Research focus
Cell death is a crucial process in ontogeny, homeostasis and pathologies. Without (cell) death there would be no life. Every day about 100 billion cells die in our bodies. It is remarkable that in most cases we are tolerized against this daily cellular massacre. However, many diseases can be traced to a deregulation of cell death either as being too sensitive (neurodegenerative diseases, autoimmunity diseases, organ transplantation), or being too resistant (cancer). Several several modalities have been identified: apoptosis, necrosis, necroptosis, pyroptosis and autophagic cell death. Many questions concerning the intracellular signaling of these cell death modes and the intercellular communication still wait for answers.
A subgroup of our unit, headed by Wim Declercq, studies a particular situation of cell death and inflammation, viz. the skin. The terminal differentiation of keratinocytes and the formation of the cornified envelope is a beautiful example of how dead cell corpses are involved in protection against UVB, water loss and infection.
The unit aims to generate fundamental knowledge about the biology and potential biomedical application of a set of important molecules (caspases, RIP kinases) and their targets in cell death and inflammation. Molecules of interest are studied at four major levels: molecules (structure function, complexes, substrates), cells (intracellular signaling), intercellular communication (Cell Death Associated Molecular Patterns or CDAMPs), and organisms (transgenic models in various disease models). Our aim is to define molecular targets in these pathways that may lead to the development of therapeutic strategies to interfere in a specific way with cell death and inflammation.
Our fundamental research may have therapeutic applications in cancer, inflammatory and neurodegenerative diseases, and skin pathologies.
Peter Vandenabeele has been chairman of the 11th and 18th Euroconference on Apoptosis organized in Ghent 2003 and 2010 by the European Cell Death Organization (ECDO).
> Watch the YouTube movies about apoptosis.
Copyright Peter Vandenabeele Lab - Vanden Berghe et al. CDD "2010",
Publications
RIP Kinase-Dependent Necrosis Drives Lethal Systemic Inflammatory Response SyndromeDuprez L, Takahashi N, Van Hauwermeiren F, Vandendriessche B, Goossens V, Vanden Berghe T, Declercq W, Libert C, Cauwels A, Vandenabeele PIMMUNITY, 35, 908-18, 2011 Necroptosis, necrosis and secondary necrosis converge on similar cellular disintegration featuresVanden Berghe T, Vanlangenakker N, Parthoens E, Deckers W, Devos M, Festjens N, Guerin C, Brunk U, Declercq W, Vandenabeele PCELL DEATH AND DIFFERENTIATION, 17, 922-30, 2010 Caspase-14 protects against epidermal UVB photodamage and water lossDenecker G, Hoste E, Gilbert B, Hochepied T, Ovaere P, Lippens S, Van Den Broecke C, Van Damme P, D'herde K, Hachem J, Borgonie G, Presland R, Schoonjans L, Libert C, Vandekerckhove J, Gevaert K, Vandenabeele P, Declercq WNATURE CELL BIOLOGY, 9, 666-74, 2007
News
27/12/2011 - By blocking necroptosis, Peter Vandenabeele and his colleagues from from VIB-UGent were able to protect mice against the lethal condition sepsis, showing the central role of the molecule RIPK in this condition. 02/02/2009 - Foamix Ltd., a leading worldwide developer of topical foams for dermatology and gynecology has entered into an agreement with VIB for the development of a unique topical drug for the treatment of Psoriasis. 21/05/2007 - VIB researchers have demonstrated that the caspase-14 protein − whose function has been unknown up to now − not only plays a role in maintaining the balance of moisture in the skin but also offers protection against UVB rays.
 Peter VandenabeeleResearch area(s)Model organism(s)BioPh.D.: Ghent University, Ghent, Belgium, 1990 VIB Group leader since 1996 Contact Info
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