Search

Your search keyword '"Lamballe, Fabienne"' showing total 35 results
Start Over Author "Lamballe, Fabienne" Search Limiters Academic (Peer-Reviewed) Journals
35 results on '"Lamballe, Fabienne"'

2. Supplementary Figures S1-S7 from Depleting MET-Expressing Tumor Cells by ADCC Provides a Therapeutic Advantage over Inhibiting HGF/MET Signaling

Author

Hultberg, Anna, primary, Morello, Virginia, primary, Huyghe, Leander, primary, De Jonge, Natalie, primary, Blanchetot, Christophe, primary, Hanssens, Valérie, primary, De Boeck, Gitte, primary, Silence, Karen, primary, Festjens, Els, primary, Heukers, Raimond, primary, Roux, Benjamin, primary, Lamballe, Fabienne, primary, Ginestier, Christophe, primary, Charafe-Jauffret, Emmanuelle, primary, Maina, Flavio, primary, Brouckaert, Peter, primary, Saunders, Michael, primary, Thibault, Alain, primary, Dreier, Torsten, primary, de Haard, Hans, primary, and Michieli, Paolo, primary

Published
2023
Full Text
View/download PDF

3. Data from Depleting MET-Expressing Tumor Cells by ADCC Provides a Therapeutic Advantage over Inhibiting HGF/MET Signaling

Author

Hultberg, Anna, primary, Morello, Virginia, primary, Huyghe, Leander, primary, De Jonge, Natalie, primary, Blanchetot, Christophe, primary, Hanssens, Valérie, primary, De Boeck, Gitte, primary, Silence, Karen, primary, Festjens, Els, primary, Heukers, Raimond, primary, Roux, Benjamin, primary, Lamballe, Fabienne, primary, Ginestier, Christophe, primary, Charafe-Jauffret, Emmanuelle, primary, Maina, Flavio, primary, Brouckaert, Peter, primary, Saunders, Michael, primary, Thibault, Alain, primary, Dreier, Torsten, primary, de Haard, Hans, primary, and Michieli, Paolo, primary

Published
2023
Full Text
View/download PDF

4. Supplementary Tables S1-S7 from Depleting MET-Expressing Tumor Cells by ADCC Provides a Therapeutic Advantage over Inhibiting HGF/MET Signaling

Author

Hultberg, Anna, primary, Morello, Virginia, primary, Huyghe, Leander, primary, De Jonge, Natalie, primary, Blanchetot, Christophe, primary, Hanssens, Valérie, primary, De Boeck, Gitte, primary, Silence, Karen, primary, Festjens, Els, primary, Heukers, Raimond, primary, Roux, Benjamin, primary, Lamballe, Fabienne, primary, Ginestier, Christophe, primary, Charafe-Jauffret, Emmanuelle, primary, Maina, Flavio, primary, Brouckaert, Peter, primary, Saunders, Michael, primary, Thibault, Alain, primary, Dreier, Torsten, primary, de Haard, Hans, primary, and Michieli, Paolo, primary

Published
2023
Full Text
View/download PDF

5. Supplementary Methods and References from Depleting MET-Expressing Tumor Cells by ADCC Provides a Therapeutic Advantage over Inhibiting HGF/MET Signaling

Author

Hultberg, Anna, primary, Morello, Virginia, primary, Huyghe, Leander, primary, De Jonge, Natalie, primary, Blanchetot, Christophe, primary, Hanssens, Valérie, primary, De Boeck, Gitte, primary, Silence, Karen, primary, Festjens, Els, primary, Heukers, Raimond, primary, Roux, Benjamin, primary, Lamballe, Fabienne, primary, Ginestier, Christophe, primary, Charafe-Jauffret, Emmanuelle, primary, Maina, Flavio, primary, Brouckaert, Peter, primary, Saunders, Michael, primary, Thibault, Alain, primary, Dreier, Torsten, primary, de Haard, Hans, primary, and Michieli, Paolo, primary

Published
2023
Full Text
View/download PDF

6. Enhanced wild-Type mET Receptor levels in mouse hepatocytes attenuates insulin-mediated signaling

Author

Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), European Commission, Comunidad de Madrid, Fundación Ramón Areces, Instituto de Salud Carlos III, Institut National du Cancer (France), Aix-Marseille Université, Fondation de France, Fondation ARC pour la Recherche sur le Cancer, Rada, Patricia, Lamballe, Fabienne, Cárcer, Guillermo de, Carceller-López, Elena, Hitos, Ana B., Sequera, Celia, Maina, Flavio, Valverde, Ángela M., Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), European Commission, Comunidad de Madrid, Fundación Ramón Areces, Instituto de Salud Carlos III, Institut National du Cancer (France), Aix-Marseille Université, Fondation de France, Fondation ARC pour la Recherche sur le Cancer, Rada, Patricia, Lamballe, Fabienne, Cárcer, Guillermo de, Carceller-López, Elena, Hitos, Ana B., Sequera, Celia, Maina, Flavio, and Valverde, Ángela M.

Abstract

Compelling evidence points to the MET receptor tyrosine kinase as a key player during liver development and regeneration. Recently, a role of MET in the pathophysiology of insulin resistance and obesity is emerging. Herein, we aimed to determine whether MET regulates hepatic insulin sensitivity. To achieve this, mice in which the expression of wild-type MET in hepatocytes is slightly enhanced above endogenous levels (Alb-R26Met mice) were analyzed to document glucose homeostasis, energy balance, and insulin signaling in hepatocytes. We found that Alb-R26Met mice exhibited higher body weight and food intake when compared to R26stopMet control mice. Metabolic analyses revealed that Alb-R26Met mice presented age-related glucose and pyruvate intolerance in comparison to R26stopMet controls. Additionally, in Alb-R26Met mice, high MET levels decreased insulin-induced insulin receptor (IR) and AKT phosphorylation compared to control mice. These results were corroborated in vitro by analyzing IR and AKT phosphorylation in primary mouse hepatocytes from Alb-R26Met and R26stopMet mice upon insulin stimulation. Moreover, co-immunoprecipitation assays revealed MET-IR interaction under both basal and insulin stimulation conditions; this effect was enhanced in Alb-R26Met hepatocytes. Altogether, our results indicate that enhanced MET levels alter hepatic glucose homeostasis, which can be an early event for subsequent liver pathologies.

Published
2022

9. Mitogen-inducible gene 6 is an endogenous inhibitor of HGF/Met-induced cell migration and neurite growth

Author

Pante, Guido, Thompson, Jane, Lamballe, Fabienne, Iwata, Tomoko, Ferby, Ingvar, Barr, Francis A., Davies, Alun M., Maina, Flavio, and Rudiger, Klein

Subjects
Liver cells -- Research, Mitogens -- Research, Cell migration -- Research, Biological sciences
Abstract

Hepatocyte growth factor (HGF)/Met signaling controls cell migration, growth and differentiation in several embryonic organs and is implicated in human cancer. The physiologic mechanisms that attenuate Met signaling are not well understood. Here we report a mechanism by which mitogen-inducible gene 6 (Mig6; also called Gene 33 and receptor-associated late transducer) negatively regulates HGF/Met-induced cell migration. The effect is observed by Mig6 overexpression and is reversed by Mig6 small interfering RNA knock-down experiments; this indicates that endogenous Mig6 is part of a mechanism that inhibits Met signaling. Mig6 functions in cells of hepatic origin and in neurons, which suggests a role for Mig6 in different cell lineages. Mechanistically, Mig6 requires an intact Cdc42/Rac interactive binding site to exert its inhibitory action, which suggests that Mig6 acts, at least in part, distally from Met, possibly by inhibiting Rho-like GTPases. Because Mig6 also is induced by HGF stimulation, our results suggest that Mig6 is part of a negative feedback loop that attenuates Met functions in different contexts and cell types.

Published
2005

10. 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
Full Text
View/download PDF

14. Tracking Dynamics of Spontaneous Tumours in Mice Using Photon Counting Computed Tomography

Author

Cassol, Franca, primary, Portal, Loriane, additional, Richelme, Sylvie, additional, Dupont, Mathieu, additional, Boursier, Yannick, additional, Arechederra, Maria, additional, Auphan-Anezin, Nathalie, additional, Chasson, Lionel, additional, Laprie, Caroline, additional, Fernandez, Samantha, additional, Balasse, Laure, additional, Lamballe, Fabienne, additional, Dono, Rosanna, additional, Guillet, Benjamin, additional, Lawrence, Toby, additional, Morel, Christian, additional, and Maina, Flavio, additional

Published
2019
Full Text
View/download PDF

15. 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
Full Text
View/download PDF

17. Depleting MET-Expressing Tumor Cells by ADCC Provides a Therapeutic Advantage over Inhibiting HGF/MET Signaling

Author

Hultberg, Anna, primary, Morello, Virginia, additional, Huyghe, Leander, additional, De Jonge, Natalie, additional, Blanchetot, Christophe, additional, Hanssens, Valérie, additional, De Boeck, Gitte, additional, Silence, Karen, additional, Festjens, Els, additional, Heukers, Raimond, additional, Roux, Benjamin, additional, Lamballe, Fabienne, additional, Ginestier, Christophe, additional, Charafe-Jauffret, Emmanuelle, additional, Maina, Flavio, additional, Brouckaert, Peter, additional, Saunders, Michael, additional, Thibault, Alain, additional, Dreier, Torsten, additional, de Haard, Hans, additional, and Michieli, Paolo, additional

Published
2015
Full Text
View/download PDF

19. Met acts through Abl to regulate p53 transcriptional outcomes and cell survival in the developing liver

Author

Furlan, Alessandro, primary, Lamballe, Fabienne, additional, Stagni, Venturina, additional, Hussain, Azeemudeen, additional, Richelme, Sylvie, additional, Prodosmo, Andrea, additional, Moumen, Anice, additional, Brun, Christine, additional, del Barco Barrantes, Ivan, additional, Arthur, J. Simon C., additional, Koleske, Anthony J., additional, Nebreda, Angel R., additional, Barilà, Daniela, additional, and Maina, Flavio, additional

Published
2012
Full Text
View/download PDF

20. Combined Drug Action of 2-Phenylimidazo[2,1-b]Benzothiazole Derivatives on Cancer Cells According to Their Oncogenic Molecular Signatures

Author

Furlan, Alessandro, primary, Roux, Benjamin, additional, Lamballe, Fabienne, additional, Conti, Filippo, additional, Issaly, Nathalie, additional, Daian, Fabrice, additional, Guillemot, Jean-François, additional, Richelme, Sylvie, additional, Contensin, Magali, additional, Bosch, Joan, additional, Passarella, Daniele, additional, Piccolo, Oreste, additional, Dono, Rosanna, additional, and Maina, Flavio, additional

Published
2012
Full Text
View/download PDF

28. Pool-Specific Regulation of Motor Neuron Survival by Neurotrophic Support.

Author

Lamballe, Fabienne, Genestine, Matthieu, Caruso, Nathalie, Arce, Vilma, Richelme, Sylvie, Helmbacher, Françoise, and Maina, Flavio

Subjects
*MOTOR neurons, *MUSCLES, *HEPATOCYTE growth factor, *CELL receptors, *NEUROTROPHIC functions, *NEUROPHYSIOLOGY
Abstract

The precise control of motor neuron (MN) death and survival following initial innervation of skeletal muscle targets is a key step in sculpting a functional motor system, but how this is regulated at the level of individual motor pools remains unclear. Hepatocyte growth factor (HGF) and its receptor Met play key developmental roles in both muscle and MNs. We generated mice (termed "Nes-Met") in which met is inactivated from midembryonic stages onward in the CNS only. Adult animals showed motor behavioral defects suggestive of impaired innervation of pectoral muscles. Correspondingly, in neonatal spinal cords of Nes-Met mutants, we observed death of a discrete population of pea3-expressing MNs at brachial levels. Axonal tracing using pea3 reporter mice revealed a novel target muscle of pea3-expressing MNs: the pectoralis minor muscle. In Nes-Met mice, the pectoralis minor pool initially innervated its target muscle, but required HGF/Met for survival, hence for proper maintenance of muscle innervation. In contrast, HGF/Met was dispensable for the survival of neighboring Met-expressing MN pools, despite its earlier functions for their specification and axon growth. Our results demonstrate the exquisite degree to which outcomes of signaling by receptor tyrosine kinases are regulated on a cell-by-cell basis. They also provide a model for one way in which the multiplicity of neurotrophic factors may allow for regulation of MN numbers in a pool-specific manner. [ABSTRACT FROM AUTHOR]

Published
2011
Full Text
View/download PDF

33. Spatiotemporal expression of noncatalytic TrkC NC2 isoform during early and late CNS neurogenesis: a comparative study with TrkC catalytic and p75NTR receptors.

Author

Menn, Bénédicte, Timsit, Serge, Represa, Alfonso, Mateos, Stéphanie, Calothy, Georges, and Lamballe, Fabienne

Subjects
PROTEIN-tyrosine kinases, DEVELOPMENTAL neurobiology, CENTRAL nervous system, CEREBELLUM, RATS, NERVOUS system
Abstract

AbstractThe TrkC subfamily of primary high-affinity neurotrophin-3 receptors is composed of catalytic (kinase-containing; TrkC K) and noncatalytic (TrkC NC) isoforms generated by alternative splicing. We previously reported the presence of the mouse noncatalytic TrkC NC2 isoform in regions of neuronal differentiation [Menn, B., Timsit, S., Calothy, G. & Lamballe, F. (1998) J. Comp. Neurol., 401, 47–64]. In order to gain insight into specific roles for TrkC NC2 receptors during CNS neurogenesis, we compared its distribution with that of its catalytic counterparts and the p75NTR receptor in in vivo and in vitro model systems of early and late neuronal differentiation. We found that TrkC NC2 expression coincided with the exit of neuronal progenitors from the cell cycle and was maintained in differentiated cerebellar neurons. We also showed that, whilst TrkC K receptors were expressed both in mitotic and postmitotic cells, TrkC NC2 was present only in differentiating neural stem cell progeny, suggesting its involvement in neuronal and glial cell differentiation. During neuritogenesis of primary neocortical neurons, both TrkC isoforms as well as p75NTR were located in axonal and dendritic processes. However, whilst these various receptors were present in the same neuronal compartments, TrkC NC2 distribution was specifically restricted to distinct areas of extending neurites. Taken together, these findings suggest that spatiotemporal localization of the noncatalytic receptor could account for specific local effects of neurotrophin-3. [ABSTRACT FROM AUTHOR]

Published
2000
Full Text
View/download PDF

34. The trkB tyrosine protein kinase is a receptor for neurotrophin-4

Author

Klein, Rüdiger, Lamballe, Fabienne, Bryant, Sherri, and Barbacid, Mariano

Abstract

Neurotrophin-4 is a novel member of the nerve growth factor family of neurotrophins recently isolated from Xenopus and viper DNA. We now report that the Xenopus NT-4 protein (XNT-4) can mediate some of its biological properties through gp 145trkBa murine tyrosine protein kinase previously identified as a primary receptor for the related brain-derived neurotrophic factor (BDNF). XNT-4 displaces 125I-labeled BDNF from binding to cells expressing gp 145trkBreceptors, induces their rapid phosphorylation on tyrosine residues, and causes the morphologic transformation of NIH 3T3 cells when coexpressed with gp 145trkB. Moreover, XNT-4 induces the differentiation of PC12 cells into sympathetic-like neurons only if they ectopically express gp 145trkBreceptors. None of these biochemical or biological effects could be observed when XNT-4 was added to cells expressing the related receptors. Replacement of one of the extracellular cysteines (Cys-345) of gp 145trkBby a serine residue prevents its activation by XNT-4 but not by BDNF. Therefore, XNT-4 and BDNF may interact with at least partially distinct domains within the gp 145trkBreceptor.

Published
1992
Full Text
View/download PDF

35. The trkBtyrosine protein kinase is a receptor for brain-derived neurotrophic factor and neurotrophin-3

Author

Klein, Rüdiger, Nanduri, Venkata, Jing, Shuqian, Lamballe, Fabienne, Tapley, Peter, Bryant, Sherri, Cordon-Cardo, Carlos, Jones, Kevin R., Reichardt, Louis F., and Barbacid, Mariano

Abstract

trkB is a tyrosine protein kinase gene highly related to trk, a proto-oncogene that encodes a receptor for nerve growth factor (NGF) and neurotrophin-3 (NT-3). trkB expression is confined to structures of the central and peripheral nervous systems, suggesting it also encodes a receptor for neurotrophic factors. Here we show that brain-derived neurotrophic factor (BDNF) and NT-3, but not NGF, can induce rapid phosphorylation on tyrosine of gp145trkB, one of the receptors encoded by trkB. BDNF and NT-3 can induce DNA synthesis in quiescent NIH 3T3 cells that express gp145trkB. Cotransfection of plasmids encoding gp145trkBand BDNF or NT-3 leads to transformation of recipient NIH 3T3 cells. In these assays, BDNF elicits a response at least two orders of magnitude higher than NT-3. Finally, 125I-NT-3 binds to NIH 3T3 cells expressing gp145trkB; binding can be competed by NT-3 and BDNF but not by NGF. These findings indicate that gp145trkBmay function as a neurotrophic receptor for BDNF and NT-3.

Published
1991
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results