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Upcoming Seminars

Maurizio Renna, PhD - "Understanding the regulation of macroautophagy in health and disease: what have we learnt, so far?"

Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Università degli Studi di Napoli “Federico II”
When Oct 30, 2018
from 12:00 PM to 01:30 PM
Where Tigem, Vesuvius Auditorium
Contact Name
Contact Phone 081-19230659
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Abstract
Autophagy is a major cellular catabolic process responsible for the removal of long-lived cytoplasmic proteins, protein complexes, as well as of entire intracellular organelles, which is fundamental for the homeostasis of eukaryotic cells. Indeed, alterations of the autophagic pathways have been implicated in a large set of human diseases. Over the years, one of the major goal of the research in the field has been to identify novel pathways and molecular mechanisms regulating autophagy with the aim of providing potential alternative approaches for the treatment of many clinically relevant conditions, such as ageing, metabolic, neurodegenerative disorders, infectious diseases and cancer.
For instance, recent data report how autophagy is compromised upon contact inhibition, a phenomenon that enables normal cells to control proliferation and growth but is lost upon malignant transformation. In particular, in 2D or 3D-soft extracellular matrix cultures of contact-inhibited cells, YAP/TAZ fail to co-transcriptionally regulate the expression of myosin-II genes, resulting in the loss of F-actin stress fibers, which in turn impairs autophagosome formation. The decreased proliferation, as well as the increased sensitivity to hypoxia and glucose starvation, resulting from contact inhibition are partly autophagy-dependent. These findings define how mechanical cues mediated via the YAP/TAZ-axis impact on autophagy to contribute to core phenotypes resulting from high cell confluency, which are lost in various cancers.
Finally, preliminary data will be presented linking the activity and homeostasis of the autophagic/lysosomal compartment to the function of TDP-43, a RNA-binding protein whose mutations have been associated to some neurodegenerative diseases, such as FTD and ALS.

Volker Haucke Ph.D. - "Lipid regulation of endocytosis and endolysosmal membrane dynamics"

Full Professor of Molecular Pharmacology, Director, Leibniz Forschungsinstitut für Molekulare Pharmakologie (FMP), Berlin, Germany
When Nov 20, 2018
from 12:00 PM to 01:30 PM
Where Tigem, Auditorium "Vesuvius"
Contact Name
Contact Phone 08119230659
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Abstract
Phosphoinositides (PIs) form a minor class of phospholipids with crucial functions in cell physiology, ranging from cell signalling and motility to a role as signposts of compartmental membrane identity. Phosphatidylinositol 3-phosphates are present at the plasma membrane and within the endolysosomal system, where they serve as key regulators of both cell signalling and of intracellular membrane traffic. In my talk I will discuss the localization, regulation, and molecular mechanism of action of class II PI 3-kinases and their roles in endocytosis and in nutrient signaling within the endolysosomal system. For example, I will cover our recent advances in the analysis of the metabolic pathways that regulate cellular synthesis of PI 3-phosphates at distinct intracellular sites and discuss the mechanisms by which these lipids regulate cell signaling and membrane traffic in different biological model systems. Our data provide a framework for how PI 3-phosphate metabolism is integrated into the cellular network and identify PI3Ks as targets for future therapeutics.

References
Posor, Y. et al. Haucke, V. (2013) Spatiotemporal Control of Endocytosis by Phosphatidylinositol 3,4-Bisphosphate. Nature, 499, 233-237
Marat, A.L., Haucke, V. (2016) Phosphatidylinositol 3-phosphates - at the interface between cell signalling and membrane traffic. EMBO J., 35, 561-579
Schöneberg, J.#, Lehmann, M.# et al. Haucke, V.*, Noe, F.* (2017) Lipid-mediated PX-BAR domain recruitment couples local membrane constriction to endocytic vesicle fission. (*co-corresponding) Nature Communications, 8:15873. doi: 10.1038/ncomms15873
Marat, A.L. et al Haucke, V. (2017) mTORC1 activity repression by late endosomal phosphatidylinositol 3,4-bisphosphate. Science 356, 968-972
Wang, H. #, Lo, W.T. #, Vujičić Žagar, A., Gulluni, F., Scapozza, L., Haucke, V.*, Vadas, O.* (2018) Autoregulation of class II alpha PI3K activity by its lipid binding PX-C2 domain module. Mol. Cell, 71, 343-351 (*co-corresponding)


Daniel Ory, MD - "Niemann-Pick C: A Disorder of Cholesterol Homeostasis"

Senior VP, Translational Medicine, Casma Therapeutics, Cambridge, MA (USA)
When Nov 27, 2018
from 12:00 PM to 01:30 PM
Where Tigem Auditorium "Vesuvius"
Contact Name
Contact Phone 08119230659
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Abstract
Niemann-Pick type C1 (NPC1) disease is an autosomal recessive neurovisceral disease characterized by progressive lipid accumulation. Mutations in NPC1 (95% of NPC cases) and NPC2 are responsible for NPC in humans. Diagnosis of the disease has been challenging, often leading to diagnostic delays of more than 4-5 years. Therapeutic options are limited. The only approved therapy for NPC is miglustat, an inhibitor of glycosphingolipid synthesis that has shown limited efficacy. In this seminar, advances in NPC diagnostics and treatments will be presented.