Wim Declercq

ORCID: 0000-0002-8218-2017
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About
Contact & Profiles
Research Areas
  • Cell death mechanisms and regulation
  • interferon and immune responses
  • NF-κB Signaling Pathways
  • Immune Response and Inflammation
  • Skin and Cellular Biology Research
  • Inflammasome and immune disorders
  • Cancer-related Molecular Pathways
  • Autophagy in Disease and Therapy
  • RNA Interference and Gene Delivery
  • Dermatology and Skin Diseases
  • Phagocytosis and Immune Regulation
  • Wnt/β-catenin signaling in development and cancer
  • Trace Elements in Health
  • Ubiquitin and proteasome pathways
  • Immunotherapy and Immune Responses
  • Autoimmune Bullous Skin Diseases
  • Hippo pathway signaling and YAP/TAZ
  • Virus-based gene therapy research
  • DNA Repair Mechanisms
  • Advancements in Transdermal Drug Delivery
  • Cytokine Signaling Pathways and Interactions
  • Skin Protection and Aging
  • Heat shock proteins research
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Wound Healing and Treatments

VIB-UGent Center for Inflammation Research
2015-2024

Ghent University
2014-2024

Cancer Research Institute Ghent
2016-2020

Vlaams Instituut voor Biotechnologie
2001-2016

Ghent University Hospital
2005-2016

VIB-UGent Center for Medical Biotechnology
2010

Ljubljana University Medical Centre
2010

University of Virginia
2005

Yale University
2005

VA Connecticut Healthcare System
2005

Murine L929 fibrosarcoma cells treated with tumor necrosis factor (TNF) rapidly die in a necrotic way, due to excessive formation of reactive oxygen intermediates. We investigated the role caspases cell death pathway. When cytokine response modifier A (CrmA), serpin-like caspase inhibitor viral origin, was stably overexpressed cells, latter became 1,000-fold more sensitive TNF-mediated death. In addition, TNF sensitization also observed when were pretreated Ac-YVAD-cmk or zDEVD-fmk, which...

10.1084/jem.187.9.1477 article EN The Journal of Experimental Medicine 1998-05-04

Although mixed lineage kinase domain-like (MLKL) protein has emerged as a specific and crucial for necroptosis induction, how MLKL transduces the death signal remains poorly understood. Here, we demonstrate that full four-helical bundle domain (4HBD) in N-terminal region of is required sufficient to induce its oligomerization trigger cell death. Moreover, found patch positively charged amino acids on surface 4HBD binds phosphatidylinositol phosphates (PIPs) allows recruitment plasma...

10.1016/j.celrep.2014.04.026 article EN cc-by-nc-nd Cell Reports 2014-05-01

Autophagy and apoptosis are two important interconnected stress-response mechanisms. However, the molecular interplay between these pathways is not fully understood. To study fate function of autophagic proteins at onset apoptosis, we used a cellular model system in which autophagy precedes apoptosis. IL-3 depletion Ba/F3 cells caused caspase (casp)-mediated cleavage Beclin-1 PI3KC3, crucial components autophagy-inducing complex. We identified casp sites Beclin-1, TDVD(133) DQLD(149), yields...

10.1038/cddis.2009.16 article EN cc-by Cell Death and Disease 2010-01-21

Murine L929 fibrosarcoma cells were transfected with the human Fas (APO-1/CD95) receptor, and role of various caspases in Fas-mediated cell death was assessed. Proteolytic activation procaspase-3 -7 shown by Western analysis. Acetyl-Tyr-Val-Ala-Asp-chloromethylketone benzyloxycarbonyl-Asp(OMe)-Glu(OMe)-Val-Asp(OMe)-fluoromethylketone, tetrapeptide inhibitors caspase-1– caspase-3–like proteases, respectively, failed to block Fas-induced apoptosis. Unexpectedly, broad-spectrum caspase...

10.1084/jem.188.5.919 article EN The Journal of Experimental Medicine 1998-09-07

Necrostatin-1 (Nec-1) is widely used in disease models to examine the contribution of receptor-interacting protein kinase (RIPK) 1 cell death and inflammation. We studied three Nec-1 analogs: Nec-1, active inhibitor RIPK1, inactive (Nec-1i), its variant, stable (Nec-1s), more variant. report that identical methyl-thiohydantoin-tryptophan, an potent immunomodulatory enzyme indoleamine 2,3-dioxygenase (IDO). Both Nec-1i inhibited human IDO, but Nec-1s did not, as predicted by molecular...

10.1038/cddis.2012.176 article EN cc-by Cell Death and Disease 2012-11-29

Successful immunogenic apoptosis in experimental cancer therapy depends on the induction of strong host anti-tumor responses. Given that tumors are often resistant to apoptosis, it is important identify alternative molecular mechanisms elicit cell death. We have developed a genetic model which direct dimerization FADD combined with inducible expression RIPK3 promotes necroptosis. report necroptotic cells release damage-associated patterns and promote maturation dendritic cells, cross-priming...

10.1016/j.celrep.2016.03.037 article EN cc-by-nc-nd Cell Reports 2016-04-01

Caspases are a family of cysteine proteases which play crucial role in apoptosis and inflammation. The involvement caspases these processes can be demonstrated by their irreversible inhibition with fluoromethyl ketone chloromethyl derivatives peptides resembling the cleavage site known caspase substrates. These inhibitors irreversibly alkylate residue active caspases. In this study we show that biotinylated peptide inhibitor (z‐VAD.fmk) also efficiently affinity‐labeled cathepsin B H....

10.1016/s0014-5793(98)01640-8 article EN FEBS Letters 1999-01-08
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