News & VeranstaltungenBiologisches Kolloquium 23.04.2013: 17:00 Helmholtzstraße 8/1 Raum 2.56
Dr. Ulrich auf dem Keller
Institute of Molecular Health Sciences, Zürich
„Proteases as modulators of intercellular communication in skin inflammation and repair“
Abteilungskolloquium 14.04.2013: 17:00 Helmholtzstr. 8/1, R. 2.56
PD Dr. rer. nat. Pamela Fischer-Posovszky
Department of Pediatrics and Adolescent Medicine, Ulm University Medical Center
"Regulation of adipose tissue mass by apoptosis"
Biologisches Kolloquium 05.03.2013: 17:00 OE/N25 H8
Matthias Kieslinger Ph.D.
Junior Group Leader, Helmholtz Zentrum München
Inst. of Clinical Molecular Biology and Tumor Genetics
“Defining niche and interactions of hematopoietic stem cells“
Biologisches Kolloquium 26.02.2013: 10:00 OE/N24 101
Dr. Mateusz Kolanczyk, Ph.D.
Max-Planck-Institut für molekulare Genetik, Berlin
"New perspectives on NF1 pathology-insights from the Nf1Prx1 model"
Biologisches Kolloquium 05.02.2013: 17:00 OE/N25 H8
Prof. Dr. Uwe JF Tietge
University Medical Center Groningen, Center for Liver, Digestive, and Metabolic Diseases, Groningen, Netherlands
"Differential Impact of ABCG5/G8 and SR-BI on Sterol Metabolism and Reverse Cholesterol Transport"
Biologisches Kolloquium 29.01.2013: 17:00 OE/N24 104
Dr. Torsten Plösch
Laboratory of Pediatrics University Medical Center Groningen, Netherlands
"Regulation of Cholesterol Metabolism: From Nuclear Receptors to Epigenetic Programming"
Biologisches Kolloquium 21.01.2013: 17:00 OE/N23 2622
Jun. Prof. Dr. Gregor Bucher
Johann Friedrich Blumenbach Institut, Georg-August-Universität, Göttingen
"Identifying genes for head and brain development: from candidates to genome wide RNAi in the red flour beetle"The insect head is composed of several segments and anterior non-segmental tissue. While pattern formation of the segmented part of the body is well understood in Drosophila , patterning of the anterior non-segmental region remains enigmatic. We use the red flour beetle Tribolium castaneum as model for head and brain development because of its insect typical non-involuted larval head.
In order to identify genes involved in anterior patterning, we systematically investigated expression and function of orthologs of vertebrate neural plate patterning genes in Tribolium . We find that most of them are required for head epidermis development. This approach has identified Tc-six3 as novel upstream regulator required for the development of the anterior most parts of the insect head including development of the neuroendocrine pars intercerebralis, where neuroendocrine markers like Tc-chx and Tc-fas are missing in Tc-six3 RNAi embryos. Further, Tc-six3 is required for central complex development.
While our candidate gene approach has been highly fruitful it will not identify a comprehensive set of insect head patterning genes. In order to gain such a comprehensive list, we are – in collaboration with the German Tribolium community – performing a genome wide RNAi screen (FOR1234 “iBeetle: Functional Genomics of Insect Embryogenesis and Metamorphosis”). With this endeavor we aim at overcoming the currently prevailing candidate gene approach, we open new fields of research and we establishing the red flour beetle as complementary screening platform, where all genes can be identified, which are required for a certain biological process.
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Wir sind stolz, die Ansiedlung der unabhängigen Nachwuchsforschungsgruppe “Metabolic Disorders” an unserem Institut bekannt geben zu können. Die Arbeitsgruppe, geführt von Dr. Maja Vujic, wird von der Deutschen Forschungsgemeinschaft großzügig unterstützt unter anderem durch die Gruppenleiterstelle und eine Doktorandenstelle.
Dr. Maja Vujic Forschungsthema befasst sich mit der hormonellen und molekularen Kontrolle der Eisen-Homöostase in einer häufigen genetischen Eisenstoffwechselkrankheit. Sie und ihre Arbeitsgruppe benutzen transgene Mäuse, komplexe Zellkulturmodelle und bioinformatische Methoden, um die Rolle von Makrophagen im Zwischenspiel von systemischer und zellulärer Antwort auf Eisenkonzentration und Entzündungsreaktionen zu untersuchen. Das Forschungsteam wird seine Arbeit im Oktober 2012 aufnehmen.
Biologisches Kolloquium 23.05.2012: 17:00 OE/N25 H8
Prof. Dr. Claude Libert
Ghent University and VIBMouse Genetics in Inflammation, Ghent, Belgium
"GR dimers control JNK-mediated inflammation and cell-death via MKP-1 in an in vivo TNF model"Glucocorticoids (GCs) are very powerful anti-inflammatory agents that function by binding on the GC receptor (GR), which is a member of the nuclear receptor family of proteins. Despite GCs are very widely used in the combat against inflammatory diseases, several problems with GCs/GR are recognized. The problem relevant to this seminar deals with the mechanism by which GR exerts its anti-inflammatory function. After binding of GCs to GR and after nuclear transport, GR can interact with inflammatory transcription factors (such as NFkB), leading to transrepression, but GR can also dimerize and bind on DNA and induce and repress gene expression, in a process called transactivation. The relative contribution of these two processes is still poorly understood. In light of the anti-cancer effects of the cytokine TNF and of its role in numerous inflammatory diseases (anti-TNF therapies belong to the top-10 best selling drugs worldwide), we are studying the GR dimerization in relation to TNF’s inflammation. Using mice expressing a GR pointmutation, leading to a GR that can hardly dimerize, we have found that GR dimerization is essential in the protection of mice against TNF’s toxicity. The extreme TNF sensitivity of such GRdim/dim mice is very comparable to the TNF sensitive phenotype of Dusp1-/- mice. Dusp1 is a gene induced by GR and encoding the major MAP kinase de-phosphorylating phosphatase MKP-1. In the TNF model, Dusp1-/- mice are unable to reverse the phosphorylation of JNK, a phenotype we also observe in GRdim/dim mice. We found that JNK2-/- mice resist TNF toxicity and that Dusp1/JNK2 --/-- mice are less sensitive to TNF compared to Dusp1-/- mice. Since we found that GRdim/dim/JNK2-/- mice are also protected compared to GRdim/dim mice, we believe that GR dimerization is essential in the induction of MKP-1, which in turn controls JNK2 phosphorylation and hence TNF-inuduced, JNK2-mediated inflammation and cell death. Since Dusp1 is not the only GR dimer-induced anti-inflammatory gene, we also focused on the gene Tsc22d3, which encodes GILZ, another such anti-inflammatory gene. I will also show data dealing with the identification of GILZ as an important protective factor in acute inflammation.
Biologisches Kolloquium 17.04.2012: 17:00 OE/N25 H8
Dr. Maja Vujic
Molecular Medicine Partnership Unit, Iron Homeostasis, Univeristätsklinikum Heidelberg, Germany
"Novel roles for Hfe and Hepcidin in metabolism"
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Seit 01. April 2012 leitetProf. Dr. Jan Peter Tuckermann das Institut (Nachfolge von Prof. Dr. Klaus-Dieter Spindler).
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Vertretungsprofessor: