Dear All,
It is my pleasure to invite you to the (special) Nencki Institute Seminar, which will take place on the 1st of December at 3 pm in the CN hall.
We will host 4 speakers:
15-15:30 Prof. Stephan Herzig, Director and Department Head of the Helmholtz Diabetes Center and Director of the Institute for Diabetes and Cancer from Helmholtz Center Munich, Germany, who will give a lecture entitled: Metabolic control through inter- and intra-organ communication.
15:30-16 Prof. Philippe Bastiaens, Director of the Max Planck Institute for Molecular Physiology and the head of the Department of Systemic Cell Biology, Max Planck Institute for Molecular Physiology, Dortmund, Germany, who will give a lecture entitled: RPTPγ is a redox-regulated suppressor of promigratory EGFR signaling.
16-16:15 Break
16:15-16:45 Prof. Ana Cuenda, from the Department of Immunology and Oncology, National Centre of Biotechnology/Consejo Superior de Investigaciones Científicas, Madrid, Spain, who will talk about: p38 signalling in inflammation and colon cancer.
16:45-17:15 Prof. Martin Klingenspor from the Chair for Molecular Nutritional Medicine, Technical University of Munich, Freising, Germany, who will give a lecture entitled: Evolution, Function and Physiology of Uncoupling Protein 1.
Below you can find all 4 abstracts.
There will be a coffee break and the seminar will be followed by a get together.
Best regards
Aleksandra Pękowska
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Stephan Herzig
Helmholtz Center Munich, Neuherberg, Germany
Metabolic control through inter- and intra-organ communication.
Systemic energy homeostasis is determined by the intricate interplay between different organ compartments, including the central nervous system, skeletal muscle, liver as well as white and brown adipose tissue (WAT/BAT). Indeed, the coordinated adaptation of metabolic pathways in different tissues to changing environmental cues is critical for systemic metabolic health. However, integrative molecular checkpoints in inter-tissue communication and/or coordination still remain largely unknown.
Here, we discuss our recent findings on both the tissue-specific and systemic roles of novel endocrine and transcriptional axes in energy homeostasis and metabolic dysfunction. Our data overall underline the notion that the coordinated regulation of distinct transcriptional hubs may represent a novel component of integrative inter-tissue communication and metabolic flexibility.
Philippe Bastiaens
Department of Systemic Cell Biology, Max Planck Institute for Molecular Physiology, Dortmund, Germany
RPTPγ is a redox-regulated suppressor of promigratory EGFR signaling
Spatially-organized interaction dynamics between proto-oncogenic epidermal growth factor receptor (EGFR) and protein tyrosine phosphatases (PTPs) determine EGFR’s phosphorylation response to growth factors and thereby cellular behavior within developing tissues. We describe how the coupling between EGFR and PTP activity leads to aberrant signal suppression while enabling migratory signaling responses to low, physiological growth factor stimuli. Single cell imaging of EGFR phosphorylation and PTP oxidation revealed that RPTPγ fully suppresses spontaneous EGFR phosphorylation, while EGF-induced NADPH-oxidase activity enables promigratory signaling responses at the plasma membrane by H2O2-mediated oxidative inhibition of RPTPγ’s phosphatase activity. The EGF-dependent toggle switch dynamics between interacting EGFR monomers and RPTPγ thereby enables autocatalytically amplified phosphorylation responses to very low, physiological, EGF levels at sparse receptor expression. Accordingly, RPTPγ knock-out results in spontaneous promigratory EGFR signaling from the plasma membrane but loss of proliferative signaling stemming from liganded endosomal EGFR complexes. We thereby provide evidence of RPTPγ’s suppressor function of oncogenic promigratory EGFR signaling from the plasma membrane.
Ana Cuenda
Department of Immunology and Oncology, National Centre of Biotechnology/Consejo Superior de Investigaciones Científicas, Madrid, Spain
p38 signalling in inflammation and colon cancer
p38MAPK pathways are central to inflammatory processes. The p38MAPK group has four members encoded by different genes, p38α, p38β, p38γ and p38δ. While the roles of the p38α isoform have been widely studied in the context of inflammation and tumour development, the knowledge of the in vivo role of p38γ and p38δ in these processes is still very limited. Our laboratory is studying essential functions of these two less studied alternative p38MAPKs, in vivo and in cultured cells. This strategy has led to the discovery of unexpected cross talk between p38γ/p38δ and ERK1/2 pathway controlling cytokine production in cells during inflammation. The regulation of inflammatory processes by p38γ/p38δ has an impact in the development of different diseases such as colon and skin inflammation, arthritis, or colon cancer associated to colitis. We will discuss how, in specific settings, the p38MAPK components, p38γ and p38δ, operate in inflammatory processes, and the mechanisms underlying these unexpected functions.
Martin Klingenspor
Chair for Molecular Nutritional Medicine, Technical University of Munich, Freising, Germany
Evolution, Function and Physiology of Uncoupling Protein 1
Orthologues of the mitochondrial carrier uncoupling protein 1(UCP1) can be found in the genome of bony fish, thus documenting >400 million years of evolutionary history. Since the discovery of UCP1 as the GDP-binding protein in mammalian brown adipose tissue, the capacity of this protein to dissipate proton-motive force for thermogenesis has been thoroughly investigated on the biochemical, cellular and systemic level. The presentation will address key questions related to the thermogenic function of UCP1 still awaiting conclusive answers.
