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Université Catholique de Louvain
1.
Gualdron Lopez, Melisa.
Study of the molecular mechanism involved in recycling of matrix protein receptor, PEX5, during glycosome biogenesis in Trypanosoma brucei.
Degree: 2012, Université Catholique de Louvain
URL: http://hdl.handle.net/2078.1/112195 
► Trypanosoma brucei is the parasitic protist that is responsible for human sleeping sickness in Africa, a disease for which no adequate, affordable and harmless treatment…
(more)
▼ Trypanosoma brucei is the parasitic protist that is responsible for human sleeping sickness in Africa, a disease for which no adequate, affordable and harmless treatment is available. The parasite lives as a so-called procyclic-form trypanosome in the midgut of the tsetse fly, the vector that transmits the trypanosomes between people. It has been previously established that glycolysis is essential for the bloodstream form of the parasite, its life-cycle stage in humans, hence representing a promising drug target. Glycolysis in trypanosomatids is compartmentalized in peroxisome-like organelles called glycosomes, a unique feature not found in cells of other eukaryotes. Biogenesis of peroxisomes, organelles found in most eukaryotes, and of glycosomes in trypanosomatids are mediated by homologous proteins called peroxins (acronym PEX). The peroxins of trypanosomes are considered potentially good drug targets not only because glycolysis is essential for the parasites, but also because trypanosomes die when proper compartmentalization of glycolytic enzymes within glycosomes is disrupted.
The import of proteins into the glycosomal matrix involves a cytosolic receptor, PEX5, which recognizes the peroxisomal-targeting signal type 1 (PTS-1) present at the C-terminus of the majority of these proteins. In yeasts and mammalian cells it has previously been shown that the cargo-loaded PEX5 associates with the peroxisomal membrane, delivers its cargo and is then ubiquitinated, a modification that serves as a signal for retrieval of PEX5 from the organelle to be used for further cycles of import (monoubiquitination) or, when recycling is impaired, for its proteasome-dependent degradation (polyubiquitination). We have found stable monoubiquitinated PEX5 in cytosolic fractions of wild-type bloodstream- and procyclic-form T. brucei. This modification appeared to be resistant to DTT, suggesting the conjugation of an ubiquitin moiety to a lysine residue of PEX5. We reason that this modified PEX5 species represents recycled molecules that have been efficiently exported by the recycling peroxin complex and that are in transit to be deubiquitinated, as a physiological step in the receptor cycle. We have identified the T. brucei orthologue of PEX4, the ubiquitin-conjugating (UBC) enzyme responsible for PEX5 monoubiquitination in yeast. This protein is expressed in both bloodstream and procyclic forms and is associated with the cytosolic face of the glycosomal membrane, probably via its interaction with the putative TbPEX22 that we also identified. Creation of a ∆PEX4 procyclic cell line by deletion of both alleles of the TbPEX4 gene enabled us to demonstrate that this peroxin is involved in TbPEX5 monoubiquitination. Surprisingly, after transfection of this mutant with a construct for expression of the Green Fluorescent Protein with a PTS-1 followed by subcellular localization studies by live cell imaging and fluorescence microscopy, only a minor defect in glycosomal matrix protein import was observed. Analysis of the ∆PEX4…
Advisors/Committee Members: UCL - BIFA - Sciences biomédicales et pharmaceutiques, Michels, Paul, Courtoy, Pierre, Decottignies, Anabelle, Collet, Jean-François, Clotman, Frédéric, Erdmann, Ralf, Matthews, Keith.
Subjects/Keywords: Trypanosoma brucei; Glycosome; Peroxin; PEX5; Ubiquitination.
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APA (6th Edition):
Gualdron Lopez, M. (2012). Study of the molecular mechanism involved in recycling of matrix protein receptor, PEX5, during glycosome biogenesis in Trypanosoma brucei. (Thesis). Université Catholique de Louvain. Retrieved from http://hdl.handle.net/2078.1/112195
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Gualdron Lopez, Melisa. “Study of the molecular mechanism involved in recycling of matrix protein receptor, PEX5, during glycosome biogenesis in Trypanosoma brucei.” 2012. Thesis, Université Catholique de Louvain. Accessed April 11, 2021.
http://hdl.handle.net/2078.1/112195.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Gualdron Lopez, Melisa. “Study of the molecular mechanism involved in recycling of matrix protein receptor, PEX5, during glycosome biogenesis in Trypanosoma brucei.” 2012. Web. 11 Apr 2021.
Vancouver:
Gualdron Lopez M. Study of the molecular mechanism involved in recycling of matrix protein receptor, PEX5, during glycosome biogenesis in Trypanosoma brucei. [Internet] [Thesis]. Université Catholique de Louvain; 2012. [cited 2021 Apr 11].
Available from: http://hdl.handle.net/2078.1/112195.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Gualdron Lopez M. Study of the molecular mechanism involved in recycling of matrix protein receptor, PEX5, during glycosome biogenesis in Trypanosoma brucei. [Thesis]. Université Catholique de Louvain; 2012. Available from: http://hdl.handle.net/2078.1/112195
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Université Catholique de Louvain
2.
Mattiussi, Marina.
The odyssey of telomerase in regulating cellular responses to cytokines and reactive oxygen species.
Degree: 2011, Université Catholique de Louvain
URL: http://hdl.handle.net/2078.1/88085
► During the multistep tumorigenic process, cancer cells progressively acquire properties that include an unlimited replicative potential, invasion, sustained proliferative signaling, metastasis and resistance to cell…
(more)
▼ During the multistep tumorigenic process, cancer cells progressively acquire properties that include an unlimited replicative potential, invasion, sustained proliferative signaling, metastasis and resistance to cell death. In addition to its well-established role in telomere synthesis, telomerase was reported to exert non-canonical functions that may promote several abilities of cancer cells, notably by lowering reactive oxygen species (ROS) levels, modulating chromatin properties and acting as transcriptional cofactor in Wnt/β-catenin signaling pathway.
The aim of this thesis was to investigate possible non-canonical functions of telomerase in regulating human fibroblasts responses to cytokines, namely Tumor Necrosis Factor-α (TNF-α) pro-inflammatory cytokine and Transforming Growth Factor-β1 (TGF-β1).
ROS have been involved in a variety of cellular events downstream of TNF-α binding to its receptor, including mitogen-activated protein kinase (MAPK) activation, apoptosis and induction of some -but not all- NF-κB target genes. The previously reported antioxidant properties of telomerase prompted us to test whether telomerase may be able to modulate ROS-dependent and/or -independent cellular responses to TNF-α, a potent inducer of NF-κB pathway. We showed that telomerase overexpression in normal human fibroblasts, strongly repress activation of ERK1/2 mitogen-activated protein kinases and cell death. In contrast, telomerase overexpression did not affect ROS-independent cellular responses to TNF-α, including NF-κB activation, nuclear translocation of phosphorylated NF-κBp65 and TNF-α-induced transcription of various NF-κB target genes. However, telomerase expression considerably repressed TNF-α-induced transcription of the ROS-sensitive NF-κB target gene SOD2 by reducing ROS contribution to SOD2 gene induction, both in normal fibroblasts and in cancer cells. Our results demonstrate that human telomerase represses ROS-dependent intracellular signaling and gene induction in response to TNF-α without affecting NF-κB activation.
Previous studies suggested a possible regulatory role of mouse telomerase on TGF-β signaling pathway. The second aim of this thesis was to investigate whether human telomerase may modulate cellular responses to TGF-β1. We showed that telomerase overexpression in human foreskin fibroblasts does not globally impact on TGF-β signaling as shown by unaltered activation of Smad regulators and similar induction of TGF-β1-target genes. However, telomerase strongly and significantly increased induction of JUNB proto-oncogene transcription in different fibroblast cell lines in response to TGF-β1 treatment. Additional experiments are required to elucidate how human telomerase increase JUNB induction in response to TGF-β1.
In summary, our work provides the first evidences for a role of human telomerase in ROS-dependent transcriptional regulation and MAPK activation and further supports the existence of antioxidant functions of telomerase in mitochondria.
(SBIM 3) – UCL, 2011
Advisors/Committee Members: UCL - SSS/DDUV/DDUV - Institut de Duve, Decottignies, Anabelle, Vikkula, Miikka, Lemaigre, Frédéric, Demoulin, Jean-Baptiste, Michiels, Thomas, Piette, Jacques, Revy, Patrick.
Subjects/Keywords: Telomerase; Reactive oxygen species; TNF-α; NF-κB; TGF-beta
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APA (6th Edition):
Mattiussi, M. (2011). The odyssey of telomerase in regulating cellular responses to cytokines and reactive oxygen species. (Thesis). Université Catholique de Louvain. Retrieved from http://hdl.handle.net/2078.1/88085
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Mattiussi, Marina. “The odyssey of telomerase in regulating cellular responses to cytokines and reactive oxygen species.” 2011. Thesis, Université Catholique de Louvain. Accessed April 11, 2021.
http://hdl.handle.net/2078.1/88085.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Mattiussi, Marina. “The odyssey of telomerase in regulating cellular responses to cytokines and reactive oxygen species.” 2011. Web. 11 Apr 2021.
Vancouver:
Mattiussi M. The odyssey of telomerase in regulating cellular responses to cytokines and reactive oxygen species. [Internet] [Thesis]. Université Catholique de Louvain; 2011. [cited 2021 Apr 11].
Available from: http://hdl.handle.net/2078.1/88085.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Mattiussi M. The odyssey of telomerase in regulating cellular responses to cytokines and reactive oxygen species. [Thesis]. Université Catholique de Louvain; 2011. Available from: http://hdl.handle.net/2078.1/88085
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Université Catholique de Louvain
3.
Campagnolo, Nathalie.
Endoplasmic Reticulum-Associated Degradation of mutated forms of yeast ABC-transporter Pdr5.
Degree: 2011, Université Catholique de Louvain
URL: http://hdl.handle.net/2078.1/86020
► One of the research activity in our laboratory focuses on the quality control and degradation of mutated versions of the yeast plasma membrane ABC-transporter Pdr5.…
(more)
▼ One of the research activity in our laboratory focuses on the quality control and degradation of mutated versions of the yeast plasma membrane ABC-transporter Pdr5. The main objective of the doctoral work was to ascertain the veracity of the ERAD model established with engineered fusion proteins featuring how newly synthesized membrane proteins are targeted for degradation by the proteasome. Depending of the localization of the mutated domain, ER lumen versus the cytosol, the ERAD model predicts that misfolded proteins are degraded via different pathways (Carvalho et al. 2006; Vashist et al. 2001; Vashist and Ng 2004). To ascertain the model, we have contructed 3 protein variants, Pdr5L183P, Pdr5C1427Y and Pdr5L183P+C1427Y. According to the model, Pdr5L183P that is misfolded as the result of a mutation in a cytosolic region should be ubiquitylated by the Ub-ligase Doa10p (ERAD-C pathway) and transported back to the cytosol in a Der1p and Sec61p-independent process. In contrast, Pdr5C1427Y with a misfolded region facing the ER lumen should be ubiquitylated by Hrd1p (ERAD-L pathway) and required Der1p and/or Sec61p for its degradation. Pdr5L183P+C1427Y variant that combines the cytosolic and luminal substitutions should be targeted by the ERAD-C pathway for degradation as this pathway predominates the ERAD-L pathway. The importance of the ER-to-Golgi transport (post-ER quality control) for proteasome-mediated degradation of mutated variants have been also tested. An other objective of this work is the identification of amino-acid determinants in the Pdr5 sequence which trigger the quality control system and subsequent degradation using C-truncated variants.
(AGRO 3) – UCL, 2011
Advisors/Committee Members: UCL - SST/ISV/ISV - Institut des sciences de la vie, Ghislain , Michel, Fastrez, Jacques, Decottignies, Anabelle, Hermand, Damien, Mahillon, Jacques, Vandenbol, Micheline.
Subjects/Keywords: Human disorders; Protein trafficking; Membrane protein; Metabolism and genetic of yeast; Molecular biology; Biochemistry
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APA ·
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APA (6th Edition):
Campagnolo, N. (2011). Endoplasmic Reticulum-Associated Degradation of mutated forms of yeast ABC-transporter Pdr5. (Thesis). Université Catholique de Louvain. Retrieved from http://hdl.handle.net/2078.1/86020
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Campagnolo, Nathalie. “Endoplasmic Reticulum-Associated Degradation of mutated forms of yeast ABC-transporter Pdr5.” 2011. Thesis, Université Catholique de Louvain. Accessed April 11, 2021.
http://hdl.handle.net/2078.1/86020.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Campagnolo, Nathalie. “Endoplasmic Reticulum-Associated Degradation of mutated forms of yeast ABC-transporter Pdr5.” 2011. Web. 11 Apr 2021.
Vancouver:
Campagnolo N. Endoplasmic Reticulum-Associated Degradation of mutated forms of yeast ABC-transporter Pdr5. [Internet] [Thesis]. Université Catholique de Louvain; 2011. [cited 2021 Apr 11].
Available from: http://hdl.handle.net/2078.1/86020.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Campagnolo N. Endoplasmic Reticulum-Associated Degradation of mutated forms of yeast ABC-transporter Pdr5. [Thesis]. Université Catholique de Louvain; 2011. Available from: http://hdl.handle.net/2078.1/86020
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Université Catholique de Louvain
4.
Szczepanowska, Karolina.
A cluster of pathogenic mutations in the 3'-5' exonuclease domain of DNA polymerase gamma defines a novel module coupling DNA synthesis and degradation.
Degree: 2011, Université Catholique de Louvain
URL: http://hdl.handle.net/2078.1/73438
► DNA polymerase gamma (pol g in human, Mip1 in yeast) is the unique DNA replicase found in mitochondria. Pol g plays a key role in…
(more)
▼ DNA polymerase gamma (pol g in human, Mip1 in yeast) is the unique DNA replicase found in mitochondria. Pol g plays a key role in fidelity of mtDNA replication through accurate selection of nucleotides and 3’-5’ exonuclease proofreading activity. Defective maintenance of mtDNA leads to mitochondrial dysfunction and disease. More than 150 POLG mutations have been identified in human.
Based on the good conservation of the pol g catalytic subunits we have used Mip1 as a model enzyme to generate yeast mutations equivalent to seven human pol g mutations associated with PEO, various neuropathies and Alpers syndrome. Five mutations clustered in a novel subdomain of the 3’-5’ exonuclease are localized in the DNA-binding channel.
We have determined the in vivo phenotypes of the yeast mutants and biochemical properties of mutant polymerases. The mip1 mutations increase the frequency of mtDNA point mutations and deletions with generally a good correlation between mtDNA instability in yeast and disease severity in human. Mutations clustered in the novel module result in increased frequency of point mutations and high instability of the mitochondrial DNA in yeast cells, and unexpectedly for mutator mutations, they favour exonucleolysis versus polymerization. This trait is associated with highly decreased DNA binding activity and poorly processive DNA synthesis. Our data show for the first time that a 3’-5’ exonuclease module of DNA polymerase gamma plays a crucial role in the coordination of the polymerase and exonuclease functions and they strongly suggest that in patients the disease is not caused by defective proofreading but results from poor mtDNA replication generated by a severe imbalance between DNA synthesis and degradation.
(AGRO 3) – UCL, 2011
Advisors/Committee Members: UCL - SST/ISV/ISV - Institut des sciences de la vie, Foury, Françoise, Fastrez, Jacques, Salas, Margarita, Decottignies, Anabelle, Van Dyck, Eric, Morsomme, Pierre.
Subjects/Keywords: Mitochondrial DNA polymerase gamma; Mitochondrial disorders; Mutations; Yeast
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APA ·
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APA (6th Edition):
Szczepanowska, K. (2011). A cluster of pathogenic mutations in the 3'-5' exonuclease domain of DNA polymerase gamma defines a novel module coupling DNA synthesis and degradation. (Thesis). Université Catholique de Louvain. Retrieved from http://hdl.handle.net/2078.1/73438
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Szczepanowska, Karolina. “A cluster of pathogenic mutations in the 3'-5' exonuclease domain of DNA polymerase gamma defines a novel module coupling DNA synthesis and degradation.” 2011. Thesis, Université Catholique de Louvain. Accessed April 11, 2021.
http://hdl.handle.net/2078.1/73438.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Szczepanowska, Karolina. “A cluster of pathogenic mutations in the 3'-5' exonuclease domain of DNA polymerase gamma defines a novel module coupling DNA synthesis and degradation.” 2011. Web. 11 Apr 2021.
Vancouver:
Szczepanowska K. A cluster of pathogenic mutations in the 3'-5' exonuclease domain of DNA polymerase gamma defines a novel module coupling DNA synthesis and degradation. [Internet] [Thesis]. Université Catholique de Louvain; 2011. [cited 2021 Apr 11].
Available from: http://hdl.handle.net/2078.1/73438.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Szczepanowska K. A cluster of pathogenic mutations in the 3'-5' exonuclease domain of DNA polymerase gamma defines a novel module coupling DNA synthesis and degradation. [Thesis]. Université Catholique de Louvain; 2011. Available from: http://hdl.handle.net/2078.1/73438
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Université Catholique de Louvain
5.
Aboubakar Nana, Frank.
Role of Focal Adhesion Kinase in the invasive phenotype of small-cell lung cancer.
Degree: 2020, Université Catholique de Louvain
URL: http://hdl.handle.net/2078.1/232632
► Small-cell lung cancer (SCLC) is a devastating illness with frequent metastases and poor survival. The molecular steps leading to SCLC development and progression are still…
(more)
▼ Small-cell lung cancer (SCLC) is a devastating illness with frequent metastases and poor survival. The molecular steps leading to SCLC development and progression are still poorly understood and this has translated into the absence of effective targeted therapies and a five-year overall survival as low as 5%. Focal Adhesion Kinase (FAK) is a non-receptor tyrosine kinase localized at sites of focal adhesions and playing an important role in signal transduction pathways initiated by integrins and G-protein-coupled-receptors. It is overexpressed in many cancers and contributes to cancer progression through a central role in cell adhesion, migration, invasion, survival, and growth, which are highly relevant in SCLC, known to be very aggressive. Since FAK has been poorly studied in SCLC, we decided to investigate it at the functional level in this cancer. We found that FAK was strongly expressed and activated in primary SCLC tumors compared to non-small-cell lung cancer and normal lung. Moreover, inhibition of FAK activity in SCLC cell lines where FAK is overexpressed and constitutively activated decreased FAK phosphorylation (Tyr397) and resulted in antitumoral effects. Inhibition of FAK activity significantly decreased cell proliferation, induced cell cycle arrest in G2/M phases, decreased DNA synthesis, increased apoptosis, and decreased motility as well as invasion in SCLC cell lines. Altogether, this work demonstrates that FAK activation plays a key role in the invasive behaviour of SCLC and suggests that FAK-targeted therapeutic strategies should be evaluated in clinical trials with the hope of reducing mortality from SCLC.
(BIFA - Sciences biomédicales et pharmaceutiques) – UCL, 2020
Advisors/Committee Members: UCL - SSS/IREC/PNEU - Pôle de Pneumologie, ORL et Dermatologie, UCL - Faculté de pharmacie et des sciences biomédicales, Ocak, Sebahat, Pilette, Charles, Decottignies, Anabelle, Vermaelen, Karim, Feron, Olivier, Planchard, David, Machiels, Jean-Pascal.
Subjects/Keywords: SCLC; FAK; Targeted therapy; FAK tyrosine kinase inhibitor; Oncogenic driver
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APA (6th Edition):
Aboubakar Nana, F. (2020). Role of Focal Adhesion Kinase in the invasive phenotype of small-cell lung cancer. (Thesis). Université Catholique de Louvain. Retrieved from http://hdl.handle.net/2078.1/232632
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Aboubakar Nana, Frank. “Role of Focal Adhesion Kinase in the invasive phenotype of small-cell lung cancer.” 2020. Thesis, Université Catholique de Louvain. Accessed April 11, 2021.
http://hdl.handle.net/2078.1/232632.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Aboubakar Nana, Frank. “Role of Focal Adhesion Kinase in the invasive phenotype of small-cell lung cancer.” 2020. Web. 11 Apr 2021.
Vancouver:
Aboubakar Nana F. Role of Focal Adhesion Kinase in the invasive phenotype of small-cell lung cancer. [Internet] [Thesis]. Université Catholique de Louvain; 2020. [cited 2021 Apr 11].
Available from: http://hdl.handle.net/2078.1/232632.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Aboubakar Nana F. Role of Focal Adhesion Kinase in the invasive phenotype of small-cell lung cancer. [Thesis]. Université Catholique de Louvain; 2020. Available from: http://hdl.handle.net/2078.1/232632
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Université Catholique de Louvain
6.
Beyaert, Maxime.
ATR signalling after DNA damage : from the discovery of a new target to the reevaluation of its function in primary chronic lymphocytic leukaemia cells.
Degree: 2017, Université Catholique de Louvain
URL: http://hdl.handle.net/2078.1/187734
► Deoxycytidine kinase (dCK) catalyses the first and rate limiting step of the deoxynucleoside salvage pathway that supplies cells with dNTPs for DNA synthesis. dCK is…
(more)
▼ Deoxycytidine kinase (dCK) catalyses the first and rate limiting step of the deoxynucleoside salvage pathway that supplies cells with dNTPs for DNA synthesis. dCK is also required for the activation of several antiviral and anticancer nucleoside analogues and plays a crucial role in their therapeutic efficacy. Given these important functions, deciphering the mechanisms that control dCK activity is of major interest for both fundamental scientists and clinician researchers. Our group demonstrated that dCK is a phosphoprotein whose activity is increased by phosphorylation of the Ser-74 residue. Moreover, it was established that increase in dCK activity in response to several genotoxic treatments, including ionizing radiation (IR), UV-C, chemotherapeutic nucleoside analogues and DNA polymerase inhibitors, was related to an increase in Ser-74 phosphorylation. These observations suggested that Ser-74 could be phosphorylated by a DNA damage-activated protein kinase, possibly ATM, ATR or DNA-PK. Two different groups identified ATM, a transducer of the DNA damage response (DDR), as the protein kinase responsible for Ser-74 phosphorylation and dCK activation following ionizing radiation (IR), a DNA double-strand break (DSB) inducer. The first objective of this thesis consisted in investigating whether ATM was also involved in dCK activation in response to other types of DNA damage, such as induced by UV-C light that causes replication stress and induces single-stranded DNA (ssDNA). Using ATM-deficient lymphoblastoid cell lines, a selective ATM inhibitor or ATM siRNA, we demonstrated that ATM was not involved in dCK activation induced by UV-C, aphidicolin or cladribine. Surprisingly, we also found that ATM was not essential for dCK activation following IR, contrary to what was stated in the literature. On the other hand, a selective inhibitor of ATR, the kinase that is activated in response to ssDNA, as well as ATR siRNA prevented dCK activation by these agents, though not IR, and also reduced basal dCK activity. Further analyses, including time-course experiments, revealed that ATR, which is also activated after IR at later time points, was responsible for IR-induced dCK activation in cells in which ATM was deficient or inhibited. We concluded that ATR controls basal dCK activity and dCK activation in response to agents that induce ssDNA and that ATM activates dCK in response to agents that induce DSBs. However, as the repair of DSBs includes a resection step that induces the formation of ssDNA and thus activates ATR, ATR can activate dCK independent of ATM in IR-treated ATM-deficient or -inhibited cells.
(BIFA - Sciences biomédicales et pharmaceutiques) – UCL, 2017
Advisors/Committee Members: UCL - SSS/DDUV/BCHM - Biochimie-Recherche métabolique, UCL - Faculté de pharmacie et des sciences biomédicales, Decottignies, Anabelle, Bontemps, Françoise, Van Den Neste, Eric, Rider, Mark, Bommer, Guido, Grégoire, Vincent, Vincent, Marie-Françoise, Habraken, Yvette, Stankovic, Tatjana.
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APA ·
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MLA ·
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to Zotero / EndNote / Reference
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APA (6th Edition):
Beyaert, M. (2017). ATR signalling after DNA damage : from the discovery of a new target to the reevaluation of its function in primary chronic lymphocytic leukaemia cells. (Thesis). Université Catholique de Louvain. Retrieved from http://hdl.handle.net/2078.1/187734
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Beyaert, Maxime. “ATR signalling after DNA damage : from the discovery of a new target to the reevaluation of its function in primary chronic lymphocytic leukaemia cells.” 2017. Thesis, Université Catholique de Louvain. Accessed April 11, 2021.
http://hdl.handle.net/2078.1/187734.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Beyaert, Maxime. “ATR signalling after DNA damage : from the discovery of a new target to the reevaluation of its function in primary chronic lymphocytic leukaemia cells.” 2017. Web. 11 Apr 2021.
Vancouver:
Beyaert M. ATR signalling after DNA damage : from the discovery of a new target to the reevaluation of its function in primary chronic lymphocytic leukaemia cells. [Internet] [Thesis]. Université Catholique de Louvain; 2017. [cited 2021 Apr 11].
Available from: http://hdl.handle.net/2078.1/187734.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Beyaert M. ATR signalling after DNA damage : from the discovery of a new target to the reevaluation of its function in primary chronic lymphocytic leukaemia cells. [Thesis]. Université Catholique de Louvain; 2017. Available from: http://hdl.handle.net/2078.1/187734
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Université Catholique de Louvain
7.
Van Tongelen, Aurélie.
Identification of a novel cancer-germline transcript within the miRNA harboring GABRA3 gene : epigenetic alterations of the locus in tumors.
Degree: 2017, Université Catholique de Louvain
URL: http://hdl.handle.net/2078.1/184987
► It is now well established that alterations in DNA methylation patterns contribute to tumor development. Both gains (DNA hypermethylation) and losses (DNA hypomethylation) of this…
(more)
▼ It is now well established that alterations in DNA methylation patterns contribute to tumor development. Both gains (DNA hypermethylation) and losses (DNA hypomethylation) of this repressive mark are observed in tumors. Our group demonstrated that DNA hypomethylation in tumors induces transcriptional activation of a defined group of genes, which normally show specific expression in the germline. These genes were grouped under the term "cancer-germline" genes (CG genes). The main goal of the laboratory is to characterize the epigenetic regulation and functional roles of CG genes. Our work focused on the GABRA3 gene locus, where we discovered the existence of two overlapping transcripts: BT-GABRA3, which is expressed specifically in brain and testis; and CT-GABRA3, starting ~250 kb upstream, which is expressed exclusively in testis. CT-GABRA3 (but not BT-GABRA3) exhibits typical features of a CG gene, as it shows promoter hypomethylation and transcriptional activation in various tumors. CT-GABRA3 carries a clustered pair of miRNAs (miR-105 and miR-767), which show concurrent expression in tumors. Interestingly, an independent group identified miR-105 as a crucial promoter of cancer metastasis, due to its ability to weaken vascular endothelial barriers following exosomal secretion. On the other hand, we demonstrated that miR-767 inhibits expression of TET1, a gene with tumor suppressive functions involved in epigenetic processes of DNA demodification. Moreover, our studies revealed that CT-GABRA3 hypomethylation/activation in tumors is correlated with hypermethylation of the downstream BT-GABRA3 promoter. The mechanism underlying this interdependent epigenetic alteration appears to involve deposition of the histone mark H3K36me3 on the entire CT-GABRA3 transcribed region, which includes the BT-GABRA3 promoter. Finally, we observed that in tumor cells where the BT-GABRA3 promoter is hypermethylated, the gene becomes sensitive to DNA demethylation, suggesting a process of epigenetic switch. Together our work revealed the existence of a novel miRNA-producing CG gene with oncogenic potential. It also uncovered a unusual mechanism of epigenetic alteration in tumors, whereby DNA hypomethylation and hypermethylation are linked via a process of transcriptional overlap.
(BIFA - Sciences biomédicales et pharmaceutiques) – UCL, 2017
Advisors/Committee Members: UCL - SSS/DDUV/GEPI - Epigénétique, UCL - Faculté de pharmacie et des sciences biomédicales, De Smet, Charles, Loriot, Axelle, Lemaigre, Frédéric, Arimodo, Paola, Arnaud, Philippe, Decottignies, Anabelle, Jacquemin, Patrick, Bommer, Guido.
Subjects/Keywords: DNA methylation; Hydroxymethylation; miRNA; Cancer; Epigenetics; GABRA3; Crispr/cas9; Cancer-germline genes; TET; Hypomethylation
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APA (6th Edition):
Van Tongelen, A. (2017). Identification of a novel cancer-germline transcript within the miRNA harboring GABRA3 gene : epigenetic alterations of the locus in tumors. (Thesis). Université Catholique de Louvain. Retrieved from http://hdl.handle.net/2078.1/184987
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Van Tongelen, Aurélie. “Identification of a novel cancer-germline transcript within the miRNA harboring GABRA3 gene : epigenetic alterations of the locus in tumors.” 2017. Thesis, Université Catholique de Louvain. Accessed April 11, 2021.
http://hdl.handle.net/2078.1/184987.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Van Tongelen, Aurélie. “Identification of a novel cancer-germline transcript within the miRNA harboring GABRA3 gene : epigenetic alterations of the locus in tumors.” 2017. Web. 11 Apr 2021.
Vancouver:
Van Tongelen A. Identification of a novel cancer-germline transcript within the miRNA harboring GABRA3 gene : epigenetic alterations of the locus in tumors. [Internet] [Thesis]. Université Catholique de Louvain; 2017. [cited 2021 Apr 11].
Available from: http://hdl.handle.net/2078.1/184987.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Van Tongelen A. Identification of a novel cancer-germline transcript within the miRNA harboring GABRA3 gene : epigenetic alterations of the locus in tumors. [Thesis]. Université Catholique de Louvain; 2017. Available from: http://hdl.handle.net/2078.1/184987
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Université Catholique de Louvain
8.
Arts, Nathalie.
Microenvironnement inflammatoire et échappement à la réponse immunitaire anti-tumorale : le microARN-155 réprime l’expression de MITF-M dans les mélanomes.
Degree: 2014, Université Catholique de Louvain
URL: http://hdl.handle.net/2078.1/153457
► Gene MITF (Microphtalmia-associated transcription factor) generates several transcripts and proteins through the use of different promoters. The MITF-M isoform is expressed exclusively in melanocytes and…
(more)
▼ Gene MITF (Microphtalmia-associated transcription factor) generates several transcripts and proteins through the use of different promoters. The MITF-M isoform is expressed exclusively in melanocytes and is a key transcription factor that regulates, among others, many genes involved in differentiation. Indeed, MITF-M induces the expression of differentiation genes like TYR (tyrosinase), MLANA (Melan-A/Mart-1) or SILV (pMel17/gp100). In melanoma cells, the expression of these genes produce antigens that can be recognized at the surface of the tumor cells by specific CTLs (Cytolytic T Lymphocytes) able to induce the death of these cells. In the course of our study, we demonstrated that an inflammatory environment characterized by the presence of IL-1ß (Interleukin-1ß) reduced the expression of differentiation antigens consecutive to a reduction of MITF-M expression. We showed that this repression reduced the recognition of melanoma cells by CTLs directed against melanocytic differentiation antigens. We also found that this process was JNK (c-Jun N-terminal Kinase) and NF-κB (Nuclear Factor-κB) dependent. The study of the mechanisms involved in this repression of MITF-M expression induced by IL-1ß allowed us to show that the classical MITF-M promoter did not seem to be involved. However, transcriptional repression seemed to occur on a sequence of the MITF gene that differs from the classical promoter and that we were unable to identify. Following this, we found that the microRNA-155 known to be induced by NF-κB has a role in this process. Indeed, we observed that the downregulation of MITF-M was paralleled by an upregulation of miR-155 in 4 melanoma cell lines treated with IL-1ß. On the other hand, the expression of miR-155 was not induced by IL-1ß in 3 melanoma cell lines which did not show any downregulation of MITF-M. We confirmed the role of miR-155 in the IL-1ß induced repression of MITF-M by using a miR-155 specific inhibitor. Finally, in a mouse model of melanoma, we observed a strong negative correlation between the expression levels of MITF-M and tyrosinase on one hand, and miR-155 and IL-1ß on the other hand. To conclude, our results allowed us to identify a new mechanism developed by tumor cells to escape the immune response in an inflammatory environment. We demonstrated for the first time that miR-155 was able to repress the expression of MITF-M in melanoma cells. Therefore, the inhibition of miR-155 could be a new therapeutic approach to improve the classical immmunotherapy or chimiotherapy of human melanomas.
(BIFA - Sciences biomédicales et pharmaceutiques) – UCL, 2014
Advisors/Committee Members: UCL - SSS/DDUV - Institut de Duve, UCL - Faculté de pharmacie et des sciences biomédicales, Lison, Dominique, De Plaen, Etienne, Decottignies, Anabelle, De Smet, Charles, Jacquemin, Patrick, Larue, Lionel, Marine, Jean-Christophe.
Subjects/Keywords: MITF; MicroRNA-155; Inflammation; Differentiation antigens; Melanoma; Interleukin-1
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Arts, N. (2014). Microenvironnement inflammatoire et échappement à la réponse immunitaire anti-tumorale : le microARN-155 réprime l’expression de MITF-M dans les mélanomes. (Thesis). Université Catholique de Louvain. Retrieved from http://hdl.handle.net/2078.1/153457
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Arts, Nathalie. “Microenvironnement inflammatoire et échappement à la réponse immunitaire anti-tumorale : le microARN-155 réprime l’expression de MITF-M dans les mélanomes.” 2014. Thesis, Université Catholique de Louvain. Accessed April 11, 2021.
http://hdl.handle.net/2078.1/153457.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Arts, Nathalie. “Microenvironnement inflammatoire et échappement à la réponse immunitaire anti-tumorale : le microARN-155 réprime l’expression de MITF-M dans les mélanomes.” 2014. Web. 11 Apr 2021.
Vancouver:
Arts N. Microenvironnement inflammatoire et échappement à la réponse immunitaire anti-tumorale : le microARN-155 réprime l’expression de MITF-M dans les mélanomes. [Internet] [Thesis]. Université Catholique de Louvain; 2014. [cited 2021 Apr 11].
Available from: http://hdl.handle.net/2078.1/153457.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Arts N. Microenvironnement inflammatoire et échappement à la réponse immunitaire anti-tumorale : le microARN-155 réprime l’expression de MITF-M dans les mélanomes. [Thesis]. Université Catholique de Louvain; 2014. Available from: http://hdl.handle.net/2078.1/153457
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Université Catholique de Louvain
9.
Onselaer, Marie-Blanche.
L'AMPKalpha1 régule la polymérisation de l'actine, la formation des lamellipodes et la rétraction du clou plaquettaire en réponse à la thrombine.
Degree: 2014, Université Catholique de Louvain
URL: http://hdl.handle.net/2078.1/153270
► Platelet activation requires sweeping morphological changes, supported by contraction and remodelling of platelet actin cytoskeleton. In epithelial and endothelial cells, AMP-activated protein kinase (AMPK) controls…
(more)
▼ Platelet activation requires sweeping morphological changes, supported by contraction and remodelling of platelet actin cytoskeleton. In epithelial and endothelial cells, AMP-activated protein kinase (AMPK) controls actin cytoskeleton organization through the phosphorylation of cytoskeletal targets, namely myosin regulatory light chains (MLC), cofilin and the vasodilator-stimulated phosphoprotein (VASP), extending the role of AMPK beyond metabolism. In this thesis, we hypothesized that AMPK was activated in thrombin-stimulated platelets and played a role in platelet secretion, aggregation and clot retraction, by regulating polymerization and/or organization of actin cytoskeleton through the phosphorylation of MLC, cofilin and VASP. We show that human platelets expressed exclusively the AMPKα1 isoform. In human purified platelets, thrombin led to a transient activation of AMPKα1 and to phosphorylation of its substrate acetyl coA carboxylase (ACC). Platelets isolated from mice lacking AMPKα1 exhibited reduced aggregation and secretion in response to thrombin, associated with a defect in ACC, MLC, cofilin and VASP phosphorylation. These changes were associated with an abrogation of thrombin-dependent F-actin formation. Moreover, the percentage of platelets able to form lamellipodia after immobilization on fibrinogen-coated coverslips and stimulation by thrombin, was significantly reduced in the absence of AMPKα1, indicating an altered cytoskeleton reorganization during spreading. More importantly, clot retraction was slower and less effective in KO platelets. Conclusion: AMPKα1 plays a critical role in platelet function in response to thrombin through the phosphorylation of cytoskeletal targets and the subsequent regulation of cytoskeleton organization -dependent processes. This conclusion is supported by clinical data showing that AMPK is also activated in vivo, in platelets of patients undergoing cardiac surgery and therefore submitted to a thrombotic process designed to counter bleeding.
(BIFA - Sciences biomédicales et pharmaceutiques) – UCL, 2014
Advisors/Committee Members: UCL - SSS/IREC/CARD - Pôle de recherche cardiovasculaire, UCL - Faculté de pharmacie et des sciences biomédicales, Horman, Sandrine, Beauloye, Christophe, Decottignies, Anabelle, Constantinescu, Stefan, Hermans, Cédric, Rider, Mark, Vanoverschelde, Jean-Louis, Oury, Cécile, Bachelot-loza, Christilla.
Subjects/Keywords: AMP-activated protein kinase; PAR-récepteur; Rho-GTPase; Thrombose; Cytosquelettte d'actine; Hémostase; Lamellipode; Calcium; Plaquette; AMPK; Thrombine; CaMKKbeta
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Onselaer, M. (2014). L'AMPKalpha1 régule la polymérisation de l'actine, la formation des lamellipodes et la rétraction du clou plaquettaire en réponse à la thrombine. (Thesis). Université Catholique de Louvain. Retrieved from http://hdl.handle.net/2078.1/153270
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Onselaer, Marie-Blanche. “L'AMPKalpha1 régule la polymérisation de l'actine, la formation des lamellipodes et la rétraction du clou plaquettaire en réponse à la thrombine.” 2014. Thesis, Université Catholique de Louvain. Accessed April 11, 2021.
http://hdl.handle.net/2078.1/153270.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Onselaer, Marie-Blanche. “L'AMPKalpha1 régule la polymérisation de l'actine, la formation des lamellipodes et la rétraction du clou plaquettaire en réponse à la thrombine.” 2014. Web. 11 Apr 2021.
Vancouver:
Onselaer M. L'AMPKalpha1 régule la polymérisation de l'actine, la formation des lamellipodes et la rétraction du clou plaquettaire en réponse à la thrombine. [Internet] [Thesis]. Université Catholique de Louvain; 2014. [cited 2021 Apr 11].
Available from: http://hdl.handle.net/2078.1/153270.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Onselaer M. L'AMPKalpha1 régule la polymérisation de l'actine, la formation des lamellipodes et la rétraction du clou plaquettaire en réponse à la thrombine. [Thesis]. Université Catholique de Louvain; 2014. Available from: http://hdl.handle.net/2078.1/153270
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Université Catholique de Louvain
10.
Amsaïlale, Rachid.
New insights into the regulation of deoxycytidine kinase activity via Ser-74 phosphorylation : toward improved activation of anticancer nucleoside analogs.
Degree: 2014, Université Catholique de Louvain
URL: http://hdl.handle.net/2078.1/144335
► Deoxycytidine kinase (dCK) catalyzes the phosphorylation of deoxycytidine, deoxyadenosine and deoxyguanosine, which constitutes the first and rate-limiting step in the synthesis of DNA precursors by…
(more)
▼ Deoxycytidine kinase (dCK) catalyzes the phosphorylation of deoxycytidine, deoxyadenosine and deoxyguanosine, which constitutes the first and rate-limiting step in the synthesis of DNA precursors by the deoxynucleoside salvage pathway. In addition, dCK phosphorylates and activates numerous chemotherapeutic nucleoside analogs. As low dCK activity is often associated with reduced nucleoside analog efficacy, it is of particular interest to gain more insights into the mechanisms that regulate its activity. Prior to this thesis project, research conducted in our laboratory had demonstrated that dCK activity is regulated by post-translational modification, and more precisely that its activity can be increased in vivo through Ser-74 phosphorylation, a finding that could be exploited to improve therapeutic efficacy of nucleoside analogs. The first objective of this thesis was to investigate the impact of Ser-74 phosphorylation on nucleoside analog activation and efficacy in cancer cells. We started by a kinetic study using recombinant dCK in which Ser-74 phosphorylation was mimicked by a S74E mutation. Although it was well demonstrated that S74E mutation increases dCK activity toward deoxycytidine and pyrimidine analogs, such as gemcitabine, its effect toward purine analogs had not yet been investigated. We found that S74E mutation enhanced the catalytic activity (Kcat) of dCK toward cladribine and clofarabine, but not fludarabine, with ATP or UTP as phosphoryl donor. However, Km values were also increased so that the catalytic efficiencies (Kcat/Km) of dCK for cladribine and clofarabine were not, or only slightly increased, and even decreased for fludarabine. In addition, increase of endogenous dCK activity, which was easily detected with deoxycytidine or gemcitabine as substrates after in vivo-induced increase of Ser-74 phosphorylation, was not observed with deoxyadenosine or purine analogs. Accordingly, treatment of CLL (chronic lymphocytic leukemia) cells with aphidicolin, which induces dCK activation through Ser-74 phosphorylation, did not enhance the conversion of cladribine or fludarabine into their active triphosphate form. Nevertheless, the same treatment induced higher activation of gemcitabine in CLL as well as in colon cancer cells and produced synergic cytotoxicity. From this study, it was concluded that increasing phosphorylation of dCK on Ser-74 might constitute a valuable strategy to enhance the clinical efficacy of particular nucleoside analogs, like gemcitabine. The second objective of my PhD work was to identify the protein phosphatase (PP) responsible for Ser-74 dephosphorylation. Studies in intact cells with cell-permeable PP inhibitors suggested that this PP could be the phosphoprotein phosphatase 2A (PP2A). Investigation of the dephosphorylation of dCK by purified PP as well as experiments performed in whole or PP2A-immunodepleted cell lysates confirmed this hypothesis. Use of siRNA allowed definitively concluding that PP2A constitutively dephosphorylates dCK at Ser-74 and negatively regulates dCK…
Advisors/Committee Members: UCL - SSS/DDUV - Institut de Duve, UCL - Faculté de pharmacie et des sciences biomédicales, Bontemps, Françoise, Decottignies, Anabelle, Bertrand, Luc, Rider, Mark, Balzarini, Jan, Janssens, Veerle, Van Den Neste, Eric.
Subjects/Keywords: Deoxycytidine kinase; Ser-74 phosphorylation; Nucleoside analogs; CLL; Ser/Thr protein phosphatase; Protein phosphatase 2A
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❌
APA ·
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MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Amsaïlale, R. (2014). New insights into the regulation of deoxycytidine kinase activity via Ser-74 phosphorylation : toward improved activation of anticancer nucleoside analogs. (Thesis). Université Catholique de Louvain. Retrieved from http://hdl.handle.net/2078.1/144335
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Amsaïlale, Rachid. “New insights into the regulation of deoxycytidine kinase activity via Ser-74 phosphorylation : toward improved activation of anticancer nucleoside analogs.” 2014. Thesis, Université Catholique de Louvain. Accessed April 11, 2021.
http://hdl.handle.net/2078.1/144335.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Amsaïlale, Rachid. “New insights into the regulation of deoxycytidine kinase activity via Ser-74 phosphorylation : toward improved activation of anticancer nucleoside analogs.” 2014. Web. 11 Apr 2021.
Vancouver:
Amsaïlale R. New insights into the regulation of deoxycytidine kinase activity via Ser-74 phosphorylation : toward improved activation of anticancer nucleoside analogs. [Internet] [Thesis]. Université Catholique de Louvain; 2014. [cited 2021 Apr 11].
Available from: http://hdl.handle.net/2078.1/144335.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Amsaïlale R. New insights into the regulation of deoxycytidine kinase activity via Ser-74 phosphorylation : toward improved activation of anticancer nucleoside analogs. [Thesis]. Université Catholique de Louvain; 2014. Available from: http://hdl.handle.net/2078.1/144335
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Université Catholique de Louvain
11.
Delhaye, Antoine.
Old dog, new tricks : how the Cpx stress response monitors multiple essential envelope biogenesis processes in E. coli.
Degree: 2019, Université Catholique de Louvain
URL: http://hdl.handle.net/2078.1/220309
► The envelope of Gram-negative bacteria is a complex compartment that is essential for viability. To ensure survival of the bacterial cells in fluctuating environments, several…
(more)
▼ The envelope of Gram-negative bacteria is a complex compartment that is essential for viability. To ensure survival of the bacterial cells in fluctuating environments, several signal transduction systems, called envelope stress response systems (ESRSs), exist to monitor envelope biogenesis and homeostasis. We show that the Cpx two-component system, an extensively studied ESRS of E. coli, can monitor two essential envelope processes: cell wall synthesis and lipoprotein trafficking. We first show that Cpx is activated when peptidoglycan (PG) integrity is challenged and that this activation provides protection to cells exposed to antibiotics inhibiting PG synthesis. We also found evidence that an outer membrane lipoprotein, NlpE is used by Cpx to detect perturbations in lipoprotein trafficking. The activation of Cpx by NlpE improves fitness in these nefarious conditions.
(BIFA - Sciences biomédicales et pharmaceutiques) – UCL, 2019
Advisors/Committee Members: UCL - SSS/DDUV/BCHM - Biochimie-Recherche métabolique, UCL - Faculté de pharmacie et des sciences biomédicales, Tyteca, Donatienne, Decottignies, Anabelle, Collet, Jean-François, Laloux, Géraldine, Ruiz, Natividad, Polissi, Alessandra, Van Melderen, Laurence.
Subjects/Keywords: E. coli; Stress response; Two-component; Bacteria; Signal transduction; Envelope stress; Lipoprotein; Stress; Petidoglycan; Cpx; Envelope; Nlpe; Beta-lactam; Trafficking; ESRS
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Delhaye, A. (2019). Old dog, new tricks : how the Cpx stress response monitors multiple essential envelope biogenesis processes in E. coli. (Thesis). Université Catholique de Louvain. Retrieved from http://hdl.handle.net/2078.1/220309
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Delhaye, Antoine. “Old dog, new tricks : how the Cpx stress response monitors multiple essential envelope biogenesis processes in E. coli.” 2019. Thesis, Université Catholique de Louvain. Accessed April 11, 2021.
http://hdl.handle.net/2078.1/220309.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Delhaye, Antoine. “Old dog, new tricks : how the Cpx stress response monitors multiple essential envelope biogenesis processes in E. coli.” 2019. Web. 11 Apr 2021.
Vancouver:
Delhaye A. Old dog, new tricks : how the Cpx stress response monitors multiple essential envelope biogenesis processes in E. coli. [Internet] [Thesis]. Université Catholique de Louvain; 2019. [cited 2021 Apr 11].
Available from: http://hdl.handle.net/2078.1/220309.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Delhaye A. Old dog, new tricks : how the Cpx stress response monitors multiple essential envelope biogenesis processes in E. coli. [Thesis]. Université Catholique de Louvain; 2019. Available from: http://hdl.handle.net/2078.1/220309
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Université Catholique de Louvain
12.
Hochstenbach, Jean-François.
The yeast proteolipid Pmp3p is a new component of the plasma membrane microdomains associated with the eisosomes.
Degree: 2010, Université Catholique de Louvain
URL: http://hdl.handle.net/2078.1/32235
► Many prokaryotic and eukaryotic organisms possess small molecular weight hydrophobic proteins that respond differently to stresses, such as cold temperature, salt and dehydration. Yeast plasma…
(more)
▼ Many prokaryotic and eukaryotic organisms possess small molecular weight hydrophobic proteins that respond differently to stresses, such as cold temperature, salt and dehydration. Yeast plasma membranes contain a small 55 amino acid hydrophobic polypeptide, Pmp3p/Sna1p, which belongs to the SNA (Sensitive to Na) proteins family and has three close homologues, called Sna2p, Sna3p and Sna4p. Previous work showed that the PMP3 deletion increases the plasma membrane potential and confers sensitivity to cytotoxic cations.
In this study we present a further characterization of the molecular function of Pmp3p. We observed that Pmp3p physically interacts with Pil1p, a component of the eisosomes which are structures associated with some plasma membrane microdomains. We confirmed the localization of Pmp3p in these microdomains via indirect immunofluorescence. Using different techniques in molecular biology, biochemistry, cell biology and proteomics, we showed that Pmp3p could protect some transporters against endocytosis and link this process to cation homeostasis. Finally, a site-directed mutagenesis approach revealed that at least 9 conserved residues (F14, P17, G25, D29, L36, L39, P43, A48, Y50) are important for the function of Pmp3p.
(AGRO 3) – UCL, 2010
Advisors/Committee Members: UCL - AGRO - Sciences agronomiques et ingénierie biologique, Morsomme, Pierre, Mahillon, Jacques, Goffeau, André, Decottignies, Anabelle, Soumillion, Patrice, Sychrova, Hana.
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Hochstenbach, J. (2010). The yeast proteolipid Pmp3p is a new component of the plasma membrane microdomains associated with the eisosomes. (Thesis). Université Catholique de Louvain. Retrieved from http://hdl.handle.net/2078.1/32235
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Hochstenbach, Jean-François. “The yeast proteolipid Pmp3p is a new component of the plasma membrane microdomains associated with the eisosomes.” 2010. Thesis, Université Catholique de Louvain. Accessed April 11, 2021.
http://hdl.handle.net/2078.1/32235.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Hochstenbach, Jean-François. “The yeast proteolipid Pmp3p is a new component of the plasma membrane microdomains associated with the eisosomes.” 2010. Web. 11 Apr 2021.
Vancouver:
Hochstenbach J. The yeast proteolipid Pmp3p is a new component of the plasma membrane microdomains associated with the eisosomes. [Internet] [Thesis]. Université Catholique de Louvain; 2010. [cited 2021 Apr 11].
Available from: http://hdl.handle.net/2078.1/32235.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Hochstenbach J. The yeast proteolipid Pmp3p is a new component of the plasma membrane microdomains associated with the eisosomes. [Thesis]. Université Catholique de Louvain; 2010. Available from: http://hdl.handle.net/2078.1/32235
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
. 
Open Access Theses and Dissertations