Bertrand team: Molecular and Cellular Signaling under stress

Research Field: Signal transduction in Inflammation and Cell Death

Team leader: Prof. Dr. Mathieu Bertrand

Tel: +32 9 33 13 720 - Fax: +32 9 221 76 73
Email: Mathieu.Bertrand.spam.detractor@irc.vib-UGentspam.corruptor.be

Research topic

Cells are continuously confronted with stress signals that initiate at the cell surface or within the cell. The ability to transduce the signal and to activate a proper cellular response, either through transcription-dependent or –independent mechanisms, relies on the recruitment of adaptor proteins and on the activation of specific signaling pathways. These processes need thigh regulation, as defective control of these pathways can lead to human pathologies.

Our research team focuses on the elucidation of the molecular mechanisms regulating stress-induced cell survival/death, as well as innate immune/inflammatory responses, with a particular interest on the role of ubiquitylation. Cell death and innate immunity are ancient evolutionary conserved, inter-connected, processes that utilize a great number of related molecular effectors and parallel signal transduction mechanisms. Research in the group is mainly conducted at the biochemical and cellular levels, but also involves in vivo studies. Our group is part of the GROUP-ID (Ghent Researchers On Unfolded Proteins in Inflammatory Disease) multidisciplinary research platform (MRP) of Ghent University. GROUP-ID is a consortium that focuses on the role of ER stress in inflammation and immunity.

Schematic representation of signaling downstream of the NOD1/2 innate immune receptors. Vandenabeele P and Bertrand MJ, Nature Reviews Immunology, 2012.
Schematic representation of signaling downstream of the NOD1/2 innate immune receptors. Vandenabeele P and Bertrand MJ, Nature Reviews Immunology, 2012. Click to enlarge.

Areas of expertise

  • Signal transduction
  • Ubiquitylation
  • Inflammatory and death pathways (downstream of death receptors and pattern recognition receptors)

Technology transfer potential

Identification of new therapeutic targets for the treatment of cell death and inflammation related diseases

Selected publications

  1. Dondelinger Y et al. RIPK3 contributes to TNF-mediated RIPK1-dependent apoptosis in conditions of cIAP1/2 deletion or TAK1 kinase inhibition.
    Cell Death and Differentiation, 20, 1381-92, 2013.
  2. Vandenabeele P and Bertrand MJ. The role of the IAP E3 ubiquitin ligases in regulating pattern-recognition receptor signaling.
    Nature Reviews Immunology, 12, 833-44, 2012.
  3. Vanlangenakker N et al. cIAP1 and TAK1 protect cells from TNF-induced necrosis by preventing RIP1/RIP3-dependent reactive oxygen species production.
    Cell Death and Differentiation, 18, 656-65, 2010.
  4. Bertrand MJ et al. Cellular inhibitors of apoptosis cIAP1 and cIAP2 are required for innate immunity signaling by the pattern recognition receptors NOD1 and NOD2.
    Immunity, 30, 789-801, 2009.
  5. Bertrand MJ et al. cIAP1 and cIAP2 facilitate cancer cell survival by functioning as E3 ligases that promote RIP1 ubiquitination.
    Molecular Cell, 30, 689-700, 2008.

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