Search

Your search keyword '"Remouchamps, Caroline"' showing total 16 results
Start Over Author "Remouchamps, Caroline"
16 results on '"Remouchamps, Caroline"'

1. Control of APOBEC3B induction and cccDNA decay by NF-κB and miR-138-5p

Author

Faure-Dupuy, Suzanne, Riedl, Tobias, Rolland, Maude, Hizir, Zoheir, Reisinger, Florian, Neuhaus, Katharina, Schuehle, Svenja, Remouchamps, Caroline, Gillet, Nicolas, Schönung, Maximilian, Stadler, Mira, Wettengel, Jochen, Barnault, Romain, Parent, Romain, Schuster, Linda Christina, Farhat, Rayan, Prokosch, Sandra, Leuchtenberger, Corinna, Öllinger, Rupert, Engleitner, Thomas, Rippe, Karsten, Rad, Roland, Unger, Kristian, Tscharahganeh, Darjus, Lipka, Daniel B., Protzer, Ulrike, Durantel, David, Lucifora, Julie, Dejardin, Emmanuel, and Heikenwälder, Mathias

Published
2021
Full Text
View/download PDF

2. A Dual Role of Caspase-8 in Triggering and Sensing Proliferation-Associated DNA Damage, a Key Determinant of Liver Cancer Development

Author

Boege, Yannick, Malehmir, Mohsen, Healy, Marc E., Bettermann, Kira, Lorentzen, Anna, Vucur, Mihael, Ahuja, Akshay K., Böhm, Friederike, Mertens, Joachim C., Shimizu, Yutaka, Frick, Lukas, Remouchamps, Caroline, Mutreja, Karun, Kähne, Thilo, Sundaravinayagam, Devakumar, Wolf, Monika J., Rehrauer, Hubert, Koppe, Christiane, Speicher, Tobias, Padrissa-Altés, Susagna, Maire, Renaud, Schattenberg, Jörn M., Jeong, Ju-Seong, Liu, Lei, Zwirner, Stefan, Boger, Regina, Hüser, Norbert, Davis, Roger J., Müllhaupt, Beat, Moch, Holger, Schulze-Bergkamen, Henning, Clavien, Pierre-Alain, Werner, Sabine, Borsig, Lubor, Luther, Sanjiv A., Jost, Philipp J., Weinlich, Ricardo, Unger, Kristian, Behrens, Axel, Hillert, Laura, Dillon, Christopher, Di Virgilio, Michela, Wallach, David, Dejardin, Emmanuel, Zender, Lars, Naumann, Michael, Walczak, Henning, Green, Douglas R., Lopes, Massimo, Lavrik, Inna, Luedde, Tom, Heikenwalder, Mathias, and Weber, Achim

Published
2017
Full Text
View/download PDF

3. Specific and Nonhepatotoxic Degradation of Nuclear Hepatitis B Virus cccDNA

Author

Lucifora, Julie, Xia, Yuchen, Reisinger, Florian, Zhang, Ke, Stadler, Daniela, Cheng, Xiaoming, Sprinzl, Martin F., Koppensteiner, Herwig, Makowska, Zuzanna, Volz, Tassilo, Remouchamps, Caroline, Chou, Wen-Min, Thasler, Wolfgang E., Hüser, Norbert, Durantel, David, Liang, T. Jake, Münk, Carsten, Heim, Markus H., Browning, Jeffrey L., Dejardin, Emmanuel, Dandri, Maura, Schindler, Michael, Heikenwalder, Mathias, and Protzer, Ulrike

Published
2014

10. NF-κB inducing kinase (NIK) inhibitors: Identification of new scaffolds using virtual screening

Author

UCL - SSS/LDRI - Louvain Drug Research Institute, Mortier, Jérémie, Masereel, Bernard, Remouchamps, Caroline, Ganeff, Corinne, Piette, Jacques, Frédérick, Raphaël, UCL - SSS/LDRI - Louvain Drug Research Institute, Mortier, Jérémie, Masereel, Bernard, Remouchamps, Caroline, Ganeff, Corinne, Piette, Jacques, and Frédérick, Raphaël

Abstract

As a wide variety of pro-inflammatory cytokines are involved in the development of rheumatoid arthritis (RA), there is an urgent need for the discovery of novel therapeutic strategies. Among these, the inhibition of the NF-κB inducing kinase (NIK), a key enzyme of the NF-κB alternative pathway activation, represents a potential interesting approach. In fact, NIK is involved downstream of many tumor necrosis factor receptors (TNFR) like CD40, RANK or LTβR, implicated in the pathogenesis of RA. But, up to now, the number of reported putative NIK inhibitors is extremely limited. In this work, we report a virtual screening (VS) study combining various filters including high-throughput docking using a 3D-homology model and ranking by using different scoring functions. This work led to the identification of two molecular fragments, 4H-isoquinoline-1,3-dione (5) and 2,7-naphthydrine-1,3,6,8-tetrone (6) which inhibit NIK with an IC50 value of 51 and 90 μM, respectively. This study opens new perspectives in the field of the NF-κB alternative pathway inhibition. © 2010 Elsevier Ltd. All rights reserved.

Published
2010

11. Induction of the Alternative NF-κB Pathway by Lymphotoxin αβ (LTαβ) Relies on Internalization of LTβ Receptor

Author

Ganeff, Corinne, primary, Remouchamps, Caroline, additional, Boutaffala, Layla, additional, Benezech, Cécile, additional, Galopin, Géraldine, additional, Vandepaer, Sarah, additional, Bouillenne, Fabrice, additional, Ormenese, Sandra, additional, Chariot, Alain, additional, Schneider, Pascal, additional, Caamaño, Jorge, additional, Piette, Jacques, additional, and Dejardin, Emmanuel, additional

Published
2011
Full Text
View/download PDF

12. A dual role of caspase-8 in triggering and sensing proliferation-associated DNA damage, a key determinant of liver cancer development

Author

Boege, Yannick, Malehmir, Mohsen, Healy, Marc E, Bettermann, Kira, Lorentzen, Anna, Vucur, Mihael, Ahuja, Akshay K, Böhm, Friederike, Mertens, Joachim C, Shimizu, Yutaka, Frick, Lukas, Remouchamps, Caroline, Mutreja, Karun, Kähne, Thilo, Sundaravinayagam, Devakumar, Wolf, Monika J, Rehrauer, Hubert, Koppe, Christiane, Speicher, Tobias, Padrissa-Altés, Susagna, Maire, Renaud, Schattenberg, Jörn M, Jeong, Ju-Seong, Liu, Lei, Zwirner, Stefan, Boger, Regina, Hüser, Norbert, Davis, Roger J, Müllhaupt, Beat, Moch, Holger, Schulze-Bergkamen, Henning, Clavien, Pierre-Alain, Werner, Sabine, Borsig, Lubor, Luther, Sanjiv A, Jost, Philipp J, Weinlich, Ricardo, Unger, Kristian, Behrens, Axel, Hillert, Laura, Dillon, Christopher, Di Virgilio, Michela, Wallach, David, Dejardin, Emmanuel, Zender, Lars, Naumann, Michael, Walczak, Henning, Green, Douglas R, Lopes, Massimo, Lavrik, Inna, Luedde, Tom, Heikenwalder, Mathias, and Weber, Achim

Subjects
Model organisms, Stem Cells, Genome Integrity & Repair, Gene Expression, Tumour Biology, Genetics & Genomics, 3. Good health
Abstract

Concomitant hepatocyte apoptosis and regeneration is a hallmark of chronic liver diseases (CLDs) predisposing to hepatocellular carcinoma (HCC). Here, we mechanistically link caspase-8-dependent apoptosis to HCC development via proliferation- and replication-associated DNA damage. Proliferation-associated replication stress, DNA damage, and genetic instability are detectable in CLDs before any neoplastic changes occur. Accumulated levels of hepatocyte apoptosis determine and predict subsequent hepatocarcinogenesis. Proliferation-associated DNA damage is sensed by a complex comprising caspase-8, FADD, c-FLIP, and a kinase-dependent function of RIPK1. This platform requires a non-apoptotic function of caspase-8, but no caspase-3 or caspase-8 cleavage. It may represent a DNA damage-sensing mechanism in hepatocytes that can act via JNK and subsequent phosphorylation of the histone variant H2AX.

13. A Dual Role of Caspase-8 in Triggering and Sensing Proliferation-Associated DNA Damage, a Key Determinant of Liver Cancer Development

Author

Boege, Yannick, Malehmir, Mohsen, Healy, Marc E., Bettermann, Kira, Lorentzen, Anna, Vucur, Mihael, Ahuja, Akshay K., Böhm, Friederike, Mertens, Joachim C., Shimizu, Yutaka, Frick, Lukas, Remouchamps, Caroline, Mutreja, Karun, Kähne, Thilo, Sundaravinayagam, Devakumar, Wolf, Monika J., Rehrauer, Hubert, Koppe, Christiane, Speicher, Tobias, Padrissa-Altés, Susagna, Maire, Renaud, Schattenberg, Jörn M., Jeong, Ju-Seong, Liu, Lei, Zwirner, Stefan, Boger, Regina, Hüser, Norbert, Davis, Roger J., Müllhaupt, Beat, Moch, Holger, Schulze-Bergkamen, Henning, Clavien, Pierre-Alain, Werner, Sabine, Borsig, Lubor, Luther, Sanjiv A., Jost, Philipp J., Weinlich, Ricardo, Unger, Kristian, Behrens, Axel, Hillert, Laura, Dillon, Christopher, Di Virgilio, Michela, Wallach, David, Dejardin, Emmanuel, Zender, Lars, Naumann, Michael, Walczak, Henning, Green, Douglas R., Lopes, Massimo, Lavrik, Inna, Luedde, Tom, Heikenwalder, Mathias, and Weber, Achim

Subjects
3. Good health
Abstract

Cancer cell 32(3), 342-359.e10 (2017). doi:10.1016/j.ccell.2017.08.010, Published by Cell Press, Cambridge, Mass.

14. A dual role of caspase-8 in triggering and sensing proliferation-associated DNA damage, a key determinant of liver cancer development

Author

Boege, Yannick, Malehmir, Mohsen, Healy, Marc E, Bettermann, Kira, Lorentzen, Anna, Vucur, Mihael, Ahuja, Akshay K, Böhm, Friederike, Mertens, Joachim C, Shimizu, Yutaka, Frick, Lukas, Remouchamps, Caroline, Mutreja, Karun, Kähne, Thilo, Sundaravinayagam, Devakumar, Wolf, Monika J, Rehrauer, Hubert, Koppe, Christiane, Speicher, Tobias, Padrissa-Altés, Susagna, Maire, Renaud, Schattenberg, Jörn M, Jeong, Ju-Seong, Liu, Lei, Zwirner, Stefan, Boger, Regina, Hüser, Norbert, Davis, Roger J, Müllhaupt, Beat, Moch, Holger, Schulze-Bergkamen, Henning, Clavien, Pierre-Alain, Werner, Sabine, Borsig, Lubor, Luther, Sanjiv A, Jost, Philipp J, Weinlich, Ricardo, Unger, Kristian, Behrens, Axel, Hillert, Laura, Dillon, Christopher, Di Virgilio, Michela, Wallach, David, Dejardin, Emmanuel, Zender, Lars, Naumann, Michael, Walczak, Henning, Green, Douglas R, Lopes, Massimo, Lavrik, Inna, Luedde, Tom, Heikenwalder, Mathias, and Weber, Achim

Subjects
Model organisms, Stem Cells, Genome Integrity & Repair, Gene Expression, Tumour Biology, Genetics & Genomics, 3. Good health
Abstract

Concomitant hepatocyte apoptosis and regeneration is a hallmark of chronic liver diseases (CLDs) predisposing to hepatocellular carcinoma (HCC). Here, we mechanistically link caspase-8-dependent apoptosis to HCC development via proliferation- and replication-associated DNA damage. Proliferation-associated replication stress, DNA damage, and genetic instability are detectable in CLDs before any neoplastic changes occur. Accumulated levels of hepatocyte apoptosis determine and predict subsequent hepatocarcinogenesis. Proliferation-associated DNA damage is sensed by a complex comprising caspase-8, FADD, c-FLIP, and a kinase-dependent function of RIPK1. This platform requires a non-apoptotic function of caspase-8, but no caspase-3 or caspase-8 cleavage. It may represent a DNA damage-sensing mechanism in hepatocytes that can act via JNK and subsequent phosphorylation of the histone variant H2AX.

15. A Dual Role of Caspase-8 in Triggering and Sensing Proliferation-Associated DNA Damage, a Key Determinant of Liver Cancer Development

Author

Boege, Yannick, Malehmir, Mohsen, Healy, Marc E., Bettermann, Kira, Lorentzen, Anna, Vucur, Mihael, Ahuja, Akshay K., Böhm, Friederike, Mertens, Joachim C., Shimizu, Yutaka, Frick, Lukas, Remouchamps, Caroline, Mutreja, Karun, Kähne, Thilo, Sundaravinayagam, Devakumar, Wolf, Monika J., Rehrauer, Hubert, Koppe, Christiane, Speicher, Tobias, Padrissa-Altés, Susagna, Maire, Renaud, Schattenberg, Jörn M., Jeong, Ju-Seong, Liu, Lei, Zwirner, Stefan, Boger, Regina, Hüser, Norbert, Davis, Roger J., Müllhaupt, Beat, Moch, Holger, Schulze-Bergkamen, Henning, Clavien, Pierre-Alain, Werner, Sabine, Borsig, Lubor, Luther, Sanjiv A., Jost, Philipp J., Weinlich, Ricardo, Unger, Kristian, Behrens, Axel, Hillert, Laura, Dillon, Christopher, Di Virgilio, Michela, Wallach, David, Dejardin, Emmanuel, Zender, Lars, Naumann, Michael, Walczak, Henning, Green, Douglas R., Lopes, Massimo, Lavrik, Inna, Luedde, Tom, Heikenwalder, Mathias, and Weber, Achim

Subjects
Hepatocellular carcinoma, replication stress, apoptosis, liver, DNA damage response, 3. Good health
Abstract

Concomitant hepatocyte apoptosis and regeneration is a hallmark of chronic liver diseases (CLDs) predisposing to hepatocellular carcinoma (HCC). Here, we mechanistically link caspase-8-dependent apoptosis to HCC development via proliferation- and replication-associated DNA damage. Proliferation-associated replication stress, DNA damage, and genetic instability are detectable in CLDs before any neoplastic changes occur. Accumulated levels of hepatocyte apoptosis determine and predict subsequent hepatocarcinogenesis. Proliferation-associated DNA damage is sensed by a complex comprising caspase-8, FADD, c-FLIP, and a kinase-dependent function of RIPK1. This platform requires a non-apoptotic function of caspase-8, but no caspase-3 or caspase-8 cleavage. It may represent a DNA damage-sensing mechanism in hepatocytes that can act via JNK and subsequent phosphorylation of the histone variant H2AX., Cancer Cell, 32 (3), ISSN:1535-6108, ISSN:1878-3686

16. Methods to assess the activation of the alternative (noncanonical) NF-κB pathway by non-death TNF receptors.

Author

Remouchamps C and Dejardin E

Subjects
Antibodies, Monoclonal pharmacology, Electrophoretic Mobility Shift Assay, Enzyme Activation, Enzyme Stability, Humans, I-kappa B Kinase metabolism, Inhibitor of Apoptosis Proteins metabolism, Ligands, NF-kappa B p52 Subunit metabolism, Phosphorylation, Protein Binding, Protein Serine-Threonine Kinases metabolism, Protein Transport, Proteolysis, Receptors, Tumor Necrosis Factor agonists, TNF Receptor-Associated Factor 2 metabolism, TNF Receptor-Associated Factor 3 metabolism, Transcription Factor RelB metabolism, NF-kappaB-Inducing Kinase, NF-kappa B metabolism, Receptors, Tumor Necrosis Factor metabolism, Signal Transduction drug effects
Abstract

The alternative or noncanonical NF-κB pathway regulates the generation of p52-containing NF-κB dimers (e.g., p52/RelB) through a partial degradation (called processing) of the precursor p100 into p52. This pathway is activated by a subset of non-death TNF receptor members, which ultimately activate two kinases: NIK (NF-κB-Inducing Kinase) and IKKα (Inhibitor of κB Kinase alpha). These kinases create a phosphodegron for the E3 ligase SCF-β-TrCP that covalently binds K48-linked polyubiquitin chain onto p100 prior to its proteasomal processing. The resulting p52-containing complexes translocate into the nucleus to activate target genes involved in secondary lymphoid organ development, B cell survival or in osteoclastogenesis. We describe in this chapter straightforward methods to monitor the activation of the alternative NF-κB pathway. These methods uncover cytosolic and nuclear biochemical modifications of key proteins of the alternative NF-κB pathway required prior to the transcription of NF-κB target genes.

Published
2015
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results