17 results on '"F. Grise"'
Search Results
2. Optical variability of the ultraluminous X-ray source NGC 1313 X-2
- Author
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F. Grise, Renato Falomo, Luca Zampieri, Roberto Soria, and D. Impiombato
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High Energy Astrophysical Phenomena (astro-ph.HE) ,Physics ,Ultraluminous X-ray source ,Space and Planetary Science ,Modulation ,FOS: Physical sciences ,Astronomy and Astrophysics ,Astrophysics ,Astrophysics - High Energy Astrophysical Phenomena ,Light curve ,V band - Abstract
We analyzed the longest phase-connected photometric dataset available for NGC 1313 X-2, looking for the ~6 day modulation reported by Liu et al. (2009). The folded B band light curve shows a 6 days periodicity with a significance slightly larger than 3 sigma. The low statistical significance of this modulation, along with the lack of detection in the V band, make its identification uncertain., Comment: 4 pages, 2 figures. Accepted for publication in the Astronomische Nachrichten (Astronomical Notes), to appear in the proceedings of the conference "Ultra-Luminous X-ray sources and Middle Weight Black Holes" (Madrid, May 24-26, 2010)
- Published
- 2011
3. The supergiant optical counterpart of ULX P13 in NGC 7793
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C. Motch, Roberto Soria, F. Grise, and M. W. Pakull
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High Energy Astrophysical Phenomena (astro-ph.HE) ,Physics ,Spiral galaxy ,Astrophysics::High Energy Astrophysical Phenomena ,FOS: Physical sciences ,Balmer series ,Astronomy and Astrophysics ,Astrophysics::Cosmology and Extragalactic Astrophysics ,Astrophysics ,Orbital period ,Galaxy ,Luminosity ,Radial velocity ,symbols.namesake ,Space and Planetary Science ,symbols ,Astrophysics::Solar and Stellar Astrophysics ,Astrophysics::Earth and Planetary Astrophysics ,Emission spectrum ,Supergiant ,Astrophysics - High Energy Astrophysical Phenomena ,Astrophysics::Galaxy Astrophysics - Abstract
We have identified the optical counterpart of the ULX source P13 in the nearby spiral galaxy NGC 7793. The object is a V ~ 20.5 mag star, ten times brighter than any other established counterpart of a ULX in nearby galaxies. Medium resolution optical spectroscopy carried out in 2008 and 2009 with the ESO-VLT reveals the presence of narrow high order Balmer, HeI and MgII absorption lines indicating a late B type supergiant companion star with mass between 10 and 20 Msol. Stellar H beta and HeII 4686 emission lines are also seen superposed on the photospheric spectrum. We detect different patterns of radial velocity variations from the emission and absorption lines over a time interval of one month. The velocity of the high order Balmer absorption lines changes by ~ 100 km/s while the H beta and HeI 4686 emission components vary by about the same amount but with a different phasing. Assuming that the observed velocity changes trace the motion of the mass-donor star and of the X-ray source implies a mass of the accreting black hole in the range of 3 to 100 Msol with a most probable value of ~ 10 to 20 Msol. We expect an orbital period in the range of 20 to 40 days based on the low density of the supergiant star. P13 is likely in a short-lived, and thus rare high X-ray luminosity evolutionary state associated with the ascension of the donor star onto the supergiant stage., 4 pages, 5 figures, accepted for publication in the Astronomische Nachrichten, to appear in the proceedings of the conference "Ultra-Luminous X-ray sources and Middle Weight Black Holes" (Madrid, May 24-26, 2010)
- Published
- 2011
4. R36: Sous-expression de Rnd3/RhoE dans le carcinome hépatocellulaire : implication dans l’invasion des hépatocytes tumoraux
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P. Bioulac-Sage, A. Bidaud-Meynard, J. Rosenbaum, F. Grise, Jessica Zucman-Rossi, A. Rullier, N. Dugot-Senant, and V. Moreau
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Cancer Research ,Oncology ,Radiology, Nuclear Medicine and imaging ,Hematology ,General Medicine ,Biology - Published
- 2010
5. 250 RND3/RHO-E IS DOWN-REGULATED IN HEPATOCELLULAR CARCINOMA AND INVOLVED IN CELLULAR INVASION
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P. Bouliac-Sage, Jean Rosenbaum, A. Bidaud-Meynard, Nathalie Dugot-Senant, J. Baud, C. Staedel, V. Moreau, F. Grise, S. Sena, and Jessica Zucman-Rossi
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Sorafenib ,medicine.medical_specialty ,Hepatology ,Tumor size ,business.industry ,Rnd3 ,Arbitrary unit ,Ultrasound ,Urology ,Tumor response ,medicine.disease ,Hepatocellular carcinoma ,Early prediction ,medicine ,business ,medicine.drug - Abstract
predict in the very early period subsequent individual response. Starting from the clinical experience in humans that subcutaneous metastases may rapidly change consistency under sorafenib and that elastosonography a new ultrasound based technique allows assessment of tissue stiffness, we investigated the role of elastonography in the very early prediction of tumor response to sorafenib in a HCC animal model. Methods: HCC (Huh7 cells) subcutaneous xenografting in mice was utilized. Mice were randomized to vehicle or treatment with sorafenib when tumor size was 5–10mm. Elastosonography (Mylab 70XVG, Esaote, Genova, Italy) of the whole tumor mass on a transversal plane with a 10MHz linear transducer was performed at different time points from treatment start (day 0, +2, +4, +7 and +14) until mice were sacrified (day +14), with the operator blind to treatment. In order to overcome variability in absolute elasticity measurement when assessing changes over time, values were expressed in arbitrary units as relative stiffness of the tumor tissue in comparison to the stiffness of a standard reference standoff pad lying on the skin over the tumor. Results: Sor-treated mice showed a smaller tumor size increase at day +14 in comparison to vehicle-treated (tumor volume increase +192.76% vs +747.56%, p =0.06). Among Sor-treated tumors, 6 mice showed a better response to treatment than the other 4 (increase in volume +177% vs +553%, p =0.011). At day +2, median tumor elasticity increased in Sor-treated group (+6.69%, range −30.17 to +58.51%), while decreased in the vehicle group (−3.19%, range −53.32 to +37.94%) leading to a significant difference in absolute values (p =0.034). From this time point onward, elasticity decreased in both groups, with similar speed over time, not being statistically different anymore. In Sor-treated mice all 6 best responders at day 14 showed an increase in elasticity at day +2 (ranging from +3.30% to +58.51%) in comparison to baseline, whereas 3 of the 4 poorer responders showed a decrease. Conclusions: Elastosonography appears a promising non-invasive new technique for the early prediction of HCC tumor response to sorafenib.
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- 2011
6. Acute abdominal symptoms from the bleeding ovary; analysis of eighty-four proved cases
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R F, GRISE and C B, MORTON
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Abdomen ,Ovary ,Humans ,Abdominal Cavity ,Female ,Hemorrhage - Published
- 1951
7. The relationship of plasma proteolytic and antiproteolytic substances to the course of experimental appendiceal peritonitis
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R F, GRISE, E M, ALRICH, and E P, LEHMAN
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Plasma ,Proteolysis ,Humans ,Blood Proteins ,Peritonitis - Published
- 1950
8. The care of patients with multiple injuries
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R F, GRISE
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Psychotherapy ,Multiple Trauma ,Humans ,Wounds and Injuries - Published
- 1960
9. Etude des phénomènes d'échange lors de l'emploi de bentonites œnologiques
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O. COLAGRANDE, F. GRISELLI, and A.A. DEL RE
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bentoninte ,winemaking process ,fining ,Agriculture ,Botany ,QK1-989 - Abstract
L'usage œnologique de la bentonite en tant que déprotéinisant est très répandu. On sait que cette substance clarifiante modifie l'équilibre chimique des vins par phénomènes d'échange et d'adsorption. On trouve dans la littérature beaucoup de résultats de nombreuses recherches sur les conditions pratiques d'emploi des bentonites ; cependant, les connaissances du mécanisme d'action sont rares et souvent contradictoires. Il est évident que le fait de prévoir la valeur d'emploi des bentonites, en œnologie, ne peut être obtenu que par la connaissance quantitative des équilibres chimiques et physico-chimiques mis en jeu. Aussi, il nous a paru opportun d'abandonner les travaux empiriques pour étudier tout d'abord le cas de systèmes simples, de composition semblable à celle du vin, en supposant, bien entendu, les mêmes lois valables tant dans ces systèmes simples que dans les systèmes naturels.
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- 1973
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10. Autocrine control of glioma cells adhesion and migration through IRE1α-mediated cleavage of SPARC mRNA.
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Dejeans N, Pluquet O, Lhomond S, Grise F, Bouchecareilh M, Juin A, Meynard-Cadars M, Bidaud-Meynard A, Gentil C, Moreau V, Saltel F, and Chevet E
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- Actin Cytoskeleton metabolism, Brain Neoplasms genetics, Cell Adhesion genetics, Cell Proliferation, Down-Regulation genetics, Extracellular Matrix Proteins genetics, Extracellular Matrix Proteins metabolism, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Glioma genetics, Humans, Models, Biological, Osteonectin genetics, RNA, Messenger genetics, RNA, Messenger metabolism, Signal Transduction genetics, Spheroids, Cellular pathology, Tumor Cells, Cultured, rhoA GTP-Binding Protein metabolism, Autocrine Communication genetics, Brain Neoplasms pathology, Cell Movement genetics, Endoribonucleases metabolism, Glioma pathology, Osteonectin metabolism, Protein Serine-Threonine Kinases metabolism
- Abstract
The endoplasmic reticulum (ER) is an organelle specialized for the folding and assembly of secretory and transmembrane proteins. ER homeostasis is often perturbed in tumor cells because of dramatic changes in the microenvironment of solid tumors, thereby leading to the activation of an adaptive mechanism named the unfolded protein response (UPR). The activation of the UPR sensor IRE1α has been described to play an important role in tumor progression. However, the molecular events associated with this phenotype remain poorly characterized. In the present study, we examined the effects of IRE1α signaling on the adaptation of glioma cells to their microenvironment. We show that the characteristics of U87 cell migration are modified under conditions where IRE1α activity is impaired (DN_IRE1). This is linked to increased stress fiber formation and enhanced RhoA activity. Gene expression profiling also revealed that loss of functional IRE1α signaling mostly resulted in the upregulation of genes encoding extracellular matrix proteins. Among these genes, Sparc, whose mRNA is a direct target of IRE1α endoribonuclease activity, was in part responsible for the phenotypic changes associated with IRE1α inactivation. Hence, our data demonstrate that IRE1α is a key regulator of SPARC expression in vitro in a glioma model. Our results also further support the crucial contribution of IRE1α to tumor growth, infiltration and invasion and extend the paradigm of secretome control in tumor microenvironment conditioning.
- Published
- 2012
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11. Rnd3/RhoE Is down-regulated in hepatocellular carcinoma and controls cellular invasion.
- Author
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Grise F, Sena S, Bidaud-Meynard A, Baud J, Hiriart JB, Makki K, Dugot-Senant N, Staedel C, Bioulac-Sage P, Zucman-Rossi J, Rosenbaum J, and Moreau V
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- Cadherins physiology, Cell Line, Tumor, Cell Proliferation, Down-Regulation, Epithelial-Mesenchymal Transition, Homeodomain Proteins physiology, Humans, Neoplasm Invasiveness, Repressor Proteins physiology, Zinc Finger E-box Binding Homeobox 2, rho GTP-Binding Proteins antagonists & inhibitors, rho GTP-Binding Proteins genetics, Carcinoma, Hepatocellular pathology, Liver Neoplasms pathology, rho GTP-Binding Proteins physiology
- Abstract
Unlabelled: We performed a review of public microarray data that revealed a significant down-regulation of Rnd3 expression in hepatocellular carcinoma (HCC), as compared to nontumor liver. Rnd3/RhoE is an atypical RhoGTPase family member because it is always under its active GTP-bound conformation and not sensitive to classical regulators. Rnd3 down-regulation was validated by quantitative real-time polymerase chain reaction in 120 independent tumors. Moreover, Rnd3 down-expression was confirmed using immunohistochemistry on tumor sections and western blotting on human tumor and cell-line extracts. Rnd3 expression was significantly lower in invasive tumors with satellite nodules. Overexpression and silencing of Rnd3 in Hep3B cells led to decreased and increased three-dimensional cell motility, respectively. The short interfering RNA-mediated down-regulation of Rnd3 expression induced a loss of E-cadherin at cell-cell junctions that was linked to epithelial-mesenchymal transition through the up-regulation of the zinc finger E-box binding homeobox protein, ZEB2, and the down-regulation of miR-200b and miR-200c. Rnd3 knockdown mediated tumor hepatocyte invasion in a matrix-metalloproteinase-independent, and Rac1-dependent manner., Conclusion: Rnd3 down-regulation provides an invasive advantage to tumor hepatocytes, suggesting that RND3 might represent a metastasis suppressor gene in HCC., (Copyright © 2012 American Association for the Study of Liver Diseases.)
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- 2012
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12. Sodium fluoride induces podosome formation in endothelial cells.
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Tatin F, Grise F, Reuzeau E, Genot E, and Moreau V
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- Actins metabolism, Animals, Cell Adhesion physiology, Cells, Cultured, Endothelial Cells metabolism, Protein Binding drug effects, Swine, cdc42 GTP-Binding Protein metabolism, rac1 GTP-Binding Protein metabolism, rhoA GTP-Binding Protein metabolism, Cell Membrane Structures drug effects, Cytoskeleton drug effects, Endothelial Cells drug effects, GTP-Binding Proteins metabolism, Sodium Fluoride pharmacology
- Abstract
Background Information: Fluoride is a well-known G-protein activator. Exposure of cultured cells to its derivatives results in actin cytoskeleton remodelling. Podosomes are actin-based structures endowed with adhesion and matrix-degradation functions. This study investigates actin cytoskeleton reorganization induced by fluoride in endothelial cells., Results: Treatment of cultured endothelial cells with sodium fluoride (NaF) results in a rapid and potent stimulation of podosome formation. Furthermore, we show that Cdc42 (cell-division cycle 42), Rac1 and RhoA activities are stimulated in NaF-treated cells. However, podosome assembly is dependent on Cdc42 and Rac1, but not RhoA. Although the sole activation of Cdc42 is sufficient to induce individual podosomes, a balance between RhoGTPase activities regulates podosome formation in response to NaF, which in this case are often found in groups or rosettes. As in other models, podosome formation in endothelial cells exposed to NaF also involves Src. Finally, we demonstrate that NaF-induced podosomes are fully competent for matrix protein degradation., Conclusions: Taken together, our findings establish NaF as a novel inducer of podosomes in endothelial cells in vitro.
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- 2010
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13. Rho GTPases in hepatocellular carcinoma.
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Grise F, Bidaud A, and Moreau V
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- 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine analogs & derivatives, 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine therapeutic use, Amides therapeutic use, Animals, Carcinoma, Hepatocellular drug therapy, Disease Progression, Farnesyltranstransferase antagonists & inhibitors, Humans, Liver Neoplasms drug therapy, Neoplasm Metastasis, Pyridines therapeutic use, Signal Transduction, rho GTP-Binding Proteins antagonists & inhibitors, rho GTP-Binding Proteins classification, Carcinoma, Hepatocellular etiology, Liver Neoplasms etiology, rho GTP-Binding Proteins physiology
- Abstract
Rho GTPases are major regulators of signal transduction pathways and play key roles in processes including actin dynamics, cell cycle progression, cell survival and gene expression, whose deregulation may lead to tumorigenesis. A growing number of in vitro and in vivo studies using tumor-derived cell lines, primary tumors and animal cancer models strongly suggest that altered Rho GTPase signaling plays an important role in the initiation as well as in the progression of hepatocellular carcinoma (HCC), one of the deadliest human cancers in the world. These alterations can occur at the level of the GTPases themselves or of one of their regulators or effectors. The participation into the tumorigenic process can occur either through the over-expression of one of these components which presents an oncogenic activity as illustrated with RhoA and C or through the attenuation of the expression of a component presenting tumor suppressor activity as for Cdc42 or the RhoGAP, DLC-1. Consequently, these observations reflect the heterogeneity and the complexity of liver carcinogenesis. Recently, pharmacological approaches targeting Rho GTPase signaling have been used in HCC-derived models with relative success but remain to be validated in more physiologically relevant systems. Therefore, therapeutic approaches targeting Rho GTPase signaling may provide a novel alternative for anti-HCC therapy.
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- 2009
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14. The calcium-sensing protein synaptotagmin 7 is expressed on different endosomal compartments in endocrine, neuroendocrine cells or neurons but not on large dense core vesicles.
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Monterrat C, Grise F, Benassy MN, Hémar A, and Lang J
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- Animals, Cell Membrane metabolism, Cell Membrane ultrastructure, Insulin-Secreting Cells cytology, Lysosomes metabolism, Microscopy, Confocal, Neurons cytology, Neurosecretory Systems cytology, PC12 Cells metabolism, PC12 Cells ultrastructure, Protein Isoforms metabolism, Rats, Secretory Vesicles ultrastructure, Endosomes metabolism, Insulin-Secreting Cells metabolism, Neurons metabolism, Neurosecretory Systems metabolism, Secretory Vesicles metabolism, Synaptotagmins metabolism
- Abstract
Synaptotagmin (syt) isoforms function as calcium sensor in post-Golgi transport although the precise transport step and compartment(s) concerned are still not fully resolved. As syt7 has been proposed to operate in lysosomal exocytosis and in exocytosis of large dense core vesicles (LDCVs), we have addressed the distribution of endogenous syt7 in insulin-secreting cells. These cells express different syt7 isoforms comparable to neurons. According to subcellular fractionation and quantitative confocal immunocytochemistry, syt7 is not found on LDCVs or on synaptic-like microvesicles but colocalizes with Rab7 on endosomes and to structures near to or at the plasma membrane. Similarly, endogenous syt7 was absent from LDCVs in pheochromocytoma PC12 cells. In contrast, syt7 localised to lysosomes in both, PC12 cells and hippocampal neurons. In conclusion, endogenous syt7 shows a wider distribution than previously reported but does not qualify as vesicular calcium sensor in SLMV or LDCV exocytosis according to its localisation.
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- 2007
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15. Distinct roles of the C2A and the C2B domain of the vesicular Ca2+ sensor synaptotagmin 9 in endocrine beta-cells.
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Grise F, Taib N, Monterrat C, Lagrée V, and Lang J
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- Animals, Cricetinae, Endosomes metabolism, Mice, Models, Molecular, Protein Structure, Tertiary, Protein Transport, Synaptotagmins chemistry, Synaptotagmins genetics, Calcium physiology, Synaptotagmins physiology
- Abstract
Synaptotagmins form a family of calcium-sensor proteins implicated in exocytosis, and these vesicular transmembrane proteins are endowed with two cytosolic calcium-binding C2 domains, C2A and C2B. Whereas the isoforms syt1 and syt2 have been studied in detail, less is known about syt9, the calcium sensor involved in endocrine secretion such as insulin release from large dense core vesicles in pancreatic beta-cells. Using cell-based assays to closely mimic physiological conditions, we observed SNARE (soluble N-ethylmaleimide-sensitive fusion protein-attachment protein receptor)-independent translocation of syt9C2AB to the plasma membrane at calcium levels corresponding to endocrine exocytosis, followed by internalization to endosomes. The use of point mutants and truncations revealed that initial translocation required only the C2A domain, whereas the C2B domain ensured partial pre-binding of syt9C2AB to the membrane and post-stimulatory localization to endosomes. In contrast with the known properties of neuronal and neuroendocrine syt1 or syt2, the C2B domain of syt9 did not undergo calcium-dependent membrane binding despite a high degree of structural homology as observed through molecular modelling. The present study demonstrates distinct intracellular properties of syt9 with different roles for each C2 domain in endocrine cells.
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- 2007
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16. Synaptotagmin 8 is expressed both as a calcium-insensitive soluble and membrane protein in neurons, neuroendocrine and endocrine cells.
- Author
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Monterrat C, Boal F, Grise F, Hémar A, and Lang J
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- Animals, Antibodies metabolism, Antibody Specificity, Calcium metabolism, Cytosol metabolism, Endocrine Glands metabolism, Exons genetics, Neurons cytology, Neurosecretory Systems metabolism, PC12 Cells, Protein Binding, Protein Transport, Qb-SNARE Proteins metabolism, RNA, Messenger genetics, RNA, Messenger metabolism, Rats, Solubility, Synaptotagmins genetics, Calcium pharmacology, Cell Membrane metabolism, Endocrine Glands cytology, Gene Expression Regulation, Neurons metabolism, Neurosecretory Systems cytology, Synaptotagmins metabolism
- Abstract
Synaptotagmins (syt) form a large family of transmembrane proteins and some of its isoforms are known to regulate calcium-induced membrane fusion during vesicular traffic. In view of the reported implication of the isoform syt8 in exocytosis we investigated the expression, localisation and calcium-sensitivity of syt8 in secretory cells. An immunopurified antipeptide antibody was generated which is directed against a C-terminal sequence and devoid of crossreactivity towards syt1 to 12. Subcellular fractionation and immunocytochemistry revealed two forms of synaptotagmin 8 (50 and 40 kDa). Whereas the 40-kDa was present in the cytosol in brain, in PC12 and in clonal beta-cells, the 50-kDa form was localised in very typical clusters and partially colocalised with the SNARE protein Vti1a. Moreover, in primary hippocampal neurons syt8 was only found within the soma. Amplification of syt8 by RT-PCR indicated that the observed protein variants were not generated by alternative splicing of the 6th exon and are most likely linked to variations in the N-terminal region. In contrast to the established calcium sensor syt2, endogenous cytosolic syt8 and transiently expressed syt8-C2AB-eGFP did not translocate upon a raise in cytosolic calcium in living cells. Syt8 is therefore not a calcium sensor in exocytotic membrane fusion in endocrine cells.
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- 2006
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17. Myoblast migration is regulated by calpain through its involvement in cell attachment and cytoskeletal organization.
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Dedieu S, Poussard S, Mazères G, Grise F, Dargelos E, Cottin P, and Brustis JJ
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- Animals, Calcium-Binding Proteins metabolism, Calpain drug effects, Calpain metabolism, Cell Adhesion, Cell Fusion, Cell Line, Cell Movement drug effects, Clone Cells, Cysteine Proteinase Inhibitors pharmacology, Cytoskeleton metabolism, Dipeptides pharmacology, Dose-Response Relationship, Drug, Glucosidases, Leupeptins pharmacology, Mice, Muscle Fibers, Skeletal metabolism, Myoblasts cytology, Myoblasts drug effects, Myristoylated Alanine-Rich C Kinase Substrate, Oligopeptides pharmacology, Phosphoproteins metabolism, Stress Fibers drug effects, Stress Fibers metabolism, Calpain antagonists & inhibitors, Cell Movement physiology, Intracellular Signaling Peptides and Proteins, Membrane Proteins, Myoblasts physiology
- Abstract
Cell migration is a fundamental cellular function particularly during skeletal muscle development. Ubiquitous calpains are well known to play a pivotal role during muscle differentiation, especially at the onset of fusion. In this study, the possible positive regulation of myoblast migration by calpains, a crucial step required to align myoblasts to permit them to fuse, was investigated. Inhibition of calpain activity by different pharmacological inhibitors argues for the involvement of these proteinases during the migration of myoblasts. Moreover, a clonal cell line that fourfold overexpresses calpastatin, the endogenous inhibitor of calpains, and that exhibits deficient calpain activities was obtained. The results showed that the migratory capacity of C2C12 and fusion into multinucleated myotubes were completely prevented in these clonal cells. Calpastatin-overexpressing myoblasts unable to migrate were characterized by rounded morphology, the loss of membrane extensions, the disorganization of stress fibers and exhibited a major defect in new adhesion formation. Surprisingly, the proteolytic patterns of desmin, talin, vinculin, focal adhesion kinase (FAK) and ezrin, radixin, moesin (ERM) proteins are the same in calpastatin-overexpressing myoblasts as compared to control cells. However, an important accumulation of myristoylated alanine-rich C kinase substrate (MARCKS) was observed in cells showing a reduced calpain activity, suggesting that the proteolysis of this actin-binding protein is calpain-dependent and could be involved in both myoblast adhesion and migration.
- Published
- 2004
- Full Text
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