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Name:      Prof. Dr. Iris Behrmann
  Signal Transduction Laboratory
Life Sciences Research Unit
University of Luxembourg
  Homepage (external link)
Date/Location: Thursday, March, 05th 2020, 5:00 pm,  Building 28 /  Room 27
Title:  Signal transduction of IL-6-type cytokines: involvement of (short and long) non-coding RNAs

 

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Talk

 

Name:      PD Dr. Heike M. Hermanns
  Department of Medicine II / Hepatology, Medical School University of Würzburg
  Homepage (external link)
Date/Location: Friday, March, 08th 2019, 2.30 pm,  Building 28 /  Room 27
Title:  JAK-STAT signaling in liver diseases

 

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Talk

 

Name:      Prof. Dr. Gerhard Müller-Newen
  Institut für Biochemie und Molekularbiologie der RWTH Aachen
  Hompage (external link)
Date/Location: Thursday, 08.11.2018 17:00 Building 28 (Pflälzer Platz) Room 27
Title:  Non-canonical aspects of Jak-STAT signaling

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Name:      PD Dr. Christoph Garbers
  Institute of Biochemistry, Christan-Albrechts-University Kiel
  Homepage (external link)
Date/Location: Thursday, March, 08th 2018, 5 pm,  Building 28 /  Room 27
Title:  Control of intracellular signaling pathways by extracellular cytokine receptors

Abstract:

Intracellular signaling cascades, e.g. the Jak/STAT pathway, have several different functions in health and disease. Their activation and the duration of signaling must be tightly controlled. Dysregulated, overshooting activities of such pathways are often associated with human diseases. The pleiotropic cytokines Interleukin-11 (IL-11) and IL-6 are secreted glycoproteins that activate their target cells via specific membrane-bound IL-6/IL-11 alpha receptors (IL-11R and IL-6R, respectively). Formation of cytokine/cytokine receptor complexes leads to the formation of a homodimer of the ubiquitously expressed signal-transducing beta-receptor gp130 (termed classic signaling), which induces signaling cascades like the Jak/STAT pathway. Thus, the cellular expression pattern of the alpha receptors determines which cells respond to IL-6 and IL-11, respectively, as gp130 is ubiquitously expressed. Importantly, the ectodomains of the IL-11R and IL-6R can be cleaved off the cells by several proteases, albeit with different preferences and specificities. The resulting soluble receptors (sIL-11R and sIL-6R) act as agonists and can activate cells via gp130 (termed trans-signaling), which widens the spectrum of cells that can be activated by IL-11 and IL-6. The presentation will give an overview how signaling on the inside is regulated by cytokine receptors on the outside of the cell, and how knowledge about these processes can be exploited therapeutically.

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Name:      Prof. Dr. Raymond Kaempfer
  Hebrew University of Jerusalem, School of Medicine, IMRIC Biochemistry and Molecular Biology, Israel
  Homepage (externer Link)
Date/Location: Monday, December 04st 2017 16:00 Uhr in Building  28 / Pfälzer Platz, Room 027
Title:  Conrol of mRNA splicing by noncoding intragenic RNA elements that evoke a cellular stress response

Abstract:

We define structure and function of novel noncoding RNA elements within the tumor necrosis factor and hemoglobin genes that by activating a cellular stress response hitherto thought only to repress translation, render splicing of their mRNAs highly efficient. These RNA elements activate the RNA-dependent kinase, PKR. PKR-mediated mRNA splicing, we show, depends strictly on phosphorylation of translation initiation factor eIF2α which is both necessary and sufficient to achieve efficient splicing,while leaving translation intact.

References:
Cell Research (http://rdcu.be/qB2k)
Cell Reports (http://dx.doi.org/10.1016/j.celrep.2017.06.035 ).

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Name:      Dr. Niamh Connolly
  Physiology & Medical Physics Department, Royal College of Surgeons in Ireland
  Homepage (external Link)
Date/Location: Thursday, November 09th 2017, 5 pm,  Building 28 /  Room 27
Title:  Using systems modelling to investigate bioenergetic dysfunction in Alzheimer’s disease

 

Abstract:

Mitochondrial bioenergetic dysfunction is implicated in neurodegenerative diseases such as Parkinson’s, Alzheimer’s and Huntington’s Diseases. It is unknown, however, whether mitochondrial dysfunction is sufficient to trigger neurodegeneration, or whether it constitutes an additional risk factor. As part of the interdisciplinary, multi-lab consortium, ‘Cellular Bioenergetics in Neurodegenerative Diseases’ (CeBioND; cebiond.org), we are combining systems modelling with in vitro experiments in a cellular model of Alzheimer’s Disease, to holistically investigate the impact of neurodegenerative defects on mitochondrial bioenergetic output.

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Name:      Dr. Manuela Benary
  Institute for Theoretical Biology, Humboldt University Berlin
  Homepage (external Link)
Date/Location: Thursday, March 09th 2017, 5 pm,  Building 28 /  Room 27
Title:  Information theory reveals the contribution of MAPK signaling to cell cycle

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Talk

 

Name:      Dr. Ulfert Rand
  Helmholtz Centre for Infection Research, Braunschweig, Research Group Immune Aging and Chronic Infection (IMCI), Department of Vaccinology (VAC)
  Homepage (external Link)
Date/Location: Monday, November 07th 2016, 5 pm,  Building 28 /  Room 27
Title:  Dynamics of the antiviral interferon response

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Name:      Dr. Chrstian Ehlting
  Department of Gastroenterology, Hepatology, and Infectiology, University Hospital Heinrich-Heine-University, Düsseldorf
  Homepage (external Link)
Date/Location: Thursday, October 20th 2016, 5 pm,  Building 28 /  Room 27
Title:  The p38MAPK-STAT3 axis as a key regulator of the inflammatory response of macrophages

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Name:      Dr. Michal Komorowski
  Polish Academy of Science
Institute of Fundamental Technological Research
  Homepage (external Link)
Date/Location: Tuesday, May 10th 2016, 5 pm,  Building 28 /  Room 27
Title:  Information flow in signalling pathways
Abstact: High throughput experimental approaches and the advances of computational capabilities continue to reshape modern biology. Thus, mathematical biology offers new possibilities for mathematicians and biologists to explore signal transduction, an important and highly complex aspect of cell biology. The molecular mechanisms how cells transduce biochemical signals are widely understood. Biochemical descriptions however failed to reveal how stimuli are translated into distinct responses. Signalling pathways are highly complex as they are functionally pleiotropic and biochemical reactions intrinsically stochastic. In the talk I will try to present how mathematical methods of information theory and probabilistic dynamical modelling can contribute to understanding of how information flows in signalling pathways.In particular, I will present developed analytical and computational tools required to improve our understanding how cellular signalling processes can derive a variety of distinct outputs from complex inputs. To overcome limitations of existing methods we have integrated advanced concepts of statistical inference with information theory and high content confocal imaging. The concepts have been applied to obtain new insights into mechanisms that govern dose dependent responses to type I interferons via STAT1 and STAT2 pathways as well as to TNF via NF-kB pathway.

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Last Modification: 17.02.2020 - Contact Person: Prof. Dr. Fred Schaper