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162 results on '"Kilhoffer, Marie-Claude"'

1. Using Data Mining to Explore Calmodulin Bibliography

Author

Haiech, Jacques and Kilhoffer, Marie-Claude

Subjects
Quantitative Biology - Quantitative Methods
Abstract

In this chapter, we present a strategy and the technics to approach a scientific field from a set of articles gathered from the bibliographic database, Web of Science. The strategy is based on methods developed to analyze social networks. We illustrate the use of such strategy in studying the calmodulin field. Such method allows to structure a huge number of articles when writing a review, to detect the key opinion leaders in a given field and to locate his own research topic in the landscape of the themes deciphered by our own community. We show that the free software VosViewer may be used without knowledge in computing science and with a short learning period. iii. more...

Published
2019

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Books, media, physical & digital resources
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3. Bisacodyl and its cytotoxic activity on human glioblastoma stem-like cells. Implication of inositol 1,4,5-triphosphate receptor dependent calcium signaling

Author

Dong, Jihu, Aulestia, Francisco J., Assad Kahn, Suzana, Zeniou, Maria, Dubois, Luiz Gustavo, El-Habr, Elias A., Daubeuf, François, Tounsi, Nassera, Cheshier, Samuel H., Frossard, Nelly, Junier, Marie-Pierre, Chneiweiss, Hervé, Néant, Isabelle, Moreau, Marc, Leclerc, Catherine, Haiech, Jacques, and Kilhoffer, Marie-Claude more...

Published
2017
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11. The anti‐hypertensive drug prazosin inhibits glioblastoma growth via the PKCδ‐dependent inhibition of the AKT pathway

Author

Assad Kahn, Suzana, Costa, Silvia Lima, Gholamin, Sharareh, Nitta, Ryan T, Dubois, Luiz Gustavo, Fève, Marie, Zeniou, Maria, Coelho, Paulo Lucas Cerqueira, El‐Habr, Elias, Cadusseau, Josette, Varlet, Pascale, Mitra, Siddhartha S, Devaux, Bertrand, Kilhoffer, Marie‐Claude, Cheshier, Samuel H, Moura‐Neto, Vivaldo, Haiech, Jacques, Junier, Marie‐Pierre, and Chneiweiss, Hervé more...

Published
2016
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17. The anti-hypertensive drug prazosin inhibits glioblastoma growth via the PKCδ-dependent inhibition of the AKT pathway

Author

Kahn, Suzana Assad, Costa, Silvia Lima, Gholamin, Sharareh, Nitta, Ryan T, Dubois, Luiz Gustavo, Fève, Marie, Zeniou, Maria, Coelho, Paulo Lucas Cerqueira, El-Habr, Elias, Cadusseau, Josette, Varlet, Pascale, Mitra, Siddhartha S, Devaux, Bertrand, Kilhoffer, Marie-Claude, Cheshier, Samuel H, Moura-Neto, Vivaldo, Haiech, Jacques, Junier, Marie-Pierre, and Chneiweiss, Hervé more...

Published
2016
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21. The Q15H mutation enables Crh, a Bacillus subtilis HPr-like protein, to carry out some regulatory HPr functions, but does not make it an effective phosphocarrier for sugar transport

Author

Martin-Verstraete, Isabelle, Galinier, Anne, Darbon, Emmanuelle, Quentin, Yves, Kilhoffer, Marie-Claude, Charrier, Veronique, Haiech, Jacques, Rapoport, Georges, and Deutscher, Josef

Subjects
Bacillus subtilis -- Research, Plasmids -- Usage, Glutamine -- Observations, Histidine -- Observations, Microbial mutation -- Methods, Amino acid sequence -- Analysis, Biological sciences
Abstract

Research was conducted to examine any changes in the catalytic and regulatory functions of catabolite repression HPr (Crh) protein by substituting glutamine-15 to a histidine residue. Results show that the modification, although it enables Crh carry out phosphorylation, it disables sugar transport function to Crh. more...

Published
1999

22. Calcium-dependent signalling in glioblastoma stem-like cells

Author

Leclerc, Catherine, Néant, Isabelle, Haiech, Jacques, Kilhoffer, Marie-Claude, Aulestia, Francisco, Moreau, Marc, Centre de Biologie Intégrative (CBI), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS), Centre de biologie du développement (CBD), Centre National de la Recherche Scientifique (CNRS)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre de Biologie Intégrative (CBI), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), Laboratoire d'Innovation Thérapeutique (LIT), Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA)-Institut de Chimie du CNRS (INC), 8th Workshop of the European Calcium Society, ANR-13-ISV1-0004,calciumGlioStem,Signalisation calcique dans les glioblastomes multiformes : associer l'oncologie et la neurogenèse avec la biologie synthétique et l'imagerie pour relier signalisation calcique et caractère-souche neural.(2013), and ANR-10-IDEX-0002,UNISTRA,Par-delà les frontières, l'Université de Strasbourg(2010) more...

Subjects
mitochondria, glioblastoma stem-like cells, Calcium imaging, KCNIP proteins, [SDV.CAN]Life Sciences [q-bio]/Cancer, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, RNAseq, [SDV.BDD]Life Sciences [q-bio]/Development Biology
Abstract

International audience; Glioblastomas (GBM) are the most aggressive and lethal primary astrocytic tumors in adults, with very poor prognosis. GBMs display significant heterogeneity within the tumor mass, among which a small sub-population of tumor cells with stem-like properties (GSLCs) is responsible for tumor growth, resistance to therapies and tumor recurrence. The high resistance of GSLCs to chemotherapies have been attributed to their capacity to enter quiescence. Quiescence is a reversible cell-cycle arrest which allows cancer stem-like cells to evade killing following therapies. By combining bioluminescent Ca2+-imaging and RNAseq analysis we explored how proliferating and quiescent GSLCs maintain Ca2+ homeostasis and showed that the remodelling of the Ca2+ homeostasis and the reshaping of mitochondria might favour quiescent GSLCs’ survival and aggressiveness in glioblastoma. The importance of the role played by Ca2+ in these last processes lead us to search for Ca2+-binding proteins which can relay Ca2+ signaling to gene expression. KCNIPs (potassium channel-interacting proteins), which constitute the class E of Ca2+ sensor family can control gene transcription directly by binding, via a Ca2+-dependent mechanism, to specific DNA sites on target genes. The presence of putative binding sites for KCNIPs on genes associated with unfavorable outcome for GBM patients suggests that KCNIP proteins may contribute to the alteration of the expression of these prognosis genes. This presentation will also discuss the role of this multifunctional Ca2+ sensors in the regulation of Ca2+ homeostasis in glioblastoma and how Ca2+ via KCNIP proteins may affect prognosis genes expression in GBM. more...

Published
2019

26. Use of engineered proteins with internal tryptophan reporter groups and pertubation techniques to probe the mechanism of ligand-protein interactions: Investigation of the mechanism of calcium binding to calmodulin

Author

Kilhoffer, Marie-Claude, Kubina, Maryline, Travers, Franck, and Haiech, Jacques

Subjects
Perturbation (Mathematics) -- Usage, Calmodulin -- Research, Calcium-binding proteins -- Research, Biological sciences, Chemistry
Abstract

Stopped-flow kinetic and fluorescence spectroscopic analysis, including solvent and temperature perturbations, of five isofunctional structural mutants of calmodulin indicate that calcium binding to calmodulin follows the order site III, site IV, site I, site II, with dissociation occurring in the reverse order. Each of the isofunctional structural mutants contains a single tryptophan residue, introduced by site-specific mutagenesis, as an internal spectroscopic reporter group that was used as a probe of local conformational change. Calcium binding was studied by using flow dialysis or by using fluorescence spectroscopy and monitoring the change in the single tryptophan residue in each calcium-binding site. Calcium removal was examined by using EDTA and monitoring tryptophan fluorescence or by using Quin 2 and monitoring the change in the chromophoric chelator. more...

Published
1992

28. Quiescence status of glioblastoma stem-like cells involves remodelling of Ca 2+ signalling and mitochondrial shape

Author

Aulestia, Francisco, Néant, Isabelle, Dong, Jihu, Haiech, Jacques, Kilhoffer, Marie-Claude, Moreau, Marc, Leclerc, Catherine, Centre de biologie du développement (CBD), Centre National de la Recherche Scientifique (CNRS)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre de Biologie Intégrative (CBI), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), Laboratoire d'Innovation Thérapeutique (LIT), Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA)-Institut de Chimie du CNRS (INC), Centre de Biologie Intégrative (CBI), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS), ANR-13-ISV1-0004,calciumGlioStem,Signalisation calcique dans les glioblastomes multiformes : associer l'oncologie et la neurogenèse avec la biologie synthétique et l'imagerie pour relier signalisation calcique et caractère-souche neural.(2013), and ANR-10-IDEX-0002,UNISTRA,Par-delà les frontières, l'Université de Strasbourg(2010) more...

Subjects
Adult, Cell Survival, lcsh:R, lcsh:Medicine, Apoptosis, [SDV.CAN]Life Sciences [q-bio]/Cancer, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, Article, Mitochondria, Young Adult, Cell Line, Tumor, Neoplastic Stem Cells, Humans, lcsh:Q, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, Calcium Signaling, lcsh:Science, Glioblastoma, Cell Division, Cell Proliferation, Signal Transduction
Abstract

International audience; Quiescence is a reversible cell-cycle arrest which allows cancer stem-like cells to evade killing following therapies. Here, we show that proliferating glioblastoma stem-like cells (GSLCs) can be induced and maintained in a quiescent state by lowering the extracellular pH. Through RNAseq analysis we identified Ca 2+ signalling genes differentially expressed between proliferating and quiescent GSLCs. Using the bioluminescent Ca 2+ reporter EGFP-aequorin we observed that the changes in Ca 2+ homeostasis occurring during the switch from proliferation to quiescence are controlled through store-operated channels (SOC) since inhibition of SOC drives proliferating GSLCs to quiescence. We showed that this switch is characterized by an increased capacity of GSLCs' mitochondria to capture Ca 2+ and by a dramatic and reversible change of mitochondrial morphology from a tubular to a donut shape. Our data suggest that the remodelling of the Ca 2+ homeostasis and the reshaping of mitochondria might favours quiescent GSLCs' survival and their aggressiveness in glioblastoma. Multiform glioblastoma (GBM) is the most aggressive brain tumours with very poor prognosis. Despite a combination of surgical resection, radiotherapy and temozolomide (TMZ)-based chemotherapy, more than 90% of the patients show recurrence and the mean survival period rarely exceeds 2 years 1. According to the cancer stem cell model, the GBM lethality is due to a small sub-population of tumour cells with stem-like properties, called Glioblastoma Stem-Like Cells (GSLCs). The GSLCs have been further characterized as slow-cycling or relatively quiescent cells 2 , identified in vivo in a mouse model of glioblastoma 3 and in human glioblastoma tumors 4. These quiescent GSLCs are highly resistant to TMZ treatment 5. Quiescence is a cell-cycle arrest state which differs from the one observed in differentiation or senescence by the fact that it is reversible. Transcriptional profiling data reveals that quiescent stem cells are characterized by a common gene signature with the down-regulation of genes associated with cell-cycle progression (i.e. CCNA2, CCNB1 and CCNE2) and the upregulation of genes classified as tumour suppressors, including the cyclin-dependent kinase inhibitor p21 (CDKN1A) and the G0/G1 switch gene 2 (G0S2) 6,7. These data also show that quiescence is a G 0 phase and not a prolonged G 1 phase 8. Furthermore, quiescence is actively regulated by signals provided by the stem cell microenvironment. In glioblastoma tumours, quiescent stem-like tumour cells are found close to necrotic tissues, in specific niches characterized by an hypoxic 4,5,9 and acidic microenviron-ment 10,11. The role of the microenvironment in the control of GSLCs quiescence is still poorly understood. Considering that quiescence represents a strategy for GSLCs to evade killing, it is of utmost importance to better characterize the quiescent GSLCs and to understand what governs the transition from a proliferative to a quiescence state. Here, we performed transcriptomic analysis using RNAseq to establish the RNA signatures of proliferative and quiescent GSLCs. We showed that genes involved in Ca 2+ signalling are modulated in GSLCs and we explored the causal role of Ca 2+ during this transition. Our data points out the reversible remodelling of mitochondrial morphology from tubular to donut shape, associated with an increased capacity of mitochon-dria to capture Ca 2+ and with the modification of the kinetics of Ca 2+ influx through SOC. The remodelling of more...

Published
2018
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29. WNK1 kinase and its partners Akt, SGK1 and NBC-family Na+/HCO3– cotransporters are potential therapeutic targets for glioblastoma stem-like cells linked to Bisacodyl signaling

Author

Chen, Wanyin, Zebaze, Leonel Nguekeu, Dong, Jihu, Chezeau, Laëtitia, Inquimbert, Perrine, Hugel, Sylvain, Niu, Songlin, Bihel, Frédéric, Boutant, Emmanuel, Real, Eleonore, Villa, Pascal, Junier, Marie-Pierre, Chneiweiss, Herve, Hibert, Marcel, Haiech, Jacques, Kilhoffer, Marie-Claude, Zeniou, Maria, Laboratoire d'Innovation Thérapeutique (LIT), Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA)-Institut de Chimie du CNRS (INC), Institut des Neurosciences Cellulaires et Intégratives (INCI), Université Louis Pasteur - Strasbourg I-Centre National de la Recherche Scientifique (CNRS), Institut de Science des Matériaux de Mulhouse (IS2M), Université de Haute-Alsace (UHA) Mulhouse - Colmar (Université de Haute-Alsace (UHA))-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Biophotonique et Pharmacologie - UMR 7213 (LBP), Centre National de la Recherche Scientifique (CNRS)-Réseau nanophotonique et optique, Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA)-Université de Haute-Alsace (UHA) Mulhouse - Colmar (Université de Haute-Alsace (UHA))-Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA)-Université de Haute-Alsace (UHA) Mulhouse - Colmar (Université de Haute-Alsace (UHA)), Neurobiologie & Développement (N&D), Centre National de la Recherche Scientifique (CNRS), Biomolécules et innovation thérapeutique (IGLBIT), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut de psychiatrie et neurosciences (U894 / UMS 1266), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Plasticité gliale et neuro-oncologie = Glial Plasticity (NPS-04), Neurosciences Paris Seine (NPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Biologie Paris Seine (IBPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Biologie Paris Seine (IBPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), Institut Gilbert-Laustriat : Biomolécules, Biotechnologie, Innovation Thérapeutique, HUGEL, Sylvain, Université de Strasbourg (UNISTRA)-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS), Université de Strasbourg (UNISTRA)-Université de Haute-Alsace (UHA) Mulhouse - Colmar (Université de Haute-Alsace (UHA))-Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA)-Université de Haute-Alsace (UHA) Mulhouse - Colmar (Université de Haute-Alsace (UHA))-Centre National de la Recherche Scientifique (CNRS), Neuroscience Paris Seine (NPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-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)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-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 National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Institut de Biologie Paris Seine (IBPS), 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)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Université de Strasbourg (UNISTRA)-Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-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)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-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) more...

Subjects
[SDV] Life Sciences [q-bio], [SDV]Life Sciences [q-bio], ComputingMilieux_MISCELLANEOUS
Abstract

International audience

Published
2018
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34. Cancer Stem Cell Quiescence and Plasticity as Major Challenges in Cancer Therapy

Author

Chen, Wanyin, Dong, Jihu, Haiech, Jacques, Kilhoffer, Marie-Claude, and Zeniou, Maria

Subjects
Article Subject
Abstract

Cells with stem-like properties, tumorigenic potential, and treatment-resistant phenotypes have been identified in many human malignancies. Based on the properties they share with nonneoplastic stem cells or their ability to initiate and propagate tumors in vivo, such cells were designated as cancer stem (stem-like) or tumor initiating/propagating cells. Owing to their implication in treatment resistance, cancer stem cells (CSCs) have been the subject of intense investigation in past years. Comprehension of CSCs’ intrinsic properties and mechanisms they develop to survive and even enhance their aggressive phenotype within the hostile conditions of the tumor microenvironment has reoriented therapeutic strategies to fight cancer. This report provides selected examples of malignancies in which the presence of CSCs has been evidenced and briefly discusses methods to identify, isolate, and functionally characterize the CSC subpopulation of cancer cells. Relevant biological targets in CSCs, their link to treatment resistance, proposed targeting strategies, and limitations of these approaches are presented. Two major aspects of CSC physiopathology, namely, relative in vivo quiescence and plasticity in response to microenvironmental cues or treatment, are highlighted. Implications of these findings in the context of the development of new therapies are discussed. more...

Published
2016
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35. Lebbeckoside C, a new triterpenoid saponin from the stem barks of Albizia lebbeck inhibits the growth of human glioblastoma cells.

Author

Noté, Olivier Placide, Ngo Mbing, Joséphine, Kilhoffer, Marie-Claude, Pegnyemb, Dieudonné Emmanuel, and Lobstein, Annelise

Subjects
ALBIZIA, HUMAN growth, SAPONINS, BARK, CELLS, CELL lines
Abstract

One new acacic acid-type saponin, named lebbeckoside C (1), was isolated from the stem barks of Albizia lebbeck. Its structure was established on the basis of extensive analysis of 1D and 2D NMR (uperscript>1H, 13C NMR, DEPT, COSY, TOCSY, ROESY, HSQC and HMBC) experiments, HRESIMS studies, and by chemical evidence as 3-O-[β-d-xylopyranosyl-(l→2)-β-d-fucopyranosyl-(1→6)-[β-d-glucopyranosyl(1→2)]-β-d-glucopyranosyl]-21-O-{(2E,6S)-6-O-{4-O-[(2E,6S)-2,6-dimethyl-6-O-(β-d-quinovopyranosyl)octa-2,7-dienoyl]-4-O-[(2E,6S)-2,6-dimethyl-6-O-(β-d-quinovopyranosyl)octa-2,7-dienoyl]-β-d-quinovopyranosyl}-2,6-dimethylocta-2,7-dienoyl}acacic acid 28 O-[β-d-quinovopyranosyl-(l→3)-[α-l-arabinofuranosyl-(l→4)]-α-l-rhamnopyranosyl-(l→2)-β-d-glucopyranosyl] ester. The isolated saponin (1) displayed significant cytotoxic activity against the human glioblastoma cell line U-87 MG and TG1 stem-like glioma cells isolated from a patient tumor with IC50 values of 1.69 and 1.44 μM, respectively. [ABSTRACT FROM AUTHOR] more...

Published
2019
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36. The anti‐hypertensive drug prazosin inhibits glioblastoma growth via the PKC δ‐dependent inhibition of the AKT pathway

Author

Assad Kahn, Suzana, primary, Costa, Silvia Lima, additional, Gholamin, Sharareh, additional, Nitta, Ryan T, additional, Dubois, Luiz Gustavo, additional, Fève, Marie, additional, Zeniou, Maria, additional, Coelho, Paulo Lucas Cerqueira, additional, El‐Habr, Elias, additional, Cadusseau, Josette, additional, Varlet, Pascale, additional, Mitra, Siddhartha S, additional, Devaux, Bertrand, additional, Kilhoffer, Marie‐Claude, additional, Cheshier, Samuel H, additional, Moura‐Neto, Vivaldo, additional, Haiech, Jacques, additional, Junier, Marie‐Pierre, additional, and Chneiweiss, Hervé, additional more...

Published
2016
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38. Chemical Library Screening and Structure-Function Relationship Studies Identify Bisacodyl as a Potent and Selective Cytotoxic Agent Towards Quiescent Human Glioblastoma Tumor Stem-Like Cells

Author

Zeniou, Maria, primary, Fève, Marie, additional, Mameri, Samir, additional, Dong, Jihu, additional, Salomé, Christophe, additional, Chen, Wanyin, additional, El-Habr, Elias A., additional, Bousson, Fanny, additional, Sy, Mohamadou, additional, Obszynski, Julie, additional, Boh, Alexandre, additional, Villa, Pascal, additional, Assad Kahn, Suzana, additional, Didier, Bruno, additional, Bagnard, Dominique, additional, Junier, Marie-Pierre, additional, Chneiweiss, Hervé, additional, Haiech, Jacques, additional, Hibert, Marcel, additional, and Kilhoffer, Marie-Claude, additional more...

Published
2015
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42. Comparative Expression Study of the Endo–G Protein Coupled Receptor (GPCR) Repertoire in Human Glioblastoma Cancer Stem-like Cells, U87-MG Cells and Non Malignant Cells of Neural Origin Unveils New Potential Therapeutic Targets

Author

Fève, Marie, primary, Saliou, Jean-Michel, additional, Zeniou, Maria, additional, Lennon, Sarah, additional, Carapito, Christine, additional, Dong, Jihu, additional, Van Dorsselaer, Alain, additional, Junier, Marie-Pierre, additional, Chneiweiss, Hervé, additional, Cianférani, Sarah, additional, Haiech, Jacques, additional, and Kilhoffer, Marie-Claude, additional more...

Published
2014
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45. Homodimerization of the Death-Associated Protein Kinase Catalytic Domain: Development of a New Small Molecule Fluorescent Reporter

Author

Zimmermann, Michael, primary, Atmanene, Cédric, additional, Xu, Qingyan, additional, Fouillen, Laetitia, additional, Van Dorsselaer, Alain, additional, Bonnet, Dominique, additional, Marsol, Claire, additional, Hibert, Marcel, additional, Sanglier-Cianferani, Sarah, additional, Pigault, Claire, additional, McNamara, Laurie K., additional, Watterson, D. Martin, additional, Haiech, Jacques, additional, and Kilhoffer, Marie-Claude, additional more...

Published
2010
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49. Deconvolution of Calcium-Binding Curves.

Author

Walker, John M., Vogel, Hans J., Haiech, Jacques, and Kilhoffer, Marie-Claude

Abstract

Ca2+signaling is of paramount importance in intracellular communication of eukaryotic cells. Many external stimuli trigger a transient change in the cytosolic-free Ca2+concentration (in the form of a Ca2+wave or Ca2+oscillations). The internal Ca2+modulation is deciphered by Ca2+-binding proteins, which undergo conformational changes upon Ca2+-binding allowing them to act as enzymatic or protein modulators. These Ca2+-binding proteins have been well described in the past three decades (1-6). Calmodulin, an ubiquitous and multifunctional protein, is considered as the prototype of the Ca2+-binding protein family containing EF-hand domains (7-16). Because of its pivotal role in many Ca2+-dependent cellular events, the understanding of the mechanism of action of this protein at the molecular level has been the aim of several research groups. For such a study, four main points have to be tackled: Description of the mechanism of Ca2+-binding to calmodulin;Understanding of the conformational changes induced by Ca2+-binding;Analysis of the interaction of calmodulin with the different targets; andDeciphering the activation or the modulation of the calmodulin/target protein complexes. [ABSTRACT FROM AUTHOR] more...

Published
2002
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