Ludwig Maximilians University of Munich

www.en.uni-muenchen.de
Munich, Germany

Ludwig Maximilian University of Munich is a public research university located in Munich, Germany.The University of Munich is among Germany's oldest universities. Originally established in Ingolstadt in 1472 by Duke Ludwig IX of Bavaria-Landshut, the university was moved in 1800 to Landshut by King Maximilian I of Bavaria when Ingolstadt was threatened by the French, before being relocated to its present-day location in Munich in 1826 by King Ludwig I of Bavaria. In 1802, the university was officially named Ludwig-Maximilians-Universität by King Maximilian I of Bavaria in his as well as the university's original founder's honour.The University of Munich has, particularly since the 19th century, been considered as one of Germany's as well as one of Europe's most prestigious universities; with 34 Nobel laureates associated with the university, it ranks 13th worldwide by number of Nobel laureates. Among these were Wilhelm Röntgen, Max Planck, Werner Heisenberg, Otto Hahn and Thomas Mann. Pope Benedict XVI was also a student and professor at the university. The LMU has recently been conferred the title of "elite university" under the German Universities Excellence Initiative.LMU is currently the second-largest university in Germany in terms of student population; in the winter semester of 2013/2014, the university had a total of 50,542 matriculated students. Of these, 8,719 were freshmen while international students totalled 7,403 or almost 15% of the student population. As for operating budget, the university records in 2013 a total of 571.3 million Euros in funding without the university hospital; with the university hospital, the university has a total funding amounting to approximately 1.5 billion Euros. Wikipedia.

SEARCH FILTERS
Time filter
Source Type

Patent
PLS Design GmbH, Ludwig Maximilians University of Munich and Helmholtz Center Munich | Date: 2015-09-14

The invention relates to a pharmaceutical composition for the modulation of T cell and B cell responses made of one or more preparations and comprising a therapeutically effective dose of at least one inhibitor of TNFR1-mediated functions and of at least one antigen or allergen.


Patent
Ludwig Maximilians University of Munich | Date: 2016-11-30

The present invention relates to a method for detecting protein-protein interactions by assessing interaction in a eukaryotic cell of a first fusion protein that specifically binds to GFP and accumulates at distinct sites in the nucleus of the cell or interacts with structures accumulated at distinct sites in the nucleus of the cell; a second fusion protein comprising GFP and a bait (poly)peptide; and a third fusion protein comprising a fluorescent (poly)peptide having an excitation and/or emission wavelength that differs from that of GFP and a prey (poly)peptide. The emissions from the fluorescent parts of the fusion proteins are observed. Co-localization of the emissions from both fluorescent fusion proteins indicates interaction of the bait and the prey (poly)peptide. Methods for identifying a compound modulating the interaction of two (poly)peptides and methods of determining the relative strength of the interaction of two proteins with a third protein.


Patent
Ludwig Maximilians University of Munich and Helmholtz Center Munich | Date: 2015-06-18

The present invention relates to peptide-based compounds comprising (i) at least one peptide comprising the amino acid sequence of TKDNNLLGRFELXG wherein X is S or T and (ii) at least one label and/or drug. The present invention further relates to the use of said peptide-based compounds for tumor imaging and/or tumor targeting. The present invention further relates to the use of said peptide-based compounds as carrier of tumor therapeutic(s). The present invention further relates to methods for the in vitro and/or in vivo visualization, identification and/or detection of tumor cells and/or metastases as well as to methods for the treatment of cancer. The present invention further relates to a screening method for anti-tumor compounds.


Potschka H.,Ludwig Maximilians University of Munich
Advanced Drug Delivery Reviews | Year: 2012

Experimental support for the transporter hypothesis of drug resistance in epilepsies has triggered efforts developing and validating approaches to overcome enhanced blood-brain barrier efflux transport. Testing in rodent models has rendered proof-of-concept for an add-on therapy with antiepileptic drugs. However, further development of the approach would require tolerability considerations as efflux transporters serve an important protective function throughout the body limiting distribution of harmful xenobiotics. Relevant progress has been made in the elucidation of mechanisms driving up-regulation of the multidrug transporter P-glycoprotein in response to seizure activity. Based on this knowledge, novel strategies have been evaluated targeting the signaling cascade that regulates P-glycoprotein in the epileptic brain. Further concepts might include by-passing blood-brain barrier transporters by intracerebral administration or by encapsulation of antiepileptic drugs in nano-sized carrier systems.It is important to note that the future perspectives of respective approaches are still questionable based on the limited evidence for a clinical relevance of transporter expression. Thus, techniques are urgently needed for non-invasive assessment of blood-brain barrier transporter function. Respective techniques would allow testing for a clinical correlation between pharmacosensitivity and transporter function, validating therapeutic strategies targeting efflux transporters and selecting patients with transporter over-expression for respective clinical trials. Provided that further clinical data render support for the transporter hypothesis, the main question remains whether patients exist in which transporter over-expression is the predominant mechanism of drug resistance and in which overcoming drug efflux is equivalent with overcoming drug resistance. Imaging techniques might provide a tool to address these questions in clinical epileptology. However, the complex pharmacological interactions between antiepileptic drugs, radiotracers, and transporter modulators used in these approaches as well as interindividual differences in the brain pathology might hamper clear-cut conclusions and limit the diagnostic significance. © 2011 Elsevier B.V.


Wilson D.N.,Ludwig Maximilians University of Munich
Nature Reviews Microbiology | Year: 2014

The ribosome is one of the main antibiotic targets in the bacterial cell. Crystal structures of naturally produced antibiotics and their semi-synthetic derivatives bound to ribosomal particles have provided unparalleled insight into their mechanisms of action, and they are also facilitating the design of more effective antibiotics for targeting multidrug-resistant bacteria. In this Review, I discuss the recent structural insights into the mechanism of action of ribosome-targeting antibiotics and the molecular mechanisms of bacterial resistance, in addition to the approaches that are being pursued for the production of improved drugs that inhibit bacterial protein synthesis. © 2014 Macmillan Publishers Limited.


Soehnlein O.,Ludwig Maximilians University of Munich
Circulation Research | Year: 2012

Because of their rare detection in atherosclerotic lesions, the involvement of neutrophils in the pathophysiology of atherosclerosis has been largely denied. However, over the past couple of years, studies have provided convincing evidence for the presence of neutrophils in atherosclerotic plaques and further revealed the causal contribution of neutrophils during various stages of atherosclerosis. This review describes mechanisms underlying hyperlipidemia-mediated neutrophilia and how neutrophils may enter atherosclerotic lesions. It also highlights possible mechanisms of neutrophil-driven atherogenesis and plaque destabilization. Knowledge of the contribution of neutrophils to atherosclerosis will allow for exploration of new avenues in the treatment of atherogenesis and atherothrombosis. © 2012 American Heart Association, Inc.


Hermeking H.,Ludwig Maximilians University of Munich
Nature Reviews Cancer | Year: 2012

In recent years, microRNAs (miRNAs) have been identified as mediators of tumour suppression and stress responses exerted by the p53 tumour suppressor. p53-regulated miRNAs contribute to tumour suppression by controlling the expression of central components of multiple processes, including cell cycle progression, epithelialg-mesenchymal transition, stemness, metabolism, cell survival and angiogenesis. The expression and activity of p53 itself is also under the control of miRNAs. Finally, genetic and epigenetic alterations identified in the p53g-miRNA network indicate that these pathways are important for the initiation and progression of tumours. In the future, knowledge about the p53g-miRNA network may be able to be exploited for diagnostic and therapeutic approaches in cancer prevention and treatment. © 2012 Macmillan Publishers Limited. All rights reserved.


Wienken C.J.,Ludwig Maximilians University of Munich
Nature communications | Year: 2010

Protein interactions inside the human body are expected to differ from the situation in vitro. This is crucial when investigating protein functions or developing new drugs. In this study, we present a sample-efficient, free-solution method, termed microscale thermophoresis, that is capable of analysing interactions of proteins or small molecules in biological liquids such as blood serum or cell lysate. The technique is based on the thermophoresis of molecules, which provides information about molecule size, charge and hydration shell. We validated the method using immunologically relevant systems including human interferon gamma and the interaction of calmodulin with calcium. The affinity of the small-molecule inhibitor quercetin to its kinase PKA was determined in buffer and human serum, revealing a 400-fold reduced affinity in serum. This information about the influence of the biological matrix may allow to make more reliable conclusions on protein functionality, and may facilitate more efficient drug development.


Hermeking H.,Ludwig Maximilians University of Munich
Cell Death and Differentiation | Year: 2010

Recently, the transcription factor encoded by tumor suppressor gene p53 was shown to regulate the expression of microRNAs. The most significant induction by p53 was observed for the microRNAs miR-34a and miR-34b/c, which turned out to be direct p53 target genes. Ectopic miR-34 expression induces apoptosis, cell-cycle arrest or senescence. In many tumor types the promoters of the miR-34a and the miR-34b/c genes are subject to inactivation by CpG methylation. MiR-34a resides on 1p36 and is commonly deleted in neuroblastomas. Furthermore, the loss of miR-34 expression has been linked to resistance against apoptosis induced by p53 activating agents used in chemotherapy. In this review, the evidence for a role of miR-34a and miR-34b/c in the apoptotic response of normal and tumor cells is surveyed. © 2010 Macmillan Publishers Limited All rights reserved.


Wagner E.,Ludwig Maximilians University of Munich
Accounts of Chemical Research | Year: 2012

Synthetic small interfering RNA (siRNA) presents an exciting novel medical opportunity. Although researchers agree that siRNA could have a great therapeutic impact, the required extracellular and intracellular delivery of these molecules into the disease-associated target cells presents the primary roadblock for the broader translation of these molecules into medicines. Thus, the design of adequate delivery technologies has utmost importance. Viruses are natural masterpieces of nucleic acid delivery and present chemists and drug delivery experts with a template for the design of artificial carriers for synthetic nucleic acids such as siRNA. They have been developed into gene vectors and have provided convincing successes in gene therapy. Optimized by biological evolution, viruses are programmed to be dynamic and bioresponsive as they enter living cells, and they carry out their functions in a precisely defined sequence. However, because they are synthesized within living cells and with naturally available nucleotides and amino acids, the chemistry of viruses is limited. With the use of diverse synthetic molecules and macromolecules, chemists can provide delivery solutions beyond the scope of the natural evolution of viruses.This Account describes the design and synthesis of "synthetic siRNA viruses." These structures contain elements that mimic the delivery functions of viral particles and surface domains that shield against undesired biological interactions and enable specific host cell receptor binding through the presentation of multiple targeting ligands. For example, cationic polymers can reversibly package one or more siRNA molecules into nanoparticle cores to protect them against a degradative bioenvironment. After internalization by receptor-mediated endocytosis into the acidifying endosomes of cells, synthetic siRNA can escape from these vesicles through the activation of membrane-disruption domains as viruses do and reach the cytoplasm, the location of RNA interference.This multistep task presents an attractive challenge for chemists. Similar to the design of prodrugs, the functional domains of these systems have to be activated in a dynamic mode, triggered by conformational changes or bond cleavages in the relevant microenvironment such as the acidic endosome or disulfide-reducing cytoplasm. These chemical analogues of viral domains are often synthetically simpler and more easily accessible molecules than viral proteins. Their precise assembly into multifunctional macromolecular and supramolecular structures is facilitated by improved analytical techniques, precise orthogonal conjugation chemistries, and sequence-defined polymer syntheses. The chemical evolution of microdomains using chemical libraries and macromolecular and supramolecular evolution could provide key strategies for optimizing siRNA carriers to selected medical indications. © 2011 American Chemical Society.

Loading Ludwig Maximilians University of Munich collaborators
Loading Ludwig Maximilians University of Munich collaborators