Margot Thome

ORCID: 0000-0002-5656-2139
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About
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Research Areas
  • NF-κB Signaling Pathways
  • Cell death mechanisms and regulation
  • Immune Response and Inflammation
  • Immune Cell Function and Interaction
  • Lymphoma Diagnosis and Treatment
  • interferon and immune responses
  • CAR-T cell therapy research
  • T-cell and B-cell Immunology
  • Cytokine Signaling Pathways and Interactions
  • Chronic Lymphocytic Leukemia Research
  • Monoclonal and Polyclonal Antibodies Research
  • T-cell and Retrovirus Studies
  • Cell Adhesion Molecules Research
  • Ubiquitin and proteasome pathways
  • Herpesvirus Infections and Treatments
  • Galectins and Cancer Biology
  • Immunotherapy and Immune Responses
  • Cytomegalovirus and herpesvirus research
  • Cancer-related gene regulation
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Chronic Myeloid Leukemia Treatments
  • Signaling Pathways in Disease
  • Cancer-related molecular mechanisms research
  • Melanoma and MAPK Pathways
  • Inflammasome and immune disorders

University of Lausanne
2016-2025

The University of Texas MD Anderson Cancer Center
2023

Assiut University
2023

University of Modena and Reggio Emilia
2023

Universität Ulm
2023

University of Virginia
2023

Massachusetts General Hospital
2023

Hautklinik Heidelberg
1999

Institut Pasteur
1994-1996

Death receptors, such as Fas and tumor necrosis factor-related apoptosis-inducing ligand recruit Fas-associated death domain pro-caspase-8 homodimers, which are then autoproteolytically activated. Active caspase-8 is released into the cytoplasm, where it cleaves various proteins including pro-caspase-3, resulting in apoptosis. The cellular domain-like interleukin-1-β-converting enzyme-inhibitory protein long form (FLIPL), a structural homologue of lacking caspase activity because several...

10.1074/jbc.m206882200 article EN cc-by Journal of Biological Chemistry 2002-11-01

The protease activity of the paracaspase Malt1 contributes to antigen receptor-mediated lymphocyte activation and lymphomagenesis. is required for optimal NF-κB activation, but little known about responsible substrate(s). Here we report that cleaved family member RelB after Arg-85. cleavage induced its proteasomal degradation specifically controlled DNA binding RelA- or c-Rel–containing complexes. Overexpression inhibited expression canonical target genes led impaired survival diffuse large...

10.1073/pnas.1105020108 article EN Proceedings of the National Academy of Sciences 2011-08-22

Abstract Objective Familial cold urticaria (FCU) and Muckle‐Wells syndrome (MWS) are dominantly inherited autoinflammatory disorders that cause rashes, fever, arthralgia, in some subjects, AA amyloidosis, have been mapped to chromosome 1q44. Sensorineural deafness MWS, provocation of symptoms by FCU, distinctive features. This study was undertaken characterize the genetic basis an overlapping disorder French Canadian, British, Indian families, respectively. Methods Mutations candidate gene...

10.1002/art.10509 article EN Arthritis & Rheumatism 2002-09-01

Two receptors for TRAIL, designated TRAIL‐R2 and TRAIL‐R3, have been identified. Both are members of the tumor necrosis factor receptor family. is structurally similar to death‐domain‐containing TRAIL‐R1 (DR‐4), capable inducing apoptosis. In contrast, TRAIL‐R3 does not promote cell death. highly glycosylated membrane bound via a putative phosphatidylinositol anchor. The extended structure due presence multiple threonine‐, alanine‐, proline‐ glutamine‐rich repeats (TAPE repeats). shows broad...

10.1016/s0014-5793(97)01231-3 article EN FEBS Letters 1997-10-27

FLICE-inhibitory protein, FLIP (Casper/I-FLICE/FLAME-1/CASH/CLARP/MRIT), which contains two death effector domains and an inactive caspase domain, binds to FADD caspase-8, thereby inhibits receptor-mediated apoptosis. Here, we characterize the inhibitory effect of on a variety apoptotic pathways. Human Jurkat T cells undergoing Fas ligand-mediated apoptosis in response CD3 activation were completely resistant when transfected with FLIP. In contrast, presence did not affect induced by...

10.4049/jimmunol.161.8.3936 article EN The Journal of Immunology 1998-10-15

Protective adaptive immune responses rely on TCR-mediated recognition of Ag-derived peptides presented by self-MHC molecules. However, self-Ag (tumor)-specific TCRs are often too low affinity to achieve best functionality. To precisely assess the relationship between TCR-peptide-MHC binding parameters and T cell function, we tested a panel sequence-optimized HLA-A(*)0201/NY-ESO-1(157-165)-specific TCR variants with affinities lying within physiological boundaries preserve antigenic...

10.4049/jimmunol.1000173 article EN The Journal of Immunology 2010-03-30

Bcl10, a caspase recruitment domain (CARD)‐containing protein identified from breakpoint in mucosa‐associated lymphoid tissue (MALT) B lymphomas, is essential for antigen‐receptor‐mediated nuclear factor κB (NF‐κB) activation lymphocytes. We have novel CARD‐containing and interaction partner of named Carma1. Carma1 predominantly expressed lymphocytes represents new member the membrane‐associated guanylate kinase family. binds Bcl10 via its CARD motif induces translocation cytoplasm into...

10.1016/s0014-5793(01)02414-0 article EN FEBS Letters 2001-05-09

A key element for the development of suitable anti-cancer drugs is identification cancer-specific enzymatic activities that can be therapeutically targeted. Mucosa-associated lymphoid tissue transformation protein 1 (MALT1) a proto-oncogene contributes to tumorigenesis in diffuse large B-cell lymphoma (DLBCL) activated (ABC) subtype, least curable subtype DLBCL. Recent data suggest MALT1 has proteolytic activity, but it unknown whether this activity relevant tumor growth. Here we report...

10.1073/pnas.0907511106 article EN Proceedings of the National Academy of Sciences 2009-11-07
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