References of "Piette, Jacques"
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See detailMAGED2 function as cell cycle regulator after a genotoxic stress
Trussart, Charlotte ULiege; Pirlot, Céline; Piette, Jacques ULiege et al

Poster (2017, May 11)

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See detailInvestigation of the glycolytic switch induced by saturated fatty acid in human macrophages
Colonval, Megan ULiege; Fettweis, Grégory; L'homme, Laurent et al

Poster (2017, May)

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See detailIncidence of MAGED2 on cell cycle after a camptothecin treatment
Trussart, Charlotte ULiege; Pirlot, Céline; Piette, Jacques ULiege et al

Poster (2017)

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See detailRIP3 antagonizes a TSC2-mediated pro-survival pathway in glioblastoma cell death.
Fettweis, Grégory ULiege; Di Valentin, Emmanuel ULiege; L'homme, Laurent et al

in Biochimica et Biophysica Acta (2017)

Glioblastomas are the deadliest type of brain cancer and are frequently associated with poor prognosis and a high degree of recurrence despite removal by surgical resection and treatment by chemo- and ... [more ▼]

Glioblastomas are the deadliest type of brain cancer and are frequently associated with poor prognosis and a high degree of recurrence despite removal by surgical resection and treatment by chemo- and radio-therapy. Photodynamic therapy (PDT) is a treatment well known to induce mainly necrotic and apoptotic cell death in solid tumors. 5-Aminolevulinic acid (5-ALA)-based PDT was recently shown to sensitize human glioblastoma cells (LN-18) to a RIP3 (Receptor Interacting Protein 3)-dependent cell death which is counter-acted by activation of autophagy. These promising results led us to investigate the pathways involved in cell death and survival mechanisms occurring in glioblastoma following PDT. In the present study, we describe a new TSC2 (Tuberous Sclerosis 2)-dependent survival pathway implicating MK2 (MAPKAPK2) kinase and 14-3-3 proteins which conducts to the activation of a pro-survival autophagy. Moreover, we characterized a new RIP3/TSC2 complex where RIP3 is suggested to promote cell death by targeting TSC2-dependent survival pathway. These results highlight (i) a new role of TSC2 to protect glioblastoma against PDT-induced cell death and (ii) TSC2 and 14-3-3 as new RIP3 partners. [less ▲]

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See detailInvolvement of membrane remodelling induced by fatty acids in the regulation of the NLRP3 inflammasome activity in human macrophages
Gianfrancesco, Marco ULiege; Dehairs, Jonas; Bloch, Katerzina et al

Poster (2016, September 12)

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See detailc-Jun regulates altered pre-mRNA splicing in response to cisplatin
Deward, Adeline; Gabriel, Maude; Klinck, Roscoe et al

Poster (2016, September 11)

Genotoxic stress is a well-known inducer of pre-mRNa alternative splicing . In this work, we aim at identifying keys componants of the signaling cascade linking the DNA lesion to the splcing machiney.and ... [more ▼]

Genotoxic stress is a well-known inducer of pre-mRNa alternative splicing . In this work, we aim at identifying keys componants of the signaling cascade linking the DNA lesion to the splcing machiney.and thus gain better knowledge od the molecular mechanism controling large scale splcing decision in stress situation. Nous avons établi que C-Jun est important pour l'épissage alternatif de nombreux ARN pré-messagers. [less ▲]

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See detailHuman herpesvirus 8-encoded chemokine vCCL2/vMIP-II is an agonist of the atypical chemokine receptor ACKR3/CXCR7
Szpakowska, Martyna; Dupuis, Nadine ULiege; Baragli, Alessandra et al

in Biochemical Pharmacology (2016), 114

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See detailInvolvement of membrane remodelling induced by fatty acids in the regulation of the NLRP3 inflammasome activity in human macrophages
Gianfrancesco, Marco ULiege; Dehairs, Jonas; Bloch, Katarzyna et al

in Diabetologia (2016, August), 59(Supplement 1), 291

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See detailMelanoma antigen-D2: a nucleolar protein undergoing delocalization during cell cycle and after cellular stress
Pirlot, Céline ULiege; Thiry, Marc ULiege; Trussart, Charlotte ULiege et al

in BBA Molecular Cell Research (2016), 1853(3), 581-595

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See detailNIK promotes tissue destruction independently of the alternative NF-kappaB pathway through TNFR1/RIP1-induced apoptosis.
Boutaffala, L.; Bertrand, M. J. M.; Remouchamps, Caroline ULiege et al

in Cell death and differentiation (2015), 10.1038/cdd.2015.69

NF-kappaB-inducing kinase (NIK) is well-known for its role in promoting p100/NF-kappaB2 processing into p52, a process defined as the alternative, or non-canonical, NF-kappaB pathway. Here we reveal an ... [more ▼]

NF-kappaB-inducing kinase (NIK) is well-known for its role in promoting p100/NF-kappaB2 processing into p52, a process defined as the alternative, or non-canonical, NF-kappaB pathway. Here we reveal an unexpected new role of NIK in TNFR1-mediated RIP1-dependent apoptosis, a consequence of TNFR1 activation observed in c-IAP1/2-depleted conditions. We show that NIK stabilization, obtained by activation of the non-death TNFRs Fn14 or LTbetaR, is required for TNFalpha-mediated apoptosis. These apoptotic stimuli trigger the depletion of c-IAP1/2, the phosphorylation of RIP1 and the RIP1 kinase-dependent assembly of the RIP1/FADD/caspase-8 complex. In the absence of NIK, the phosphorylation of RIP1 and the formation of RIP1/FADD/caspase-8 complex are compromised while c-IAP1/2 depletion is unaffected. In vitro kinase assays revealed that recombinant RIP1 is a bona fide substrate of NIK. In vivo, we demonstrated the requirement of NIK pro-death function, but not the processing of its substrate p100 into p52, in a mouse model of TNFR1/LTbetaR-induced thymus involution. In addition, we also highlight a role for NIK in hepatocyte apoptosis in a mouse model of virus-induced TNFR1/RIP1-dependent liver damage. We conclude that NIK not only contributes to lymphoid organogenesis, inflammation and cell survival but also to TNFR1/RIP1-dependent cell death independently of the alternative NF-kappaB pathway.Cell Death and Differentiation advance online publication, 5 June 2015; doi:10.1038/cdd.2015.69. [less ▲]

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See detailMelanoma antigen D2, a substrate of ATM, is a nucleolar protein that shuttles with cell cycle and cellular stress.
Pirlot, Céline; Thiry, Marc ULiege; Trussart, Charlotte ULiege et al

Poster (2015, November 03)

ATM coordinates numerous facets of the highly regulated DDR network. In order to identify new ATM substrates we have performed a yeast two hybrid experiment with HEAT domains of ATM and an HeLa cDNA ... [more ▼]

ATM coordinates numerous facets of the highly regulated DDR network. In order to identify new ATM substrates we have performed a yeast two hybrid experiment with HEAT domains of ATM and an HeLa cDNA library. Melanoma antigen D2 (MAGED2) was one of the interacting proteins identified in this screen. MAGED2 belongs to the type II Melanoma AntiGEn (MAGE) family. MAGE homology domain, shared by all MAGE proteins, was shown to enhance E3 ligase activity. Actually, little is known about MAGED2 functions. Like every type II MAGE protein, it is expressed in all adult tissues. However, MAGE-D2 has the particularity to be over-expressed in numerous primary cancer and metastasis and it is now recognized as a tumour marker. This over-expression suggests that MAGED2 could be important for the process of cancerisation. MAGED2 was also shown to be a negative regulator of p53, but we did not confirm this property. Proteomic analyses also detected numerous phosphorylated or acetylated residues in response to stress and during cell cycle progression, suggesting a role in cellular signal transduction. We identified the residues targeted by ATM in MAGE-D2 and analysed the localisation of MAGED2 during the interphase and after genotoxic/nucleolar stresses. [less ▲]

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See detailMelanoma AntiGEn D2 : a new nucleolar protein undergoing delocalization during cell cycle and after cellular stress
Pirlot, Céline; Thiry, Marc ULiege; Trussart, Charlotte ULiege et al

Poster (2015, September 28)

MAGED2 belongs to the Melanoma AntiGEn (MAGE) family of proteins. Actually, little is known on MAGED2 function. It contributes to the initiation of melanoma when its overexpression is associated with the ... [more ▼]

MAGED2 belongs to the Melanoma AntiGEn (MAGE) family of proteins. Actually, little is known on MAGED2 function. It contributes to the initiation of melanoma when its overexpression is associated with the mutation of BRAF and it increases apoptosis induced by TRAIL in a p53-dependent manner. MAGED2 was also shown to be a negative regulator of p53, bur we did not confirm this properties. Moreover, proteomic analyses detected numerous phosphorylated or acetylated residues in response to stess and within cell cycle suggesting its involvement in cellular signal transduction. We investigated the intra-cellular re-localization of MAGED2 during cell cycle and after genotixc stress. Both nucleolar and nuclear signals were identifed. [less ▲]

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See detailc-Jun : a new regulatory element for cisplatin induced alternative splicing
Deward, Adeline; Gabriel, Maude; Delforge, Yves et al

Poster (2015, September 28)

DNA damaging agents induce a large scale reorganisation of the proteome through pre messenger alternative splicing. We present evidence that c-Jun is required to induce this altered stress related ... [more ▼]

DNA damaging agents induce a large scale reorganisation of the proteome through pre messenger alternative splicing. We present evidence that c-Jun is required to induce this altered stress related proteome. [less ▲]

Detailed reference viewed: 19 (3 ULiège)
See detailDeciphering the molecular mechanisms underlying NLRP3 inflammasome activation by saturated fatty acids
Gianfrancesco, Marco ULiege; Bloch, Katarzyna; Dehairs, Jonas et al

Poster (2015, September)

Detailed reference viewed: 50 (22 ULiège)
See detailMelanoma AntiGEn D2 (MAGED2): a new nucleolar protein undergoing re-localization after cellular stress
Pirlot, Céline; Thiry, Marc ULiege; Trussart, Charlotte ULiege et al

Poster (2015, February 06)

MAGED2 belongs to the Melanoma AntiGEn (MAGE) family of proteins. Actually, the only known function of this protein is its involvement in the p53 pathway. Indeed, MAGED2 could be a negative regulator of ... [more ▼]

MAGED2 belongs to the Melanoma AntiGEn (MAGE) family of proteins. Actually, the only known function of this protein is its involvement in the p53 pathway. Indeed, MAGED2 could be a negative regulator of p53. It contributes to the initiation of melanoma when its overexpression is associated with the mutation of BRAF and it increases apoptosis induced by TRAIL in a p53 dependent manner. Moreover, phosphoproteomic experiments have shown that this protein is likely phosphorylated by kinases implicated in the DNA damage response (DDR). We decided to investigate the intra-cellular localization of MAGED2 in order to find new functions of this protein. In resting cell, MAGE D2 is detected is the nucleus, the nucleolus and the cytoplasm. We observed that MAGED2 localization change during cell cycle and genotoxic stress. Nuclear and nucleolar localization signals were identified. Though present in the nucleolus, the depletion of MAGED2 does not affect the structure of this organel. [less ▲]

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See detailThe phosphorylation of RelA on Ser547 does not modulate NF-kB activation after TNFa treatment like after a genotoxic stress
Trussart, Charlotte ULiege; Orban, Tanguy ULiege; Di Valentin, Emmanuel ULiege et al

Poster (2015, February 06)

NF-kB controls the expression of hundred of genes involved in inflammatory and innate responses, proliferation, survival, cancer initiation and progression. Numerous post-translational modifications of ... [more ▼]

NF-kB controls the expression of hundred of genes involved in inflammatory and innate responses, proliferation, survival, cancer initiation and progression. Numerous post-translational modifications of p65 modulating NF-kB transcriptional activity are known. We identified Ser547 as a new site of p65 phosphorylation targeted by ATM kinase, which coordinates the “DNA Damage Response” pathway in the event of DNA double-strand breaks. We demonstrated that the phosphorylation of Ser547 regulates the transcription of a sub-set of NF-κB dependent genes after genotoxic stress by modifying HDAC1 recruitment(1). Presently, we are investigating the role of this specific phosphorylation in an inflammatory context. We observe that the mutations of p65 (S547A or S547D) also affect the transcriptional potential of the NF-κB in a promoter specific manner after an exposition to TNFα and H2O2. The study of the molecular mechanism of this regulation after TNFα and H2O2 exposition are both in progress. [less ▲]

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See detailTSC2 and 14-3-3 proteins down-regulate a RIP3 dependent PDT-induced Necroptosis in Glioblastoma
Fettweis, Grégory ULiege; Coupienne, Isabelle; Fillet, Marianne ULiege et al

Poster (2014, October)

Detailed reference viewed: 50 (7 ULiège)