A5070497880- Protein Kinase Regulation and GTPase Signaling
- Adipose Tissue and Metabolism
- Blood Coagulation and Thrombosis Mechanisms
- PI3K/AKT/mTOR signaling in cancer
- Cell death mechanisms and regulation
- Cancer, Hypoxia, and Metabolism
- Melanoma and MAPK Pathways
- Cancer-related gene regulation
- interferon and immune responses
- Metabolism, Diabetes, and Cancer
- Receptor Mechanisms and Signaling
- Adipokines, Inflammation, and Metabolic Diseases
- Fibroblast Growth Factor Research
- Neonatal Respiratory Health Research
- Coagulation, Bradykinin, Polyphosphates, and Angioedema
- TGF-β signaling in diseases
- Exercise and Physiological Responses
- Ubiquitin and proteasome pathways
- Growth Hormone and Insulin-like Growth Factors
- Trace Elements in Health
- Signaling Pathways in Disease
- NF-κB Signaling Pathways
- Ion channel regulation and function
- Estrogen and related hormone effects
- ATP Synthase and ATPases Research
Université Côte d'Azur
1988-2017
Centre National de la Recherche Scientifique
2000-2017
Inserm
2000-2017
Institut de Biologie Valrose
1982-2015
Centre National pour la Recherche Scientifique et Technique (CNRST)
2015
Institut de Recherche sur le Cancer et le Vieillissement de Nice
2009
Centre Antoine Lacassagne
2000-2003
University of California, San Diego
1992-1993
University of California, San Francisco
1992
Université Paris-Est Créteil
1986
The mitogen-activated protein kinases (MAP kinases) p42mapk and p44mapk are serine/threonine rapidly activated in cells stimulated with various extracellular signals by dual phosphorylation of tyrosine threonine residues. They thought to play a pivotal role integrating transmitting transmembrane required for growth differentiation. Here we demonstrate that activation these ubiquitously expressed MAP is essential growth. To specifically suppress kinase fibroblasts, transiently either the...
Myogenin and MyoD belong to a family of muscle-specific helix-loop-helix (HLH) proteins that have the potential activate genes in nonmyogenic cells. Peptide growth factors can block ability myogenin their target genes. Here, we show factor-inducible proto-oncogenes c-fos, c-jun, junB mimic effects exogenous suppress trans-activation muscle creatine kinase (MCK) enhancer by MyoD. In contrast, JunD, which shares DNA-binding specificity with JunB c-Jun but is expressed constitutively cells, an...
Chinese hamster lung fibroblast cells (CCl39) enter the G0/G1 nonproliferative state after serum deprivation. In this report, we show that reinitiation of DNA synthesis by or combination purified human thrombin and insulin (1-10 microgram/ml) is preceded very early stimulation ionic fluxes (Na+/Rb+) protein phosphorylation (27,000 daltons, 62,000 ribosomal S6 proteins). The potentiating action on thrombin-stimulated also observed Na+ influx, Rb+ phosphorylation. Moreover, demonstrate CCl39...
Basic or acidic fibroblast growth factor (FGF), alone, was found to be as potent alpha-thrombin reinitiate DNA synthesis in G0-arrested Chinese hamster lung fibroblasts (CCL39). FGF at 50 ng/ml thrombin 1 unit/ml rapidly initiated early events such cytoplasmic alkalinization (0.2-0.3 pH units), rise Ca2+, phosphorylation of ribosomal protein S6 and increased c-myc expression, followed by a 30-40-fold increase labeled nuclei. Whereas is activator phospholipase C judged the rapid release...
Disruption of the endothelial barrier by tumour-derived secreted factors is a critical step in cancer cell extravasation and metastasis. Here, comparative proteomic analysis melanoma secretomes, we identify matricellular protein SPARC as novel vascular permeability factor. deficiency abrogates tumour-initiated lung capillaries prevents extravasation, whereas overexpression enhances leakiness, SPARC-induced paracellular dependent on VCAM1 receptor p38 MAPK signalling. Blocking impedes...
Brown adipose tissue is the primary site for thermogenesis and can consume, in addition to free fatty acids, a very high amount of glucose from blood, which both acutely chronically affect homeostasis. Here, we show that mechanistic target rapamycin (mTOR) complex 2 has novel role β3-adrenoceptor–stimulated uptake brown tissue. We β3-adrenoceptors stimulate via signaling pathway comprised two different parts: one part dependent on cAMP-mediated increases GLUT1 transcription de novo synthesis...
Thermogenic adipocytes (i.e. brown or brite/beige adipocytes) are able to burn large amounts of lipids and carbohydrates as a result highly active mitochondria enhanced uncoupled respiration, due UCP1 activity. Although the key organelles for this thermogenic function, limited human data available. We characterized changes in mitochondrial function brite adipocytes, using hMADS cells model white- brite-adipocyte conversion. found that profound molecular modifications were associated with...
Anchorage removal like growth factor induces apoptosis. In the present study we have characterized signaling pathways that can prevent this cell death using a highly factor– and anchorage-dependent line of lung fibroblasts (CCL39). After anchorage from exponentially growing cells, annexin V-FITC labeling be detected after 8 h. Apoptosis was confirmed by analysis sub-G1 DNA content Western blotting caspase substrate poly (ADP-ribose) polymerase. Growth withdrawal accelerates potentiates...
In this work, we analyzed the role of PI3K-p70 S6 kinase (S6K) signaling cascade in stimulation endothelial cell proliferation. We found that inhibitors p42/p44 MAPK pathway (PD98059) and S6K (wortmannin, Ly294002, rapamycin) all block thymidine incorporation stimulated by fetal calf serum resting mouse line 1G11. The action rapamycin can be generalized, since it completely inhibits mitogenic effect primary cultures (human umbilical vein cells) another established capillary (LIBE cells)....
Mitogen-activated protein (MAP) kinase phosphatases (MKPs) are dual-specificity that dephosphorylate phosphothreonine and phosphotyrosine residues within MAP kinases. Here, we describe a novel posttranslational mechanism for regulating MKP-3/Pyst1/DUSP6, member of the MKP family is highly specific extracellular signal-regulated 1 2 (ERK1/2) inactivation. Using fibroblast model in which expression either MKP-3 or more stable MKP-3-green fluorescent (GFP) chimera was induced by tetracycline,...
Brite adipocytes are inducible energy-dissipating cells expressing UCP1 which appear within white adipose tissue of healthy adult individuals. Recruitment these represents a potential strategy to fight obesity and associated diseases. Using human Multipotent Adipose-Derived Stem cells, able convert into brite adipocytes, we show that arachidonic acid strongly inhibits adipocyte formation via cyclooxygenase pathway leading secretion PGE2 PGF2α. Both prostaglandins induce an oscillatory Ca++...
Abstract Transforming growth factor beta (TGF‐β) was found to inhibit (IC 50 =0.1 ng/ml) α‐thrombin or FGF‐induced mitogenicity in G0‐arrested Chinese hamster lung fibroblasts. Growth factor‐stimulated cells became rapidly insensitive TGF‐β addition during their progression through G0/G1 suggesting that an early step of the mitogenic response target action. Surprisingly, none well characterized events commonly triggered by factors be affected addition. These responses included:...
Protein phosphorylation of G0/G1-arrested Chinese hamster lung fibroblasts (CC139 line) has been analyzed following stimulation by fetal calf serum (FCS) or a variety growth factors. FCS stimulated the three major polypeptides separated on sodium dodecyl sulfate-polyacrylamide gel electrophoresis: nuclear protein with Mr 62,000 daltons, ribosomal S6, and cytosoluble peptide 27,000 daltons. These phosphorylations occurred rapidly after (1 min for 27,000-dalton peptide, 5 S6 62,000-dalton...
In rodents and humans, besides brown adipose tissue (BAT), islands of thermogenic adipocytes, termed "brite" (brown-in-white) or beige emerge within white (WAT) after cold exposure β3-adrenoceptor stimulation, which may protect from obesity associated diseases. microRNAs are novel modulators development function. The purpose this work was to characterize the role in control brite adipocyte formation. Using human multipotent derived stem cells, we identified miR-125b-5p as downregulated upon...
Bcl-xL, a member of the Bcl-2 family, inhibits apoptosis, and its expression is regulated at transcriptional level, yet nothing known about transcription factors specifically activating this promoter. The bcl-x promoter contains potential Ets binding sites, we show that factor, Ets2, first identified by sequence identity to v-ets E26 retrovirus, can transactivate Transient Ets2 results in upregulation Bcl-xL but not Bcl-xS, an alternatively spliced gene product which induces apoptosis....
AlFa and vanadate have been shown to induce inositol phosphate formation in resting hamster fibroblasts (CCL39).In this study, we show that these two analogs are good tools explore the causal relationship between phosphoinositide breakdown early mitogenic events.A1F; can activate, very similarly mitogen a-thrombin: 1) amiloride-sensitive Na+/H+ antiport, 2) bumetanide-sensitive Na+/K+/Clcotransport, 3) expression of c-myc mRNA.The link phospholipase C activation events response is...