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  1. AU="Le Cann, Fabienne"
  2. AU="Ng, Kenneth K S"
  3. AU="Rodes, Virginia" AU="Rodes, Virginia"
  4. AU="Neumann, Katja"
  5. AU="de Santana, Luiz R P"
  6. AU="Çınkooğlu, Akın"
  7. AU="N. Ameer Ahammad"
  8. AU=Schmelzle T AU=Schmelzle T
  9. AU="MacIntosh, Josephine"
  10. AU="Dinh, Thị Thanh Thuy"
  11. AU="Silva, José A C"
  12. AU="Wieland, I"
  13. AU="I. L. Smirnova"
  14. AU=Mayer Gert
  15. AU="Burns, Jane"
  16. AU="Lin, Yung-Chun"
  17. AU="van de Klundert, Manouk A W"
  18. AU="Rustam, F R Mohammed"
  19. AU="Zhou, Jialiang"
  20. AU="Galotto, María José"
  21. AU="Hackell, Jesse M"
  22. AU=Nathan Carl
  23. AU="de Vasconcelos, Paulo R L"
  24. AU="Rhebergen, Koenraad S"
  25. AU="Bo Wen"
  26. AU=Brown C. Hendricks
  27. AU="Bacchetta, N."
  28. AU="Marquis, Krista"
  29. AU="Milena Alec"
  30. AU="Carfagna, Charles S"
  31. AU="Chakraborti, Udipta"
  32. AU="Uson, Jesus"
  33. AU="Riotto, A W"
  34. AU="Candel, Bart Gj"
  35. AU="Brinken, Tatjana"
  36. AU="Korkmaz, Asli"

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  1. Artikel ; Online: Sibiriline, a new small chemical inhibitor of receptor-interacting protein kinase 1, prevents immune-dependent hepatitis.

    Le Cann, Fabienne / Delehouzé, Claire / Leverrier-Penna, Sabrina / Filliol, Aveline / Comte, Arnaud / Delalande, Olivier / Desban, Nathalie / Baratte, Blandine / Gallais, Isabelle / Piquet-Pellorce, Claire / Faurez, Florence / Bonnet, Marion / Mettey, Yvette / Goekjian, Peter / Samson, Michel / Vandenabeele, Peter / Bach, Stéphane / Dimanche-Boitrel, Marie-Thérèse

    The FEBS journal

    2017  Band 284, Heft 18, Seite(n) 3050–3068

    Abstract: Necroptosis is a regulated form of cell death involved in several disease models including in particular liver diseases. Receptor-interacting protein kinases, RIPK1 and RIPK3, are the main serine/threonine kinases driving this cell death pathway. We ... ...

    Abstract Necroptosis is a regulated form of cell death involved in several disease models including in particular liver diseases. Receptor-interacting protein kinases, RIPK1 and RIPK3, are the main serine/threonine kinases driving this cell death pathway. We screened a noncommercial, kinase-focused chemical library which allowed us to identify Sibiriline as a new inhibitor of necroptosis induced by tumor necrosis factor (TNF) in Fas-associated protein with death domain (FADD)-deficient Jurkat cells. Moreover, Sib inhibits necroptotic cell death induced by various death ligands in human or mouse cells while not protecting from caspase-dependent apoptosis. By using competition binding assay and recombinant kinase assays, we demonstrated that Sib is a rather specific competitive RIPK1 inhibitor. Molecular docking analysis shows that Sib is trapped closed to human RIPK1 adenosine triphosphate-binding site in a relatively hydrophobic pocket locking RIPK1 in an inactive conformation. In agreement with its RIPK1 inhibitory property, Sib inhibits both TNF-induced RIPK1-dependent necroptosis and RIPK1-dependent apoptosis. Finally, Sib protects mice from concanavalin A-induced hepatitis. These results reveal the small-molecule Sib as a new RIPK1 inhibitor potentially of interest for the treatment of immune-dependent hepatitis.
    Mesh-Begriff(e) Alkaloids/chemistry ; Alkaloids/pharmacology ; Animals ; Apoptosis/drug effects ; Apoptosis/genetics ; Caspase 3/genetics ; Caspase 3/immunology ; Cell Line, Transformed ; Concanavalin A ; Cycloheximide/pharmacology ; Fibroblasts/cytology ; Fibroblasts/drug effects ; Fibroblasts/metabolism ; Gene Expression Regulation ; HT29 Cells ; Hepatitis, Animal/chemically induced ; Hepatitis, Animal/genetics ; Hepatitis, Animal/immunology ; Hepatitis, Animal/prevention & control ; Humans ; Imidazoles/pharmacology ; Immunologic Factors/chemistry ; Immunologic Factors/pharmacology ; Indoles/pharmacology ; Jurkat Cells ; Male ; Mice ; Molecular Docking Simulation ; Necrosis/chemically induced ; Necrosis/genetics ; Necrosis/immunology ; Protein Kinase Inhibitors/chemistry ; Protein Kinase Inhibitors/pharmacology ; Receptor-Interacting Protein Serine-Threonine Kinases/antagonists & inhibitors ; Receptor-Interacting Protein Serine-Threonine Kinases/genetics ; Receptor-Interacting Protein Serine-Threonine Kinases/immunology ; Signal Transduction ; Spiro Compounds/chemistry ; Spiro Compounds/pharmacology ; TNF-Related Apoptosis-Inducing Ligand/pharmacology ; Tumor Necrosis Factor-alpha/pharmacology
    Chemische Substanzen Alkaloids ; Imidazoles ; Immunologic Factors ; Indoles ; Protein Kinase Inhibitors ; Spiro Compounds ; TNF-Related Apoptosis-Inducing Ligand ; TNFSF10 protein, human ; Tumor Necrosis Factor-alpha ; necrostatin-1 ; sibirine ; Concanavalin A (11028-71-0) ; Cycloheximide (98600C0908) ; RIPK1 protein, human (EC 2.7.11.1) ; RIPK3 protein, human (EC 2.7.11.1) ; Receptor-Interacting Protein Serine-Threonine Kinases (EC 2.7.11.1) ; CASP3 protein, human (EC 3.4.22.-) ; Caspase 3 (EC 3.4.22.-)
    Sprache Englisch
    Erscheinungsdatum 2017-09
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 2173655-8
    ISSN 1742-4658 ; 1742-464X
    ISSN (online) 1742-4658
    ISSN 1742-464X
    DOI 10.1111/febs.14176
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Volltext online

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  2. Artikel ; Online: The Disintegrin and Metalloprotease ADAM12 Is Associated with TGF-β-Induced Epithelial to Mesenchymal Transition.

    Ruff, Michaël / Leyme, Anthony / Le Cann, Fabienne / Bonnier, Dominique / Le Seyec, Jacques / Chesnel, Franck / Fattet, Laurent / Rimokh, Ruth / Baffet, Georges / Théret, Nathalie

    PloS one

    2015  Band 10, Heft 9, Seite(n) e0139179

    Abstract: The increased expression of the Disintegrin and Metalloprotease ADAM12 has been associated with human cancers, however its role remain unclear. We have previously reported that ADAM12 expression is induced by the transforming growth factor, TGF-β and ... ...

    Abstract The increased expression of the Disintegrin and Metalloprotease ADAM12 has been associated with human cancers, however its role remain unclear. We have previously reported that ADAM12 expression is induced by the transforming growth factor, TGF-β and promotes TGF-β-dependent signaling through interaction with the type II receptor of TGF-β. Here we explore the implication of ADAM12 in TGF-β-mediated epithelial to mesenchymal transition (EMT), a key process in cancer progression. We show that ADAM12 expression is correlated with EMT markers in human breast cancer cell lines and biopsies. Using a non-malignant breast epithelial cell line (MCF10A), we demonstrate that TGF-β-induced EMT increases expression of the membrane-anchored ADAM12L long form. Importantly, ADAM12L overexpression in MCF10A is sufficient to induce loss of cell-cell contact, reorganization of actin cytoskeleton, up-regulation of EMT markers and chemoresistance. These effects are independent of the proteolytic activity but require the cytoplasmic tail and are specific of ADAM12L since overexpression of ADAM12S failed to induce similar changes. We further demonstrate that ADAM12L-dependent EMT is associated with increased phosphorylation of Smad3, Akt and ERK proteins. Conversely, inhibition of TGF-β receptors or ERK activities reverses ADAM12L-induced mesenchymal phenotype. Together our data demonstrate that ADAM12L is associated with EMT and contributes to TGF-β-dependent EMT by favoring both Smad-dependent and Smad-independent pathways.
    Mesh-Begriff(e) ADAM Proteins/metabolism ; ADAM12 Protein ; Adult ; Aged ; Aged, 80 and over ; Biocatalysis/drug effects ; Biomarkers, Tumor/metabolism ; Breast Neoplasms/genetics ; Cell Line, Tumor ; Cytoplasm/metabolism ; Drug Resistance, Neoplasm/drug effects ; Drug Resistance, Neoplasm/genetics ; Epithelial Cells/drug effects ; Epithelial Cells/metabolism ; Epithelial-Mesenchymal Transition/drug effects ; Female ; Humans ; MAP Kinase Signaling System/drug effects ; Membrane Proteins/metabolism ; Mesoderm/metabolism ; Middle Aged ; Phenotype ; Receptors, Transforming Growth Factor beta/metabolism ; Signal Transduction/drug effects ; Signal Transduction/genetics ; Transforming Growth Factor beta/pharmacology
    Chemische Substanzen Biomarkers, Tumor ; Membrane Proteins ; Receptors, Transforming Growth Factor beta ; Transforming Growth Factor beta ; ADAM Proteins (EC 3.4.24.-) ; ADAM12 Protein (EC 3.4.24.-) ; ADAM12 protein, human (EC 3.4.24.-)
    Sprache Englisch
    Erscheinungsdatum 2015
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0139179
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel: Sibiriline, a new small chemical inhibitor of receptor‐interacting protein kinase 1, prevents immune‐dependent hepatitis

    Le Cann, Fabienne / Arnaud Comte / Aveline Filliol / Blandine Baratte / Claire Delehouzé / Claire Piquet‐Pellorce / Florence Faurez / Isabelle Gallais / Marie‐Thérèse Dimanche‐Boitrel / Marion Bonnet / Michel Samson / Nathalie Desban / Olivier Delalande / Peter Goekjian / Peter Vandenabeele / Sabrina Leverrier‐Penna / Stéphane Bach / Yvette Mettey

    FEBS journal. 2017 Sept., v. 284, no. 18

    2017  

    Abstract: Necroptosis is a regulated form of cell death involved in several disease models including in particular liver diseases. Receptor‐interacting protein kinases, RIPK1 and RIPK3, are the main serine/threonine kinases driving this cell death pathway. We ... ...

    Abstract Necroptosis is a regulated form of cell death involved in several disease models including in particular liver diseases. Receptor‐interacting protein kinases, RIPK1 and RIPK3, are the main serine/threonine kinases driving this cell death pathway. We screened a noncommercial, kinase‐focused chemical library which allowed us to identify Sibiriline as a new inhibitor of necroptosis induced by tumor necrosis factor (TNF) in Fas‐associated protein with death domain (FADD)‐deficient Jurkat cells. Moreover, Sib inhibits necroptotic cell death induced by various death ligands in human or mouse cells while not protecting from caspase‐dependent apoptosis. By using competition binding assay and recombinant kinase assays, we demonstrated that Sib is a rather specific competitive RIPK1 inhibitor. Molecular docking analysis shows that Sib is trapped closed to human RIPK1 adenosine triphosphate‐binding site in a relatively hydrophobic pocket locking RIPK1 in an inactive conformation. In agreement with its RIPK1 inhibitory property, Sib inhibits both TNF‐induced RIPK1‐dependent necroptosis and RIPK1‐dependent apoptosis. Finally, Sib protects mice from concanavalin A‐induced hepatitis. These results reveal the small‐molecule Sib as a new RIPK1 inhibitor potentially of interest for the treatment of immune‐dependent hepatitis.
    Schlagwörter apoptosis ; disease models ; hepatitis ; humans ; hydrophobicity ; ligands ; mice ; molecular models ; necroptosis ; protein-serine-threonine kinases ; tumor necrosis factors
    Sprache Englisch
    Erscheinungsverlauf 2017-09
    Umfang p. 3050-3068.
    Erscheinungsort John Wiley & Sons, Ltd
    Dokumenttyp Artikel
    Anmerkung JOURNAL ARTICLE
    ZDB-ID 2173655-8
    ISSN 1742-4658 ; 1742-464X
    ISSN (online) 1742-4658
    ISSN 1742-464X
    DOI 10.1111/febs.14176
    Datenquelle NAL Katalog (AGRICOLA)

    Volltext online

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    Verfügbar in ZB MED Bonn

    Z 2006/704: Hefte anzeigen

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