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28 results on '"Cayrou, Christelle"'

1. mTert induction in p21-positive cells counteracts capillary rarefaction and pulmonary emphysema

Author

Lipskaia, Larissa, Breau, Marielle, Cayrou, Christelle, Churikov, Dmitri, Braud, Laura, Jacquet, Juliette, Born, Emmanuelle, Fouillade, Charles, Curras-Alonso, Sandra, Bauwens, Serge, Jourquin, Frederic, Fiore, Frederic, Castellano, Rémy, Josselin, Emmanuelle, Sánchez-Ferrer, Carlota, Giovinazzo, Giovanna, Lachaud, Christophe, Gilson, Eric, Flores, Ignacio, Londono-Vallejo, Arturo, Adnot, Serge, and Géli, Vincent

Published
2024
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6. Modeling Heterogeneity of Triple‐Negative Breast Cancer Uncovers a Novel Combinatorial Treatment Overcoming Primary Drug Resistance

Author

Lamballe, Fabienne, primary, Ahmad, Fahmida, additional, Vinik, Yaron, additional, Castellanet, Olivier, additional, Daian, Fabrice, additional, Müller, Anna‐Katharina, additional, Köhler, Ulrike A., additional, Bailly, Anne‐Laure, additional, Josselin, Emmanuelle, additional, Castellano, Rémy, additional, Cayrou, Christelle, additional, Charafe‐Jauffret, Emmanuelle, additional, Mills, Gordon B., additional, Géli, Vincent, additional, Borg, Jean‐Paul, additional, Lev, Sima, additional, and Maina, Flavio, additional

Published
2020
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7. ING2 PHD domain links histone H3 lysine 4 methylation to active gene repression

Author

Shi, Xiaobing, Hong, Tao, Walter, Kay L., Ewalt, Mark, Michishita, Eriko, Hung, Tiffany, Carney, Dylan, Peña, Pedro, Lan, Fei, Kaadige, Mohan R., Lacoste, Nicolas, Cayrou, Christelle, Davrazou, Foteini, Saha, Anjanabha, Cairns, Bradley R., Ayer, Donald E., Kutateladze, Tatiana G., Shi, Yang, Côté, Jacques, Chua, Katrin F., and Gozani, Or

Published
2006

9. Modeling Heterogeneity of Triple‐Negative Breast Cancer Uncovers a Novel Combinatorial Treatment Overcoming Primary Drug Resistance.

Author

Lamballe, Fabienne, Ahmad, Fahmida, Vinik, Yaron, Castellanet, Olivier, Daian, Fabrice, Müller, Anna‐Katharina, Köhler, Ulrike A., Bailly, Anne‐Laure, Josselin, Emmanuelle, Castellano, Rémy, Cayrou, Christelle, Charafe‐Jauffret, Emmanuelle, Mills, Gordon B., Géli, Vincent, Borg, Jean‐Paul, Lev, Sima, and Maina, Flavio

Subjects
TRIPLE-negative breast cancer, DRUG resistance, MET receptor, HETEROGENEITY, BREAST cancer
Abstract

Triple‐negative breast cancer (TNBC) is a highly aggressive breast cancer subtype characterized by a remarkable molecular heterogeneity. Currently, there are no effective druggable targets and advanced preclinical models of the human disease. Here, a unique mouse model (MMTV‐R26Met mice) of mammary tumors driven by a subtle increase in the expression of the wild‐type MET receptor is generated. MMTV‐R26Met mice develop spontaneous, exclusive TNBC tumors, recapitulating primary resistance to treatment of patients. Proteomic profiling of MMTV‐R26Met tumors and machine learning approach show that the model faithfully recapitulates intertumoral heterogeneity of human TNBC. Further signaling network analysis highlights potential druggable targets, of which cotargeting of WEE1 and BCL‐XL synergistically kills TNBC cells and efficiently induces tumor regression. Mechanistically, BCL‐XL inhibition exacerbates the dependency of TNBC cells on WEE1 function, leading to Histone H3 and phosphoS33RPA32 upregulation, RRM2 downregulation, cell cycle perturbation, mitotic catastrophe, and apoptosis. This study introduces a unique, powerful mouse model for studying TNBC formation and evolution, its heterogeneity, and for identifying efficient therapeutic targets. [ABSTRACT FROM AUTHOR]

Published
2021
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10. Histone H4K20 tri‐methylation at late‐firing origins ensures timely heterochromatin replication

Author

Brustel, Julien, primary, Kirstein, Nina, additional, Izard, Fanny, additional, Grimaud, Charlotte, additional, Prorok, Paulina, additional, Cayrou, Christelle, additional, Schotta, Gunnar, additional, Abdelsamie, Alhassan F, additional, Déjardin, Jérôme, additional, Méchali, Marcel, additional, Baldacci, Giuseppe, additional, Sardet, Claude, additional, Cadoret, Jean‐Charles, additional, Schepers, Aloys, additional, and Julien, Eric, additional

Published
2017
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13. Conserved Molecular Interactions within the HBO1 Acetyltransferase Complexes Regulate Cell Proliferation

Author

Avvakumov, Nikita, primary, Lalonde, Marie-Eve, additional, Saksouk, Nehmé, additional, Paquet, Eric, additional, Glass, Karen C., additional, Landry, Anne-Julie, additional, Doyon, Yannick, additional, Cayrou, Christelle, additional, Robitaille, Geneviève A., additional, Richard, Darren E., additional, Yang, Xiang-Jiao, additional, Kutateladze, Tatiana G., additional, and Côté, Jacques, additional

Published
2012
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14. Genome-scale analysis of metazoan replication origins reveals their organization in specific but flexible sites defined by conserved features

Author

Cayrou, Christelle, primary, Coulombe, Philippe, additional, Vigneron, Alice, additional, Stanojcic, Slavica, additional, Ganier, Olivier, additional, Peiffer, Isabelle, additional, Rivals, Eric, additional, Puy, Aurore, additional, Laurent-Chabalier, Sabine, additional, Desprat, Romain, additional, and Méchali, Marcel, additional

Published
2011
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15. MOF and Histone H4 Acetylation at Lysine 16 Are Critical for DNA Damage Response and Double-Strand Break Repair

Author

Sharma, Girdhar G., primary, So, Sairei, additional, Gupta, Arun, additional, Kumar, Rakesh, additional, Cayrou, Christelle, additional, Avvakumov, Nikita, additional, Bhadra, Utpal, additional, Pandita, Raj K., additional, Porteus, Matthew H., additional, Chen, David J., additional, Cote, Jacques, additional, and Pandita, Tej K., additional

Published
2010
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16. HBO1 HAT Complexes Target Chromatin throughout Gene Coding Regions via Multiple PHD Finger Interactions with Histone H3 Tail

Author

Saksouk, Nehmé, primary, Avvakumov, Nikita, additional, Champagne, Karen S., additional, Hung, Tiffany, additional, Doyon, Yannick, additional, Cayrou, Christelle, additional, Paquet, Eric, additional, Ullah, Mukta, additional, Landry, Anne-Julie, additional, Côté, Valérie, additional, Yang, Xiang-Jiao, additional, Gozani, Or, additional, Kutateladze, Tatiana G., additional, and Côté, Jacques, additional

Published
2009
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17. Molecular Architecture of Quartet MOZ/MORF Histone Acetyltransferase Complexes

Author

Ullah, Mukta, primary, Pelletier, Nadine, additional, Xiao, Lin, additional, Zhao, Song Ping, additional, Wang, Kainan, additional, Degerny, Cindy, additional, Tahmasebi, Soroush, additional, Cayrou, Christelle, additional, Doyon, Yannick, additional, Goh, Siew-Lee, additional, Champagne, Nathalie, additional, Côté, Jacques, additional, and Yang, Xiang-Jiao, additional

Published
2008
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23. ING2 PHD domain links histone H3 lysine 4 methylation to active gene repression.

Author

Xiaobing Shi, Tao Hong, Walter, Kay L., Ewalt, Mark, Michishita, Eriko, Hung, Tiffany, Carney, Dylan, Peña, Pedro, Fei Lan, Kaadige, Mohan R., Lacoste, Nicolas, Cayrou, Christelle, Davrazou, Foteini, Saha, Anjanabha, Cairns, Bradley R., Ayer, Donald E., Kutateladze, Tatiana G., Yang Shi, Côté, Jacques, and Chua, Katrin F.

Subjects
CHROMATIN, METHYLATION, LYSINE, GENETIC regulation, HISTONE deacetylase, TUMOR suppressor genes, GENE expression
Abstract

Dynamic regulation of diverse nuclear processes is intimately linked to covalent modifications of chromatin. Much attention has focused on methylation at lysine 4 of histone H3 (H3K4), owing to its association with euchromatic genomic regions. H3K4 can be mono-, di- or tri-methylated. Trimethylated H3K4 (H3K4me3) is preferentially detected at active genes, and is proposed to promote gene expression through recognition by transcription-activating effector molecules. Here we identify a novel class of methylated H3K4 effector domains—the PHD domains of the ING (for inhibitor of growth) family of tumour suppressor proteins. The ING PHD domains are specific and highly robust binding modules for H3K4me3 and H3K4me2. ING2, a native subunit of a repressive mSin3a–HDAC1 histone deacetylase complex, binds with high affinity to the trimethylated species. In response to DNA damage, recognition of H3K4me3 by the ING2 PHD domain stabilizes the mSin3a–HDAC1 complex at the promoters of proliferation genes. This pathway constitutes a new mechanism by which H3K4me3 functions in active gene repression. Furthermore, ING2 modulates cellular responses to genotoxic insults, and these functions are critically dependent on ING2 interaction with H3K4me3. Together, our findings establish a pivotal role for trimethylation of H3K4 in gene repression and, potentially, tumour suppressor mechanisms. [ABSTRACT FROM AUTHOR]

Published
2006
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24. Conserved Molecular Interactions within the HBO1 Acetyltransferase Complexes Regulate Cell Proliferation.

Author

Awakumov, Nikita, Lalonde, Marie-Eve, Saksouk, Nehmé, Paquet, Eric, Glass, Karen C., Landry, Anne-Julie, Doyon, Yannick, Cayrou, Christelle, Robitaille, Geneviève A., Richard, Darren E., Yang, Xiang-Jiao, Kutateladze, Tatiana G., and Côté, Jacques

Subjects
ACETYLTRANSFERASES, CELLULAR control mechanisms, CELL proliferation, TUMOR suppressor proteins, DNA replication
Abstract

Acetyltransferase complexes of the MYST family with distinct substrate specificities and functions maintain a conserved association with different ING tumor suppressor proteins. ING complexes containing the HBO1 acetylase are a major source of histone H3 and H4 acetylation in vivo and play critical roles in gene regulation and DNA replication. Here, our molecular dissection of HBO1/ING complexes unravels the protein domains required for their assembly and function. Multiple PHD finger domains present in different subunits bind the histone H3 N-terminal tail with a distinct specificity toward lysine 4 methylation status. We show that natively regulated association of the ING4/5 PHD domain with HBO1-JADE determines the growth inhibitory function of the complex, linked to its tumor suppressor activity. Functional genomic analyses indicate that the p53 pathway is a main target of the complex, at least in part through direct transcription regulation at the initiation site of p21/CDKN1A. These results demonstrate the importance of ING association with MYST acetyltransferases in controlling cell proliferation, a regulated link that accounts for the reported tumor suppressor activities of these complexes. [ABSTRACT FROM AUTHOR]

Published
2012

25. ERRATUM: A Human Protein Complex Homologous to the Drosophila MSL Complex Is Responsible for the Majority of Histone H4 Acetylation at Lysine 16.

Author

Smith, Edwin R., Cayrou, Christelle, Rong Huang, Lane, William S., Côté, Jacques, and Lucchesi, John C.

Subjects
*DROSOPHILA
Abstract

A correction to the article "A Human Protein Complex Homologous to the Drosophila MSL Complex is Responsible for the Majority of Histone H4 Acetylation at Lysine 16" that was published in the January 2006 issue is presented.

Published
2006
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26. Telomerase Prevents Emphysema in Old Mice by Sustaining Subpopulations of Endothelial and AT2 Cells

Author

Marielle Breau, Christelle Cayrou, Dmitri Churikov, Charles Fouillade, Sandra Curras-Alonso, Serge Bauwens, Frederic Jourquin, Laura Braud, Frederic Fiore, Rémy Castellano, Emmanuelle Josselin, Carlota Sánchez-Ferrer, Giovanna Giovinazzo, Eric Gilson, Ignacio Flores, Arturo Londono-Vallejo, Serge Adnot, Vincent Géli, Centre de Recherche en Cancérologie de Marseille (CRCM), Aix Marseille Université (AMU)-Institut Paoli-Calmettes, Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut Curie [Paris], Institut de Recherche sur le Cancer et le Vieillissement (IRCAN), Université Nice Sophia Antipolis (1965 - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Côte d'Azur (UCA), Centre d'Immunophénomique (CIPHE), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centre de neurosciences intégratives et cognitives (CNIC), Université Bordeaux Segalen - Bordeaux 2-Université Sciences et Technologies - Bordeaux 1 (UB)-Centre National de la Recherche Scientifique (CNRS), Université Côte d'Azur (UCA), Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Paoli-Calmettes, Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Aix Marseille Université (AMU), Université Nice Sophia Antipolis (... - 2019) (UNS), Université Bordeaux Segalen - Bordeaux 2-Université Sciences et Technologies - Bordeaux 1-Centre National de la Recherche Scientifique (CNRS), and CAYROU, CHRISTELLE

Subjects
0303 health sciences, telomere, [SDV.BIBS] Life Sciences [q-bio]/Quantitative Methods [q-bio.QM], senescence, aging, [SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC], respiratory system, [SDV.BIBS]Life Sciences [q-bio]/Quantitative Methods [q-bio.QM], lung, stem cell, 03 medical and health sciences, 0302 clinical medicine, emphysema, [SDV.BC.BC] Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC], Telomerase, 030217 neurology & neurosurgery, 030304 developmental biology
Abstract

Accumulation of senescent cells has been causally linked to the development of age-related pathologies. Here, we characterized a new mouse model (p21+/Tert) whose telomerase (TERT) is expressed from the p21 promoter that can be activated in response to telomere dysfunction. Lung parenchyma from p21+/Tert old mice accumulated fewer senescent cells with age and this correlated with a reduction in age-related alveolar space enlargement, a feature of pulmonary emphysema. This protection against emphysema depends on TERT catalytic activity and is associated with increased proliferation of pulmonary endothelial cells (EC) and capillary density. Single-cell RNA sequencing of lung cells revealed that TERT expression was associated with the enrichment of ECs expressing genes involved in vessel regeneration and in AT2 cells overexpressing S/G2M markers. These findings indicate that p21-promoter-dependent expression of catalytically active telomerase prevents emphysema by sustaining the proliferation of subclasses of EC and AT2 cells.

Published
2022

27. Modeling Heterogeneity of Triple‐Negative Breast Cancer Uncovers a Novel Combinatorial Treatment Overcoming Primary Drug Resistance

Author

Ulrike A. Köhler, Vincent Géli, Fahmida Ahmad, Fabrice Daian, Emmanuelle Josselin, Rémy Castellano, Sima Lev, Gordon B. Mills, Anna Katharina Müller, Christelle Cayrou, Olivier Castellanet, Jean-Paul Borg, Fabienne Lamballe, Yaron Vinik, Emmanuelle Charafe-Jauffret, Anne-Laure Bailly, Flavio Maina, Institut de Biologie du Développement de Marseille (IBDM), Aix Marseille Université (AMU)-Collège de France (CdF (institution))-Centre National de la Recherche Scientifique (CNRS), Weizmann Institute of Science [Rehovot, Israël], Centre de Recherche en Cancérologie de Marseille (CRCM), Aix Marseille Université (AMU)-Institut Paoli-Calmettes, Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Knight Cancer Institute, ANR-10-INBS-0004,France-BioImaging,Développment d'une infrastructure française distribuée coordonnée(2010), Poulain, Sébastien, Développment d'une infrastructure française distribuée coordonnée - - France-BioImaging2010 - ANR-10-INBS-0004 - INBS - VALID, Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Paoli-Calmettes, Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Aix Marseille Université (AMU), and CAYROU, CHRISTELLE

Subjects
BCL‐XL, General Chemical Engineering, [SDV]Life Sciences [q-bio], Druggability, General Physics and Astronomy, Medicine (miscellaneous), Bcl-xL, [SDV.CAN]Life Sciences [q-bio]/Cancer, 02 engineering and technology, 010402 general chemistry, 01 natural sciences, Biochemistry, Genetics and Molecular Biology (miscellaneous), 03 medical and health sciences, Histone H3, 0302 clinical medicine, Breast cancer, [SDV.CAN] Life Sciences [q-bio]/Cancer, Downregulation and upregulation, medicine, General Materials Science, WEE1, lcsh:Science, Mitotic catastrophe, Triple-negative breast cancer, 030304 developmental biology, 0303 health sciences, drug resistance, Full Paper, biology, General Engineering, Full Papers, 021001 nanoscience & nanotechnology, medicine.disease, 0104 chemical sciences, 3. Good health, [SDV] Life Sciences [q-bio], Wee1, signaling reprogramming, triple‐negative breast cancer, Apoptosis, 030220 oncology & carcinogenesis, cancer mouse model, biology.protein, Cancer research, MET, lcsh:Q, 0210 nano-technology
Abstract

Triple‐negative breast cancer (TNBC) is a highly aggressive breast cancer subtype characterized by a remarkable molecular heterogeneity. Currently, there are no effective druggable targets and advanced preclinical models of the human disease. Here, a unique mouse model (MMTV‐R26Met mice) of mammary tumors driven by a subtle increase in the expression of the wild‐type MET receptor is generated. MMTV‐R26Met mice develop spontaneous, exclusive TNBC tumors, recapitulating primary resistance to treatment of patients. Proteomic profiling of MMTV‐R26Met tumors and machine learning approach show that the model faithfully recapitulates intertumoral heterogeneity of human TNBC. Further signaling network analysis highlights potential druggable targets, of which cotargeting of WEE1 and BCL‐XL synergistically kills TNBC cells and efficiently induces tumor regression. Mechanistically, BCL‐XL inhibition exacerbates the dependency of TNBC cells on WEE1 function, leading to Histone H3 and phosphoS33RPA32 upregulation, RRM2 downregulation, cell cycle perturbation, mitotic catastrophe, and apoptosis. This study introduces a unique, powerful mouse model for studying TNBC formation and evolution, its heterogeneity, and for identifying efficient therapeutic targets., Triple‐negative breast cancer (TNBC) is highly aggressive and currently lacks effective treatment. This study reports the generation of a unique mouse model developing spontaneous, exclusive TNBC, recapitulating heterogeneity and primary resistance to treatments. Its clinical relevance is further strengthened by the identification of a potent drug combination for TNBC treatment, based on WEE1 and BCL‐XL targeting.

Published
2020

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