References of "Piette, Jacques"
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See detailNOD2 interactome
Lecat, Aurore ULg; Di Valentin, Emmanuel ULg; Fillet, Marianne ULg et al

Poster (2010, January 28)

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See detailTNFL–Induced p100 processing (TIPP) relies on the internalization of the cognate TNFR
Ganeff, Corinne; Galopin, Géraldine; Remouchamps, Caroline ULg et al

Conference (2010, January)

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See detailThe protein Nod2: an innate receptor more complex than previously assumed.
Lecat, Aurore ULg; Piette, Jacques ULg; Legrand-Poels, Sylvie ULg

in Biochemical Pharmacology (2010), 80(12), 2021-31

For almost 10 years, Nod2 has been known as a cytosolic innate receptor able to sense peptidoglycan from Gram-positive and -negative bacteria and to trigger RIP2- and NF-kappaB-mediated pro-inflammatory ... [more ▼]

For almost 10 years, Nod2 has been known as a cytosolic innate receptor able to sense peptidoglycan from Gram-positive and -negative bacteria and to trigger RIP2- and NF-kappaB-mediated pro-inflammatory and antibacterial response. Mutations in the gene encoding Nod2 in humans have been associated with Crohn's disease (CD). Mechanisms by which Nod2 variants can lead to CD development are still under investigation. The most admitted hypothesis suggests that the impaired function of Nod2 variants in intestinal epithelial and phagocytic cells results in deficiencies in epithelial-barrier function which subsequently lead to increased bacterial invasion and inflammation at intestinal sites. Very recent results have just reinforced this hypothesis by demonstrating that Nod2 wild-type (unlike Nod2 variants) could mediate autophagy, allowing an efficient bacterial clearance and adaptative immune response. Other recent data have attributed new roles to Nod2. Indeed, Nod2 has been shown to activate antiviral innate immune responses involving IRF3-dependent IFN-beta production after viral ssRNA recognition through a RIP2-independent mechanism requiring the mitochondrial adaptor protein MAVS. Recently, Nod2 has been also shown to be exquisitely tuned to detect mycobacterial infections and mount a protective immunity against these pathogens. [less ▲]

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See detailSHIP-1 inhibits CD95/APO-1/Fas-induced apoptosis in primary T lymphocytes and T leukemic cells by promoting CD95 glycosylation independently of its phosphatase activity
Charlier, Edith ULg; Condé, Claude ULg; Zhang, Jing et al

in Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K (2010)

SHIP-1 functions as a negative regulator of immune responses by hydrolyzing phosphatidylinositol-3,4,5-triphosphate generated by PI 3-kinase activity. As a result, SHIP-1 deficiency in mice results in ... [more ▼]

SHIP-1 functions as a negative regulator of immune responses by hydrolyzing phosphatidylinositol-3,4,5-triphosphate generated by PI 3-kinase activity. As a result, SHIP-1 deficiency in mice results in myeloproliferation and B cell lymphoma. On the other hand, SHIP-1 deficient mice have a reduced T cell population, but the underlying mechanisms are unknown. In this work, we hypothesized that SHIP-1 plays anti-apoptotic functions in T cells upon stimulation of the death receptor CD95/APO-1/Fas. Using primary T cells from SHIP-1-/- mice and T leukemic cell lines, we report here that SHIP-1 is a potent inhibitor of CD95-induced death. We observed that a small fraction of the SHIP-1 pool is localized to the endoplasmic reticulum where it promotes CD95 glycosylation. This post-translational modification requires an intact SH2 domain of SHIP-1, but is independent of its phosphatase activity. The glycosylated CD95 fails to oligomerize upon stimulation, resulting in impaired DISC formation and downstream apoptotic cascade. These results uncover an unanticipated inhibitory function for SHIP-1 and emphasize the role of glycosylation in the regulation of CD95 signaling in T cells. This work may also provide a new basis for therapeutic strategies using compounds inducing apoptosis through the CD95 pathway on SHIP-1 negative leukemic T cells. [less ▲]

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See detailTNFR-induced activation of MAP3K14/NIK enhances TNFR1-induced cell death
Boutafalla, Layla; Bertrand, Mathieu; Remouchamps, Caroline ULg et al

Conference (2010)

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See detailHow to monitor NF-kappaB activation after photodynamic therapy.
Coupienne, Isabelle ULg; Piette, Jacques ULg; Bontems, Sébastien ULg

in Methods in Molecular Biology (Clifton, N.J.) (2010), 635

The nuclear factor-kappa B (NF-kappaB) is a multipotent factor involved in many cellular processes such as inflammation, immune response and embryonic development and it can be activated by a large number ... [more ▼]

The nuclear factor-kappa B (NF-kappaB) is a multipotent factor involved in many cellular processes such as inflammation, immune response and embryonic development and it can be activated by a large number of stimuli. Consequently, this transcription factor plays a pivotal role in many natural processes but also in different pathologies. For several years, photodynamic therapy (PDT) has emerged as an attractive alternative approach for the treatment of different affections involving various forms of cancer and an increasing number of reports have highlighted the activation of the NF-kappaB following PDT treatment. Furthermore, it has been shown that the mechanism of activation of the NF-kappaB as well as its target genes depends on the nature of the photosensitizers and the cell type used. As this transcription factor is known to be a key regulator of the immune response but also controls cell survival and proliferation, it is important to assess its activation status and its impact on the target genes. In this review, we will present different techniques allowing identification of the activation status of this factor, from the degradation of its inhibitor in the cytoplasm to its ability to induce the expression of a reporter gene under the control of a target promoter. As a working model we will present results obtained from a 5-aminolevulinic acid-PDT treatment on cervix adenocarcinoma cells. [less ▲]

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See detailVaricella-Zoster Virus IE4 Protein Interacts with SR Proteins and Exports mRNAs through the TAP/NXF1 Pathway.
Ote, Isabelle ULg; Lebrun, Murielle ULg; Vandevenne, P. ULg et al

in PLoS ONE (2009), 4(11), 7882

Available data suggest that the Varicella-Zoster virus (VZV) IE4 protein acts as an important regulator on VZV and cellular genes expression and could exert its functions at post-transcriptional level ... [more ▼]

Available data suggest that the Varicella-Zoster virus (VZV) IE4 protein acts as an important regulator on VZV and cellular genes expression and could exert its functions at post-transcriptional level. However, the molecular mechanisms supported by this protein are not yet fully characterized. In the present study, we have attempted to clarify this IE4-mediated gene regulation and identify some cellular partners of IE4. By yeast two-hybrid and immunoprecipitation analysis, we showed that IE4 interacts with three shuttling SR proteins, namely ASF/SF2, 9G8 and SRp20. We positioned the binding domain in the IE4 RbRc region and we showed that these interactions are not bridged by RNA. We demonstrated also that IE4 strongly interacts with the main SR protein kinase, SRPK1, and is phosphorylated in in vitro kinase assay on residue Ser-136 contained in the Rb domain. By Northwestern analysis, we showed that IE4 is able to bind RNA through its arginine-rich region and in immunoprecipitation experiments the presence of RNA stabilizes complexes containing IE4 and the cellular export factors TAP/NXF1 and Aly/REF since the interactions are RNase-sensitive. Finally, we determined that IE4 influences the export of reporter mRNAs and clearly showed, by TAP/NXF1 knockdown, that VZV infection requires the TAP/NXF1 export pathway to express some viral transcripts. We thus highlighted a new example of viral mRNA export factor and proposed a model of IE4-mediated viral mRNAs export. [less ▲]

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See detailRedox regulation of nuclear post-translational modifications during NF-kappaB activation.
Gloire, Geoffrey ULg; Piette, Jacques ULg

in Antioxidants & Redox Signaling (2009)

The transcription factor NF-kappaB controls the expression of hundreds of genes involved in the regulation of the immune/inflammatory response, development, and apoptosis. In resting cells, NF-kappaB ... [more ▼]

The transcription factor NF-kappaB controls the expression of hundreds of genes involved in the regulation of the immune/inflammatory response, development, and apoptosis. In resting cells, NF-kappaB proteins are sequestered in the cytoplasm through their tight association with IkappaB proteins. NF-kappaB activation relies on the signal-induced IkappaB phosphorylation and degradation, thereby allowing the nuclear translocation of NF-kappaB proteins. In the nucleus, several post-translational modifications of NF-kappaB and chromatin remodeling of target genes are mandatory for NF-kappaB DNA binding and full transcription. Since 1991, reactive oxygen species (ROS) have been implicated in NF-kappaB activation. ROS enhance the cytoplasmic signaling pathways leading to NF-kappaB nuclear translocation, but reduction/oxidation (redox) also controls several key steps in the nuclear phase of the NF-kappaB program, including chromatin remodeling, recruitment of co-activators, and DNA binding. Here we describe the redox regulation of NF-kappaB activity in the nucleus. [less ▲]

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See detailEffects of marginal iron overload on iron homeostasis and immune function in alveolar macrophages isolated from pregnant and normal rats.
Ward, Roberta J; Wilmet, Stephanie; Legssyer, Rachida et al

in Biometals (2009), 22(2), 211-23

The effects of changes in macrophage iron status, induced by single or multiple iron injections, iron depletion or pregnancy, on both immune function and mRNA expression of genes involved in iron influx ... [more ▼]

The effects of changes in macrophage iron status, induced by single or multiple iron injections, iron depletion or pregnancy, on both immune function and mRNA expression of genes involved in iron influx and egress have been evaluated. Macrophages isolated from iron deficient rats, or pregnant rats at day 21 of gestation, either supplemented with a single dose of iron dextran, 10 mg, at the commencement of pregnancy, or not, showed significant increases of macrophage ferroportin mRNA expression, which was paralleled by significant decreases in hepatic Hamp mRNA expression. IRP activity in macrophages was not significantly altered by iron status or the inducement of pregnancy +/- a single iron supplement. Macrophage immune function was significantly altered by iron supplementation and pregnancy. Iron supplementation, alone or combined with pregnancy, increased the activities of both NADPH oxidase and nuclear factor kappa B (NFkappaB). In contrast, the imposition of pregnancy reduced the ability of these parameters to respond to an inflammatory stimuli. Increasing iron status, if only marginally, will reduce the ability of macrophages to mount a sustained response to inflammation as well as altering iron homeostatic mechanisms. [less ▲]

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