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10 results on '"Bailly, Anne-Laure"'

1. Niche-expressed Galectin-1 is involved in pre-B acute lymphoblastic leukemia relapse through pre-B cell receptor activation

Author

Pelletier, Jeoffrey, Balzano, Marielle, Destin, Jérôme, Montersino, Camille, Delahaye, Marjorie C., Marchand, Tony, Bailly, Anne-Laure, Bardin, Florence, Coppin, Emilie, Goubard, Armelle, Castellano, Remy, de Bruijn, Marjolein J.W., Rip, Jasper, Collette, Yves, Dubreuil, Patrice, Tarte, Karin, Broccardo, Cyril, Hendriks, Rudi W., Schiff, Claudine, Vey, Norbert, Aurrand-Lions, Michel, and Mancini, Stéphane J.C.

Published
2023
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3. Comparison of pharmacokinetics and biodistribution of laser-synthesized plasmonic Au and TiN nanoparticles

Author

Popov, Anton A, primary, Zelepukin, Ivan V, additional, Tikhonowski, Gleb V, additional, Popova-Kuznecova, Elena A, additional, Tselikov, Gleb I, additional, Al-Kattan, Ahmed, additional, Bailly, Anne-Laure, additional, Correard, Florian, additional, Braguer, Diane, additional, Esteve, Marie-Anne, additional, Klimentov, Sergey M, additional, Deyev, Sergey M, additional, and Kabashin, Andrei V, additional

Published
2021
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4. 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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5. Abstract 5105: Unravelling the mystery of cancer-associated fibroblast populations in the tumor microenvironment by a fully automated sequential chromogenic multiplex assay

Author

Sbarrato, Thomas, primary, Filahi, Mounia, additional, Frayssinet, Véronique, additional, Bailly, Anne-Laure, additional, Laugé, Caroline, additional, Davin, Caroline, additional, Girardi, Hélène, additional, Martirosyan, Anna, additional, and Fieschi, jacques, additional

Published
2020
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6. Nidogen-1 Contributes to the Interaction Network Involved in Pro-B Cell Retention in the Peri-sinusoidal Hematopoietic Stem Cell Niche

Author

Balzano, Marielle, De Grandis, Maria, Vu Manh, Thien-Phong, Chasson, Lionel, Bardin, Florence, Farina, Anne, Sergé, Arnauld, Bidaut, Ghislain, Charbord, Pierre, Hérault, Léonard, Bailly, Anne-Laure, Cartier-Michaud, Amandine, Boned, Annie, Dalod, Marc, Duprez, Estelle, Genever, Paul, Coles, Mark, Bajenoff, Marc, Xerri, Luc, Aurrand-Lions, Michel, Schiff, Claudine, Mancini, Stéphane, Mancini, Stéphane J.C., 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), Centre d'Immunologie de Marseille - Luminy (CIML), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Aix Marseille Université (AMU), Génétique, immunothérapie, chimie et cancer (GICC), UMR 6239 CNRS [2008-2011] (GICC UMR 6239 CNRS), Université de Tours-Centre National de la Recherche Scientifique (CNRS), Informatique, Biologie Intégrative et Systèmes Complexes (IBISC), Université d'Évry-Val-d'Essonne (UEVE), University of York [York, UK], Institut de pharmacologie moléculaire et cellulaire (IPMC), Université Nice Sophia Antipolis (... - 2019) (UNS), Université Côte d'Azur (UCA)-Université Côte d'Azur (UCA)-Centre National de la Recherche Scientifique (CNRS), Département de Biopathologie, Institut Paoli-Calmettes, Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Fédération nationale des Centres de lutte contre le Cancer (FNCLCC), Laboratoire des images et des signaux (LIS), Centre National de la Recherche Scientifique (CNRS)-Institut National Polytechnique de Grenoble (INPG)-Université Joseph Fourier - Grenoble 1 (UJF), 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), Fédération nationale des Centres de lutte contre le Cancer (FNCLCC), Mi-mAbs (C/O CIML), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Aix Marseille Université (AMU), Laboratoire de Biologie du Développement [Paris] (LBD), Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Institut de Biologie Paris Seine (IBPS), Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut de Biologie Paris Seine (IBPS), Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Aix Marseille Université (AMU), Groupe innovation et ciblage cellulaire (GICC), EA 7501 [2018-...] (GICC EA 7501), Université de Tours, University of Oxford [Oxford], Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Biologie du Développement [IBPS] (LBD), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), CCSD, Accord Elsevier, and ANR-17-CE14-0019,OSTEOVALYMPH,Autocrinie et paracrinie de l'axe de signalisation CXCL12/CXCR4-CXCR7 dans la niche ostéo-vasculaire: impact sur la spécification et l'engagement lymphoïde des cellules souches hématopoïétiques(2017)

Subjects
[SDV.MHEP.HEM] Life Sciences [q-bio]/Human health and pathology/Hematology, bone marrow, interaction network, [SDV]Life Sciences [q-bio], [SDV.CAN]Life Sciences [q-bio]/Cancer, Mice, [SDV.CAN] Life Sciences [q-bio]/Cancer, [SDV.BC.IC]Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB], B cell development, Animals, Stem Cell Niche, lcsh:QH301-705.5, ComputingMilieux_MISCELLANEOUS, Mice, Knockout, [SDV.MHEP] Life Sciences [q-bio]/Human health and pathology, Membrane Glycoproteins, Interleukin-7, Precursor Cells, B-Lymphoid, stromal cell niche, [SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/Hematology, Hematopoietic Stem Cells, [SDV] Life Sciences [q-bio], [SDV.IMM.IA]Life Sciences [q-bio]/Immunology/Adaptive immunology, lcsh:Biology (General), hematopoietic stem cell, Stromal Cells, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract

Summary: In the bone marrow, CXCL12 and IL-7 are essential for B cell differentiation, whereas hematopoietic stem cell (HSC) maintenance requires SCF and CXCL12. Peri-sinusoidal stromal (PSS) cells are the main source of IL-7, but their characterization as a pro-B cell niche remains limited. Here, we characterize pro-B cell supporting stromal cells and decipher the interaction network allowing pro-B cell retention. Preferential contacts are found between pro-B cells and PSS cells, which homogeneously express HSC and B cell niche genes. Furthermore, pro-B cells are frequently located in the vicinity of HSCs in the same niche. Using an interactome bioinformatics pipeline, we identify Nidogen-1 as essential for pro-B cell retention in the peri-sinusoidal niche as confirmed in Nidogen-1−/− mice. Finally, human pro-B cells and hematopoietic progenitors are observed close to similar IL-7+ stromal cells. Thus, a multispecific niche exists in mouse and human supporting both early progenitors and committed hematopoietic lineages. : Balzano et al. show that bone marrow peri-sinusoidal stromal cells, which form the hematopoietic stem cell niche, also express B cell niche genes including IL-7 and Nidogen-1. Loss of Nidogen-1 expression specifically affects access of pro-B cells to IL-7, resulting in impaired expansion and differentiation of early B cells. Keywords: B cell development, hematopoietic stem cell, stromal cell niche, interaction network, bone marrow

Published
2019

7. 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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8. Genetic, structural, and chemical insights into the dual function of GRASP55 in germ cell Golgi remodeling and JAM-C polarized localization during spermatogenesis

Author

Cartier-Michaud, Amandine, Bailly, Anne-Laure, Betzi, Stéphane, Shi, Xiaoli, Lissitzky, Jean-Claude, Zarubica, Ana, Sergé, Arnauld, ROCHE, Philippe, Lugari, Adrien, HAMON, Véronique, Bardin, Florence, Derviaux, Carine, Lembo, Frédérique, Audebert, Stéphane, Marchetto, Sylvie, Durand, Bénédicte, Borg, Jean-Paul, Shi, Ning, Morelli, Xavier, Aurrand-Lions, Michel, Institut Paoli-Calmettes, Fédération nationale des Centres de lutte contre le Cancer (FNCLCC), 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), Centre d'Immunologie de Marseille - Luminy (CIML), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), ANR-11-IDEX-0001,Amidex,INITIATIVE D'EXCELLENCE AIX MARSEILLE UNIVERSITE(2011), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Aix Marseille Université (AMU)

Subjects
Male, Physiology, [SDV]Life Sciences [q-bio], Golgi Apparatus, Mice, Animal Cells, Reproductive Physiology, Spermatocytes, Medicine and Health Sciences, Cell Cycle and Cell Division, Testes, Cells, Cultured, Staining, Chromosome Biology, Intracellular Signaling Peptides and Proteins, Specimen preparation and treatment, Spermatids, humanities, Protein Transport, Meiosis, Seminiferous tubules, Cell Processes, cardiovascular system, Cellular Types, Anatomy, Cellular Structures and Organelles, Genital Anatomy, Protein Binding, Research Article, endocrine system, lcsh:QH426-470, education, Immunoglobulins, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, Germ cells, Acrosomes, Animals, Spermatogenesis, Binding Sites, fungi, Reproductive System, DAPI staining, Membrane Proteins, Biology and Life Sciences, Cell Biology, Spermatogonia, Sperm, Mice, Inbred C57BL, Research and analysis methods, lcsh:Genetics, Nuclear staining, Carrier Proteins, Cell Adhesion Molecules
Abstract

Spermatogenesis is a dynamic process that is regulated by adhesive interactions between germ and Sertoli cells. Germ cells express the Junctional Adhesion Molecule-C (JAM-C, encoded by Jam3), which localizes to germ/Sertoli cell contacts. JAM-C is involved in germ cell polarity and acrosome formation. Using a proteomic approach, we demonstrated that JAM-C interacted with the Golgi reassembly stacking protein of 55 kDa (GRASP55, encoded by Gorasp2) in developing germ cells. Generation and study of Gorasp2-/- mice revealed that knock-out mice suffered from spermatogenesis defects. Acrosome formation and polarized localization of JAM-C in spermatids were altered in Gorasp2-/- mice. In addition, Golgi morphology of spermatocytes was disturbed in Gorasp2-/- mice. Crystal structures of GRASP55 in complex with JAM-C or JAM-B revealed that GRASP55 interacted via PDZ-mediated interactions with JAMs and induced a conformational change in GRASP55 with respect of its free conformation. An in silico pharmacophore approach identified a chemical compound called Graspin that inhibited PDZ-mediated interactions of GRASP55 with JAMs. Treatment of mice with Graspin hampered the polarized localization of JAM-C in spermatids, induced the premature release of spermatids and affected the Golgi morphology of meiotic spermatocytes., Author summary Spermatogenesis defects are a common cause of male sterility. Spermatogenesis occurs in the seminiferous tubules of the testes and involves adhesive interactions between developing germ cells and Sertoli cells. Knock-out mouse models identified several adhesion molecules that are critically involved in spermatogenesis. We previously demonstrated that the Junctional Adhesion Molecule-C (JAM-C) plays a crucial role in establishing spermatids polarity. The latter involves rearrangements of the Golgi apparatus in spermatids which contribute to acrosome formation. The present study demonstrated that the C-terminal cytosolic region of JAM-C interacted with the Golgi reassembly stacking protein of 55 kDa (GRASP55) encoded by Gorasp2 and that spermatogenesis was impaired in Gorasp2-deficient mice. We developed an inhibitor of GRASP55 interaction with JAM-C and demonstrated that treatment of wild-type mice with the inhibitory compound induced germ cell loss. Therefore, the male infertility-associated pathway identified in this study is important not only from a genetic point of view, but also as a potential target for male contraception.

Published
2017

9. J’agis!

Author

Gelb, Adrian W., primary, Mainland, Phoebe, additional, Phillips, Peter, additional, Sharpe, Paul, additional, Kinsella, Stephen Michael, additional, Bailly, Anne-Laure, additional, and Jaffe, Rory, additional

Published
2016
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10. Genetic, structural, and chemical insights into the dual function of GRASP55 in germ cell Golgi remodeling and JAM-C polarized localization during spermatogenesis.

Author

Cartier-Michaud A, Bailly AL, Betzi S, Shi X, Lissitzky JC, Zarubica A, Sergé A, Roche P, Lugari A, Hamon V, Bardin F, Derviaux C, Lembo F, Audebert S, Marchetto S, Durand B, Borg JP, Shi N, Morelli X, and Aurrand-Lions M

Subjects
Animals, Binding Sites, Carrier Proteins chemistry, Carrier Proteins genetics, Cells, Cultured, Golgi Apparatus ultrastructure, Intracellular Signaling Peptides and Proteins, Male, Membrane Proteins chemistry, Membrane Proteins genetics, Mice, Mice, Inbred C57BL, Protein Binding, Protein Transport, Spermatogonia cytology, Carrier Proteins metabolism, Cell Adhesion Molecules metabolism, Golgi Apparatus metabolism, Immunoglobulins metabolism, Membrane Proteins metabolism, Spermatogenesis, Spermatogonia metabolism
Abstract

Spermatogenesis is a dynamic process that is regulated by adhesive interactions between germ and Sertoli cells. Germ cells express the Junctional Adhesion Molecule-C (JAM-C, encoded by Jam3), which localizes to germ/Sertoli cell contacts. JAM-C is involved in germ cell polarity and acrosome formation. Using a proteomic approach, we demonstrated that JAM-C interacted with the Golgi reassembly stacking protein of 55 kDa (GRASP55, encoded by Gorasp2) in developing germ cells. Generation and study of Gorasp2-/- mice revealed that knock-out mice suffered from spermatogenesis defects. Acrosome formation and polarized localization of JAM-C in spermatids were altered in Gorasp2-/- mice. In addition, Golgi morphology of spermatocytes was disturbed in Gorasp2-/- mice. Crystal structures of GRASP55 in complex with JAM-C or JAM-B revealed that GRASP55 interacted via PDZ-mediated interactions with JAMs and induced a conformational change in GRASP55 with respect of its free conformation. An in silico pharmacophore approach identified a chemical compound called Graspin that inhibited PDZ-mediated interactions of GRASP55 with JAMs. Treatment of mice with Graspin hampered the polarized localization of JAM-C in spermatids, induced the premature release of spermatids and affected the Golgi morphology of meiotic spermatocytes.

Published
2017
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