Navet Benjamin, Vargas-Franco Jorge William, Gama Andrea, Amiaud Jérome, Choi Yongwon, Yagita Hideo, Mueller Christopher G, Rédini Françoise, Heymann Dominique, Castaneda Beatriz, Lézot Frédéric
Maternal RANKL Reduces the Osteopetrotic Phenotype of Null Mutant Mouse Pups Article de journal
Dans: Journal of Clinical Medicine, vol. 7, no. 11, 2018, ISSN: 2077-0383.
Résumé | Liens | BibTeX | Étiquettes: bone, mandible, Morphogenesis, OSTEOCLAST, RANKL, skeletal growth, Team-Mueller, Tooth
@article{navet_maternal_2018,
title = {Maternal RANKL Reduces the Osteopetrotic Phenotype of Null Mutant Mouse Pups},
author = {Benjamin Navet and Jorge William Vargas-Franco and Andrea Gama and Jérome Amiaud and Yongwon Choi and Hideo Yagita and Christopher G Mueller and Françoise Rédini and Dominique Heymann and Beatriz Castaneda and Frédéric Lézot},
doi = {10.3390/jcm7110426},
issn = {2077-0383},
year = {2018},
date = {2018-11-01},
journal = {Journal of Clinical Medicine},
volume = {7},
number = {11},
abstract = {RANKL signalization is implicated in the morphogenesis of various organs, including the skeleton. Mice invalidated for Rankl present an osteopetrotic phenotype that was less severe than anticipated, depending on RANKL's implication in morphogenesis. The hypothesis of an attenuated phenotype, as a result of compensation during gestation by RANKL of maternal origin, was thus brought into question. In order to answer this question, Rankl null mutant pups from null mutant parents were generated, and the phenotype analyzed. The results validated the presence of a more severe osteopetrotic phenotype in the second-generation null mutant with perinatal lethality. The experiments also confirmed that RANKL signalization plays a part in the morphogenesis of skeletal elements through its involvement in cell-to-cell communication, such as in control of osteoclast differentiation. To conclude, we have demonstrated that the phenotype associated with Rankl invalidation is attenuated through compensation by RANKL of maternal origin.},
keywords = {bone, mandible, Morphogenesis, OSTEOCLAST, RANKL, skeletal growth, Team-Mueller, Tooth},
pubstate = {published},
tppubtype = {article}
}
Reichhart Jean-Marc, Gubb David, Leclerc Vincent
The Drosophila serpins: multiple functions in immunity and morphogenesis Article de journal
Dans: Meth. Enzymol., vol. 499, p. 205–225, 2011, ISSN: 1557-7988.
Résumé | Liens | BibTeX | Étiquettes: Animals, Immunity, Innate, M3i, Morphogenesis, reichhart, Serpins, Signal Transduction
@article{reichhart_drosophila_2011,
title = {The Drosophila serpins: multiple functions in immunity and morphogenesis},
author = {Jean-Marc Reichhart and David Gubb and Vincent Leclerc},
doi = {10.1016/B978-0-12-386471-0.00011-0},
issn = {1557-7988},
year = {2011},
date = {2011-01-01},
journal = {Meth. Enzymol.},
volume = {499},
pages = {205--225},
abstract = {Members of the serpin superfamily of proteins have been found in all living organisms, although rarely in bacteria or fungi. They have been extensively studied in mammals, where many rapid physiological responses are regulated by inhibitory serpins. In addition to the inhibitory serpins, a large group of noninhibitory proteins with a conserved serpin fold have also been identified in mammals. These noninhibitory proteins have a wide range of functions, from storage proteins to molecular chaperones, hormone transporters, and tumor suppressors. In contrast, until recently, very little was known about insect serpins in general, or Drosophila serpins in particular. In the last decade, however, there has been an increasing interest in the serpin biology of insects. It is becoming clear that, like in mammals, a similar wide range of physiological responses are regulated in insects and that noninhibitory serpin-fold proteins also play key roles in insect biology. Drosophila is also an important model organism that can be used to study human pathologies (among which serpinopathies or other protein conformational diseases) and mechanisms of regulation of proteolytic cascades in health or to develop strategies for control of insect pests and disease vectors. As most of our knowledge on insect serpins comes from studies on the Drosophila immune response, we survey here the Drosophila serpin literature and describe the laboratory techniques that have been developed to study serpin-regulated responses in this model genetic organism.},
keywords = {Animals, Immunity, Innate, M3i, Morphogenesis, reichhart, Serpins, Signal Transduction},
pubstate = {published},
tppubtype = {article}
}
Goulev Youlian, Fauny Jean Daniel, Gonzalez-Marti Beatriz, Flagiello Domenico, Silber Joël, Zider Alain
SCALLOPED interacts with YORKIE, the nuclear effector of the hippo tumor-suppressor pathway in Drosophila Article de journal
Dans: Current Biology: CB, vol. 18, no. 6, p. 435–441, 2008, ISSN: 0960-9822.
Résumé | Liens | BibTeX | Étiquettes: Animals, Cell Proliferation, Drosophila, Drosophila Proteins, HeLa Cells, Humans, I2CT, Imagerie, Intracellular Signaling Peptides and Proteins, Morphogenesis, Nuclear Proteins, Protein Kinases, Protein-Serine-Threonine Kinases, Signal Transduction, Trans-Activators, Transcription Factors, Tumor Suppressor Proteins, Wing
@article{goulev_scalloped_2008,
title = {SCALLOPED interacts with YORKIE, the nuclear effector of the hippo tumor-suppressor pathway in Drosophila},
author = {Youlian Goulev and Jean Daniel Fauny and Beatriz Gonzalez-Marti and Domenico Flagiello and Joël Silber and Alain Zider},
url = {http://www.ncbi.nlm.nih.gov/pubmed/18313299},
doi = {10.1016/j.cub.2008.02.034},
issn = {0960-9822},
year = {2008},
date = {2008-01-01},
urldate = {2011-10-24},
journal = {Current Biology: CB},
volume = {18},
number = {6},
pages = {435--441},
abstract = {In Drosophila, SCALLOPED (SD) belongs to a family of evolutionarily conserved proteins characterized by the presence of a TEA/ATTS DNA-binding domain [1, 2]. SD physically interacts with the product of the vestigial (vg) gene, where the dimer functions as a master gene controlling wing formation [3, 4]. The VG-SD dimer activates the transcription of several specific wing genes, including sd and vg themselves [5, 6]. The dimer drives cell-cycle progression by inducing expression of the dE2F1 transcription factor [7], which regulates genes involved in DNA replication and cell-cycle progression. Recently, YORKIE (YKI) was identified as a transcriptional coactivator that is the downstream effector of the Hippo signaling pathway, which controls cell proliferation and apoptosis in Drosophila[8]. We identified SD as a partner for YKI. We show that interaction between YKI and SD increases SD transcriptional activity both ex vivo in Drosophila S2 cells and in vivo in Drosophila wing discs and promotes YKI nuclear localization. We also show that YKI overexpression induces vg and dE2F1 expression and that proliferation induced by YKI or by a dominant-negative form of FAT in wing disc is significantly reduced in a sd hypomorphic mutant context. Contrary to YKI, SD is not required in all imaginal tissues. This indicates that YKI-SD interaction acts in a tissue-specific fashion and that other YKI partners must exist.},
keywords = {Animals, Cell Proliferation, Drosophila, Drosophila Proteins, HeLa Cells, Humans, I2CT, Imagerie, Intracellular Signaling Peptides and Proteins, Morphogenesis, Nuclear Proteins, Protein Kinases, Protein-Serine-Threonine Kinases, Signal Transduction, Trans-Activators, Transcription Factors, Tumor Suppressor Proteins, Wing},
pubstate = {published},
tppubtype = {article}
}
Gubb David, Robertson Andrew S, Troxler Laurent, Reichhart Jean-Marc
Drosophila Serpins: Regulatory Cascades in Innate Immunity and Morphogenesis Book Section
Dans: Molecular and Cellular Aspects of the Serpinopathies and Disorders in Serpin Activity, p. 207–227, Silverman GA and Lomas DA, London UK, 2007.
BibTeX | Étiquettes: bioinformatic, innate immunity, M3i, Morphogenesis, regulatory Cascades, reichhart, Serpins
@incollection{gubb_drosophila_2007,
title = {Drosophila Serpins: Regulatory Cascades in Innate Immunity and Morphogenesis},
author = {David Gubb and Andrew S Robertson and Laurent Troxler and Jean-Marc Reichhart},
year = {2007},
date = {2007-01-01},
booktitle = {Molecular and Cellular Aspects of the Serpinopathies and Disorders in Serpin Activity},
pages = {207--227},
publisher = {Silverman GA and Lomas DA},
address = {London UK},
edition = {World Scientific Pub.},
keywords = {bioinformatic, innate immunity, M3i, Morphogenesis, regulatory Cascades, reichhart, Serpins},
pubstate = {published},
tppubtype = {incollection}
}
Kambris Zakaria, Bilak Hana, D'Alessandro Rosalba, Belvin Marcia, Imler Jean-Luc, Capovilla Maria
DmMyD88 controls dorsoventral patterning of the Drosophila embryo Article de journal
Dans: EMBO reports, vol. 4, no. 1, p. 64–69, 2003, ISSN: 1469-221X.
Résumé | Liens | BibTeX | Étiquettes: Adaptor Proteins, Alleles, Animals, Antigens, Base Sequence, Cell Surface, Complementary, Developmental, Differentiation, DNA, DNA Transposable Elements, Egg Proteins, Embryo, Exons, Female, Gene Expression Regulation, Genetically Modified, Genotype, imler, Immunity, Immunologic, Innate, Insertional, M3i, Male, messenger, Morphogenesis, Mutagenesis, Myeloid Differentiation Factor 88, Nonmammalian, Oocytes, Protein Biosynthesis, Protein Structure, Receptors, Reverse Transcriptase Polymerase Chain Reaction, RNA, Signal Transducing, Tertiary, Toll-Like Receptors, Zygote
@article{kambris_dmmyd88_2003,
title = {DmMyD88 controls dorsoventral patterning of the Drosophila embryo},
author = {Zakaria Kambris and Hana Bilak and Rosalba D'Alessandro and Marcia Belvin and Jean-Luc Imler and Maria Capovilla},
doi = {10.1038/sj.embor.embor714},
issn = {1469-221X},
year = {2003},
date = {2003-01-01},
journal = {EMBO reports},
volume = {4},
number = {1},
pages = {64--69},
abstract = {MyD88 is an adapter protein in the signal transduction pathway mediated by interleukin-1 (IL-1) and Toll-like receptors. A Drosophila homologue of MyD88 (DmMyD88) was recently shown to be required for the Toll-mediated immune response. In Drosophila, the Toll pathway was originally characterized for its role in the dorsoventral patterning of the embryo. We found that, like Toll, DmMyD88 messenger RNA is maternally supplied to the embryo. Here we report the identification of a new mutant allele of DmMyD88, which generates a protein lacking the carboxy-terminal extension, normally located downstream of the Toll/IL-1 receptor domain. Homozygous mutant female flies lay dorsalized embryos that are rescued by expression of a transgenic DmMyD88 complementary DNA. The DmMyD88 mutation blocks the ventralizing activity of a gain-of-function Toll mutation. These results show that DmMyD88 encodes an essential component of the Toll pathway in dorsoventral pattern formation.},
keywords = {Adaptor Proteins, Alleles, Animals, Antigens, Base Sequence, Cell Surface, Complementary, Developmental, Differentiation, DNA, DNA Transposable Elements, Egg Proteins, Embryo, Exons, Female, Gene Expression Regulation, Genetically Modified, Genotype, imler, Immunity, Immunologic, Innate, Insertional, M3i, Male, messenger, Morphogenesis, Mutagenesis, Myeloid Differentiation Factor 88, Nonmammalian, Oocytes, Protein Biosynthesis, Protein Structure, Receptors, Reverse Transcriptase Polymerase Chain Reaction, RNA, Signal Transducing, Tertiary, Toll-Like Receptors, Zygote},
pubstate = {published},
tppubtype = {article}
}