkan." München : Universitätsbibliothek der TU München, 2020. http://d-nb.info/1216996520/34.
Marr, Jörg [Verfasser], Kay [Akademischer Betreuer] Raum, and Raimund [Akademischer Betreuer] Kinne. "Ultraschallbasiert Untersuchungen struktureller Parameter und elastomechanischer Knocheneigenschaften unter dem Einfluss einer Leptindefizienz am genetisch veränderten C57Bl-6J-Mausmodell / Jörg Marr. Betreuer: Kay Raum ; Raimund Kinne." Halle, Saale : Universitäts- und Landesbibliothek Sachsen-Anhalt, 2010. http://d-nb.info/1024976114/34.
Haumann, Hannah Marie [Verfasser]. "Der hepato-metabolische Phänotyp genetisch gesunder Nachkommen heterozygoter eNOS-knock-out-Elterntiere vor dem Hintergrund des Konzepts der fetalen Programmierung im Mausmodell / Hannah Marie Haumann." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2012. http://d-nb.info/102730706X/34.
Albrecht, Martin [Verfasser], Ansgar Michael [Gutachter] Chromik, and Stephan [Gutachter] Hahn. "Zytokinexpression im Mausmodell der DSS-Colitis nach genetischer Inaktivierung von JNK1 und JNK2 sowie nach pharmakologischer Therapie mit Taurolidin / Martin Albrecht ; Gutachter: Ansgar Michael Chromik, Stephan Hahn." Bochum : Ruhr-Universität Bochum, 2017. http://d-nb.info/1131354850/34.
Nordmeyer, Philipp [Verfasser], Thomas A. [Akademischer Betreuer] Bayer, Walter J. [Akademischer Betreuer] Schulz-Schaeffer, and Margarete [Akademischer Betreuer] Schön. "Untersuchungen über die Auswirkungen von Geschlecht und genetischem Hintergrund auf die Alzheimerpathologie im 5xFAD-Mausmodell / Philipp Nordmeyer. Gutachter: Walter J. Schulz-schaeffer ; Margarete Schön. Betreuer: Thomas A. Bayer." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2015. http://d-nb.info/1072550776/34.
Günther, Sophie Verfasser], Joachim [Akademischer Betreuer] Neumann, Reinhard H. H. [Akademischer Betreuer] [Neubert, and Wolfram-Hubertus [Akademischer Betreuer] Zimmermann. "Untersuchungen über den Einfluss von Losartan auf die Symptome der Herzinsuffizienz am Beispiel eines genetischen Mausmodells der kardialen Überexpression von Calsequestrin / Sophie Günther. Betreuer: Joachim Neumann ; Reinhard Neubert ; Wolfram-Hubertus Zimmermann." Halle, Saale : Universitäts- und Landesbibliothek Sachsen-Anhalt, 2012. http://d-nb.info/1025302230/34.
Neuhaus, Victor [Verfasser], Lars [Akademischer Betreuer] Maier, Blanche [Gutachter] Schwappach-Pignataro, and Martin [Gutachter] Oppermann. "Einfluss der Ca2+/Calmodulin-abhängigen Proteinkinase II delta auf den L-Typ Ca2+-Strom -Untersuchungen anhand eines genetischen Knock-outs im Mausmodell / Victor Neuhaus ; Gutachter: Blanche Schwappach-Pignataro, Martin Oppermann ; Betreuer: Lars Maier." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2016. http://d-nb.info/1149954159/34.
Wölk, Guido [Verfasser]. "Beeinflussung der Allergieentstehung durch genetische und umweltbedingte Faktoren im Mausmodell / vorgelegt von Guido Wölk." 2006. http://d-nb.info/980820626/34.
Bader, Verian [Verfasser]. "Untersuchung von chemischen und genetischen Mausmodellen des Morbus Parkinson / vorgelegt von Verian Bader." 2006. http://d-nb.info/983329869/34.
Mischke, Jutta. "Blockade des Renin-Angiotensin-Aldosteron-Systems in einem Mausmodell mit genetisch determiniertem metabolischen Syndrom /." 2005. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=014580021&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.
Gerstenberger, Julia. "Sensomotorische Phänotypisierung von Mausmodellen für zentralnervöse Bewegungsstörungen." Doctoral thesis, 2016. https://ul.qucosa.de/id/qucosa%3A15646.
Nordmeyer, Philipp Johannes. "Untersuchungen über die Auswirkungen von Geschlecht und genetischem Hintergrund auf die Alzheimerpathologie im 5xFAD-Mausmodell." Doctoral thesis, 2015. http://hdl.handle.net/11858/00-1735-0000-0022-6015-4.
Meffert, Nina [Verfasser]. "Untersuchungen zur genetischen Disposition für die Helicobacter-pylori-Infektion im Mausmodell / vorgelegt von Nina Meffert." 2002. http://d-nb.info/967196019/34.
Christel, Carl Johannes [Verfasser]. "Genetische Analyse der Bedeutung von Cav1.2-Kalziumkanälen für synaptische Plastizität und Angstlernen im Mausmodell / Carl Johannes Christel." 2008. http://d-nb.info/993212301/34.
Keß, Daniel [Verfasser]. "Genetische und zelluläre Analyse der Pathogenese des psoriasiformen Phänotyps im CD18-hypomorphen Mausmodell / vorgelegt von Daniel Keß." 2004. http://d-nb.info/972710949/34.
Rohde, Franziska [Verfasser]. "Die Rolle von onkogenem Beta-Catenin bei der Entstehung von Kolorektalkarzinomen : Analyse genetisch definierter Mausmodelle / Franziska Rohde." 2008. http://d-nb.info/991118596/34.
Meyring, Wilhelm Heinrich. "Genetisch modifizierte dendritische Zellen für die Immunisierung : Einfluss einer Hitzeschockprotein-Bindedomäne in einem Hämagglutinin-spezifischen Mausmodell /." 2008. http://www.gbv.de/dms/bs/toc/571697542.pdf.
Sedelis, Marco [Verfasser]. "Suszeptibilitätsunterschiede im MPTP-Mausmodell für Morbus Parkinson : Untersuchung genetischer Einflußfaktoren anhand von Stammvergleichen / vorgelegt von Marco Sedelis." 2001. http://d-nb.info/961802324/34.
Meyring, Wilhelm Heinrich [Verfasser]. "Genetisch modifizierte dendritische Zellen für die Immunisierung : Einfluss einer Hitzeschockprotein-Bindedomäne in einem Hämagglutinin-spezifischen Mausmodell / von Wilhelm Heinrich Meyring." 2008. http://d-nb.info/989648346/34.
Kobsar, Igor V. "Die Rolle von Immunzellen bei der primär genetisch-vermittelten Demyelinisierung in einem Mausmodell für die Charcot-Marie-Tooth-Neuropathie, Typ 1X." Doctoral thesis, 2005. https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-17047.
An aim of the presented work was to investigate whether immune cells could influence upon the severity of a peripheral neuropathy in a mouse model of CMT1X (Cx32def (Cx32-deficient mouse). Using immunohistochemical methods of staining, light-, immunelectron microscopy and computerised conventional electron microscopy we analysed a number of endoneurial macrophages and CD8+ T-cells as well as morphology of N. Quadriceps and ventral spinal roots. Taking into account our results, we could make such a conclusion: 1. Macrophages and CD8+ T-cells are upregulated in the N. Quadriceps and the number of endoneurial macrophages is significantly higher in comparison with the number of endoneurial CD8+ T-cells. These numbers are correlated with the age of the mice and with the severity of patholomorphological signs of peripheral neuropathy. 2. With the help of immunelectronmicroscopy we could definitely identify endoneurial macrophages inside of endoneurial tubes in close contact with axons during or after the process of demyelination. The endoneurial macrophages included rather often the rest of phagocyted myelin. 3. By means of immun- and conventional electron microscopy we have also observed close contacts between macrophages and fibroblasts inside of investigated nerves. 4. In Cx32def/RAG-1-/- double mutants, which in addition to myelin mutation contained no mature lymphocytes, we observed significantly lower upregulation of endoneurial macrophages as well as amelioration of pathological changes of N. Quadriceps and ventral spinal roots in comparison with Cx32def/ RAG-1+/? littermates. These results lead us to conclusion that macrophages and CD8+ T-cells could significantly aggravate genetically-mediated demyelination in a mouse model of CMT1X. Taking into account similar literature data concerning a mouse model of CMT1B (P0+/- mutants), we could assume, that interaction between Schwann- and immune cells is an important component of the pathogenesis of peripheral demyelination in mouse models of CMT1
Neuhaus, Victor. "Einfluss der Ca2+/Calmodulin-abhängigen Proteinkinase II delta auf den L-Typ Ca2+-Strom -Untersuchungen anhand eines genetischen Knock-outs im Mausmodell." Doctoral thesis, 2016. http://hdl.handle.net/11858/00-1735-0000-002B-7CEA-8.
Sultan, Arian [Verfasser]. "Untersuchung zur antioxidativen Rolle des zellulären Prionproteins und dessen Rolle im oxidativen Stress-Stoffwechsel an genetisch veränderten Mausmodellen / vorgelegt von Arian Sultan." 2008. http://d-nb.info/990368211/34.
Kobsar, Igor V. [Verfasser]. "Die Rolle von Immunzellen bei der primär genetisch-vermittelten Demyelinisierung in einem Mausmodell für die Charcot-Marie-Tooth-Neuropathie, Typ 1X / vorgelegt von Igor V. Kobsar." 2006. http://d-nb.info/97879687X/34.