Literatura académica sobre el tema "Décision de destin cellulaire"
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Artículos de revistas sobre el tema "Décision de destin cellulaire"
Cicciarello, Delia y Isabella Scionti. "Le rôle inattendu des gouttelettes lipidiques dans la régulation du destin des cellules souches musculaires". médecine/sciences 39 (noviembre de 2023): 28–31. http://dx.doi.org/10.1051/medsci/2023144.
Texto completoCoulombel, Laure. "Première décision embryonnaire : adopter un destin de trophectoderme ou de masse interne ?" médecine/sciences 33, n.º 2 (febrero de 2017): 133–35. http://dx.doi.org/10.1051/medsci/20173302006.
Texto completoDjian, Aurélien. "L’horizon et le destin de la phénoménologie". Varia 45, n.º 2 (8 de enero de 2019): 343–64. http://dx.doi.org/10.7202/1055267ar.
Texto completoSalisu, Waliu Jawula, Jila Mirlashari, Khatereh Seylani, Shokoh Varaei y Sally Thorne. "Fatalisme, méfiance et refus des traitements contre le cancer du sein au Ghana". Canadian Oncology Nursing Journal 32, n.º 2 (21 de abril de 2022): 206–13. http://dx.doi.org/10.5737/23688076322206213.
Texto completoClouet, J., D. Audureau, B. Lefranc, N. Maillard, R. Guile, É. Frampas, C. Perret y G. Grimandi. "Aide à la décision médico-économique pour la prise en charge du carcinome hépato-cellulaire par chimio-embolisation". Journal de Radiologie Diagnostique et Interventionnelle 95, n.º 4 (abril de 2014): 431–38. http://dx.doi.org/10.1016/j.jradio.2013.07.008.
Texto completoLabelle Eastaugh, Érik. "Les droits linguistiques aux limites de la rationalité juridique : le curieux destin de la partie VII de la Loi sur les langues officielles". Articles, n.º 17 (21 de diciembre de 2021): 162–95. http://dx.doi.org/10.7202/1084704ar.
Texto completoHomola, Stéphanie. "La fabrique des restes". Anthropologie et Sociétés 42, n.º 2-3 (5 de octubre de 2018): 37–68. http://dx.doi.org/10.7202/1052636ar.
Texto completoMassin, Veerle. "« Défense sociale » et protection de l’enfance en Belgique. Les filles délinquantes de l’école de bienfaisance de l’État à Namur (1914-1922)". Revue d’histoire de l’enfance « irrégulière » N° 9, n.º 2 (1 de noviembre de 2007): 173–90. http://dx.doi.org/10.3917/rhei.009.0173.
Texto completoGandégnon, Médéssè Carol F. "10 propositions théoriques pour renouveler l’étude de la décision de financement dans la petite entreprise par le dirigeant". Vie & sciences de l'entreprise N° 216-217, n.º 1 (21 de agosto de 2023): 92–118. http://dx.doi.org/10.3917/vse.216.0092.
Texto completoJAMMES, H. y J. P. RENARD. "Epigénétique et construction du phénotype, un enjeu pour les productions animales ?" INRAE Productions Animales 23, n.º 1 (8 de febrero de 2010): 23–42. http://dx.doi.org/10.20870/productions-animales.2010.23.1.3283.
Texto completoTesis sobre el tema "Décision de destin cellulaire"
Kim, Jang-Mi. "Quantitative live imaging analysis of proneural factor dynamics during lateral inhibition in Drosophila". Electronic Thesis or Diss., Sorbonne université, 2022. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2022SORUS585.pdf.
Texto completoLateral inhibition by Notch is a conserved mechanism that regulates the formation of regular patterns of cell fates1. In many tissues, intercellular Delta-Notch signaling coordinates in time and space binary fate decisions thought to be stochastic. In the context of sensory organ development in Drosophila, it has been proposed that fate symmetry breaking between equipotent cells relies on random fluctuations in the level of Delta/Notch2 (or one of their upstream regulators, e.g. YAP1 in the mouse gut3), with small differences being amplified and stabilized to generate distinct fates. Notch-mediated stochastic fate choices may also be biased by intrinsic, i.e. cell history4, or extrinsic factors. Although lateral inhibition has been extensively studied in many developmental contexts, a detailed in vivo analysis of fate and signaling dynamics is still lacking. Here, we used a quantitative live imaging approach to study the dynamics of sensory organ fate specification in the Drosophila abdomen. The accumulation of the transcription factor Scute (Sc), a key regulator of sensory organ formation in the abdomen, was used as a proxy to monitor proneural competence and SOP fate acquisition in developing pupae expressing GFP-tagged Sc. We generated high spatial and temporal resolution movies and segmented/tracked all nuclei using a custom-made pipeline. This allowed us to quantitatively study Sc dynamics in all cells. Having defined a fate difference index (FDI), we found that symmetry breaking can be detected early, when cells expressed very low and heterogeneous levels of Sc. We also observed rare cases of late fate resolution, e.g. when two cells close to each other accumulate high levels of GFP-Scute before being pulled away from each other. Interestingly, we did not observe a rapid decrease in GFP-Sc levels in non-selected cells right after symmetry breaking. Also, the rate of change of FDI values after symmetry breaking appeared to positively correlate with cell-to-cell heterogeneity in Sc levels. Whether increased heterogeneity is causally linked to symmetry breaking remains to be tested. We next addressed if this stochastic fate decision is biased by birth order (as proposed in the context of the AC/VU decision in worms4) or by the size and geometry of cell-cell contacts (as modeling suggested5). We found that neither appeared to significantly influence Notch-mediated binary fate decisions in the Drosophila abdomen. In conclusion, our live imaging data provide a detailed analysis of proneural dynamics during lateral inhibition in Drosophila
Bonnet, Frédéric. "Choix du destin cellulaire et cinétique du cycle cellulaire : rôle de CDC25B durant la neurogenèse embryonnaire". Thesis, Toulouse 3, 2016. http://www.theses.fr/2016TOU30107/document.
Texto completoGenerating cell diversity is essential in developmental biology and to preserve tissue homeostasis in adulthood. This results from the choice of stem cells and progenitor cells to commit into a particular fate in response to extrinsic cues and to intrinsic properties. The aim of my PhD was to elucidate the role of the cell cycle in the neurogenesis process (i.e. in neuron generation) using the embryonic chick neural tube as a paradigm. On the one hand, I have developed a new real time imaging strategy to measure the length of the four cell cycle phases in neural progenitors. On the other hand, I performed gain and loss of function experiments of a regulator that control mitosis input, the CDC25B phosphatase, in neural progenitors and showed that this cell cycle regulator promotes neurogenic divisions at the expense of proliferative divisions, thus controlling neuronal production
Lemey, Camille. "Manipulation du destin cellulaire pour améliorer la régénération tissulaire au cours du vieillissement". Thesis, Montpellier, 2017. http://www.theses.fr/2017MONTT052.
Texto completoAging is a complex process which is often punctuated by the appearing of age-related diseases such as arthritis, idiopathic pulmonary fibrosis or osteoporosis, and which is associated with a decrease of regeneration abilities and of adult stem cells number. In 2007, Dr. Yamanaka and his collaborators showed for the first time that human fibroblasts could be converted into pluripotent stem cells by inducing the expression of 4 transcription factors: OCT4, SOX2, KLF4 and c-MYC. In the laboratory, it was showed in 2011 that it is possible to reprogram senescent cells which are accumulating in aging organisms and to differentiate them into rejuvenated somatic cells.In vivo, a total reprogramming would lead to teratomas formation but if the reprogramming process is induced and stopped before getting pluripotent stem cells, we think that it is possible to restore altered cell physiology and to delay tissues aging and its deleterious consequences. Dr. Izpisua Belmonte validated this hypothesis in December 2016. He designed a murine transgenic model which recapitulates the premature aging phenotype of Hutchinson Gilford syndrome and which can be induced to express OCT4, SOX2, KLF4 and c-MYC, and he proved that it is possible to increase mice lifespan and to delay the appearing of pathological aging phenotype. We built a similar murine model and showed that a transient reprogramming can not only increase lifespan, but also delay age-related weight loss and pathological aging phenotype. Moreover, we were able to maintain a higher regenerative capacity until mice death. We also modeled age-related pathologies such as arthritis or idiopathic pulmonary fibrosis in mice which were inducible for the Yamanaka’s transcription factors and we showed that transient reprogramming could prevent damages. This study will have allowed to confirm the importance that cellular reprogramming can have in the fight against aging
Mayeuf, Alicia. "Choix du destin cellulaire des progéniteurs multipotents du somite, chez l'embryon de souris". Paris 6, 2013. http://www.theses.fr/2013PA066495.
Texto completoThe dorsal part of the somite, the dermomyotome contains multipotent Pax3+ progenitors, which give rise to different cell types such as skeletal muscle, dermal, endothelial, mural and brown adipose cells. The aim of this thesis was to understand mechanisms underlying cell fate decisions in this context in the mouse embryo. We have first shown that the Notch signaling pathway directs multipotent progenitors towards a vascular instead of a myogenic fate, by acting on the Pax3 :Foxc2 genetic equilibrium. To determine if Foxc1, the homologue of Foxc2, is also implicated in this mecanism, we have conditionally deleted both genes in Pax3+ progenitors. We document new phenotypes, including a reduction in vascular, cells, notably endothelial cells in the forelimb, where, surprisingly myogenic cells are also absent, leading to a number of possible hypotheses. Foxc2 is also implicated in the differentiation of brown adipose tissue, which we show is a derivative of Pax3+ cells in the dermomyotome. We have studied the development of this tissue in the embryo and propose a model in two steps, with initial formation of an “undifferentiated adipogenic mass” which subsequently differentiates into brown adipocytes. Gain and loss of function approaches suggest that Foxc1/2 play a role in the control of mitochodrial function during the differentiation of brown adipocytes in the embryo. This role may also be played by Foxc1 in the slow fibers of skeletal muscle where it is specifically expressed in the adult
Bolz, Marianne. "Régulation du destin cellulaire pendant la neurogénèse postnatale : rôle de l'innervation dopaminergique issue du mésencéphale". Thesis, Aix-Marseille, 2013. http://www.theses.fr/2013AIXM4098.
Texto completoIn the postnatal and adult mammalian brain neurogenesis persists in the subgranular zone of the hippocampal dentate gyrus and the subventricular zone (SVZ). In the SVZ slowly dividing stem cells give rise to neuroblasts that migrate to the olfactory bulb (OB) where they reach the granule and glomerular cell layer of the OB and differentiate into different interneuron subtypes including a small fraction of dopaminergic interneurons. The discovery of postnatal and adult neurogenesis has changed the view of the plasticity of the brain remarkably and raised the hope for new therapeutical approaches in the field of neurodegenerative diseases. Since in Parkinson’s disease the main motor symptoms are caused by the dopaminergic denervation of the striatum adjacent to SVZ, the understanding of the generation and differentiation of OB dopaminergic neurons has received special attention. Interestingly, the neurotransmitter dopamine itself has been suggested to influence olfactory bulb neurogenesis via direct innervation of SVZ by midbrain dopaminergic neurons. However, data on this topic have been contradictory. In this study, I investigated how dopaminergic innervation influences SVZ neurogenesis and the fate of SVZ progenitors. I combined a 6-OHDA model of dopaminergic denervation in postnatal mice with in vivo forebrain electroporation to specifically label lateral and dorsal SVZ progenitors and to follow their fate in the olfactory bulb
Andriatsilavo, Rakoto Mahéva. "La régulation des cellules souches adultes intestinales de drosophila melanogaster : Comment SPEN influence un destin cellulaire". Electronic Thesis or Diss., Paris 6, 2015. http://www.theses.fr/2015PA066381.
Texto completoAdult stem cells are non-differentiated cells that maintain tissue homeostasis by supplying differentiated cells while at the same time self-renewing. How is this balance between stem cell state and differentiated state controlled? This question became one of the major interests of the Stem cell research and Translation, mostly due to the potential therapeutic perspectives that it gives. Regarding this effort, this thesis work describes a new function of a gene call split-ends/spen in adult stem cell regulation in Drosophila intestine. SPEN familly is composed by essential genes, which codes conserved proteins from Plants to Metazoa. They are involved in key cellular processes such as cell death, differentiation or proliferation, and are associated with various molecular functions controlling transcriptional and post-transcriptional gene expression. We found that a spen inactivation in Drosophila intestine leads to an abnormal increase in adult stem cells. In this work, by combining genetics tools and in vivo stem cell analysis methods, we could show that Spen works as a key factor of intestinal stem cell commitment and plays a role in their proliferation control. How does genetics programs control cellular identity? In order to investigate the molecular signature of intestinal stem cells and progenitor cells knockdowned for spen, we combined genetics, cell sorting and mRNA sequencing analysis to uncovered Spen target genes regulated in intestinal stem cells. Here, we provide a new function of spen in adult stem cell regulation, which may also shed light on its mode of action in other developmental and pathological contexts
Andriatsilavo, Rakoto Mahéva. "La régulation des cellules souches adultes intestinales de drosophila melanogaster : Comment SPEN influence un destin cellulaire". Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066381/document.
Texto completoAdult stem cells are non-differentiated cells that maintain tissue homeostasis by supplying differentiated cells while at the same time self-renewing. How is this balance between stem cell state and differentiated state controlled? This question became one of the major interests of the Stem cell research and Translation, mostly due to the potential therapeutic perspectives that it gives. Regarding this effort, this thesis work describes a new function of a gene call split-ends/spen in adult stem cell regulation in Drosophila intestine. SPEN familly is composed by essential genes, which codes conserved proteins from Plants to Metazoa. They are involved in key cellular processes such as cell death, differentiation or proliferation, and are associated with various molecular functions controlling transcriptional and post-transcriptional gene expression. We found that a spen inactivation in Drosophila intestine leads to an abnormal increase in adult stem cells. In this work, by combining genetics tools and in vivo stem cell analysis methods, we could show that Spen works as a key factor of intestinal stem cell commitment and plays a role in their proliferation control. How does genetics programs control cellular identity? In order to investigate the molecular signature of intestinal stem cells and progenitor cells knockdowned for spen, we combined genetics, cell sorting and mRNA sequencing analysis to uncovered Spen target genes regulated in intestinal stem cells. Here, we provide a new function of spen in adult stem cell regulation, which may also shed light on its mode of action in other developmental and pathological contexts
Pontis, Julien. "Rôles d'histones méthyltransférases dans le destin cellulaire : coopération entre des méthyltransférases des lysines 9 et 27 de l'histone H3". Paris 7, 2014. http://www.theses.fr/2014PA077220.
Texto completoThe genome expression program is regulated by the composition of DNA sequences and the factors that may be associated. These factors may either be transcription factors or cofactors. Cofactors, even if they do not recognize specific DNA sequences, can strongly regulate the expression of the genome. In eukaryotes, some of these cofactors can post-translationally modify structural DNA proteins (histones). These enzymes and their catalized modifications can recruit other cofactors and/or directly regulate chromatin structure allowing fine modulation of the expression of the genome. For example, this allows to control the transcription program during embryonic development or terminal muscle differentiation. Thus, methylation of lysines 9 and 27 of histone H3 (H3K9, H3K27) at gene promoters is essentially associated with transcriptional répression. These lysines are methylated by different specific enzymes called lysine methyltransferases (KMT). The laboratory has previously demonstrated the existence of a complex containing 4 H3K9 methyltransferases (G9A, GLP, and SETDB1 and SUV39H1). During these experiments, the team was able to identify the interaction between H3K9 methyltransferases and H3K27 (PRC2). The main aim of my thesis project was to identify the different genomic targets of KMTs. In these experiments we mainly were able to demonstrate a cooperation between G9A and PRC2 complex
Robert, Rémi. "Étude des mécanismes contrôlant l’expression des gènes HOX et implications pour la génération in vitro de tissus humains". Electronic Thesis or Diss., Sorbonne université, 2023. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2023SORUS399.pdf.
Texto completoDuring embryogenesis, the formation of the vertebrate body plan depends on the spatial organization of different cell types along the anterior-posterior axis. This process is orchestrated by HOX transcription factors, which are differentially expressed along this axis, conferring positional identity on developing tissues. HOX patterns of expression are initiated by the sequential activation of HOX genes in axial progenitors, a population of stem cells fueling the progressive elongation of the body of developing embryos, forming notably the somites and the spinal cord. In parallel with the progressive induction of this gene family, these progenitors generate increasingly caudal structures, transforming the temporal sequence of activation into spatial domains of expression along the anterior-posterior axis. Nevertheless, the mechanisms that regulate the temporality of this induction and its transformation into spatial domains remain poorly understood, particularly in humans. To address these questions, during my thesis I generated progenitors from human pluripotent stem cells that display the molecular and functional characteristics of axial progenitors. Indeed, we have shown that these progenitors sequentially activate HOX genes and can give rise to organoids recapitulating multiple aspects of the generation and organization of the anterior-posterior axis, such as the formation of somites surrounding a neural tube along which the spatial expression patterns of several HOXs are recapitulated. Using these in vitro-produced axial progenitors, we first demonstrated that the tempo of induction of HOX genes is dynamically modulated by the graded activity of two extrinsic factors, FGFs and GDF11, which are sequentially expressed in the caudal region of vertebrate embryos during development. Then, we showed that 1) activated HOX genes are direct targets of signaling pathways downstream of these factors and 2) that the speed of activation of genes expressed later and later is determined by the duration of pathway activation in axial progenitors, a property of the pathways regulated by intrinsic negative feedback mechanisms. Overall, my results suggest a new model in which the timing of HOX gene activation is an emergent property of the dynamics of signaling pathways downstream of extrinsic factors. In parallel, my studies have led to improved cellular and tissue engineering of trunk cells from human pluripotent stem cells, culminating in protocols for generating the different motor neuron subtypes present along the body axis, and a new organoid model mimicking morphogenesis and the formation of cellular diversity along the human body axis
André-Ratsimbazafy, Marie. "Phenotype plasticity and populations’ dynamics : social interactions among cancer cells". Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCB032/document.
Texto completoIt is commonly accepted that tumors arise from cells that escape the homeostatic controls which underlie the healthy histological structure and that cell phenotype is not the result of deterministic biochemical and genetic processes, but rather the stochastic and dynamic outcome of multiple intra- and intercellular regulation networks. This PhD aims to quantitatively study the phenotypic homeostasis of the cell populations and to present an approach to the fundamental question, never heretofore studied, regarding the autonomy versus collective control of cell fate. We studied in the long run, using flow cytometry and in 2D and 3D conditions, the level of expression of CD24 and CD44 of two breast cancer cell lines (SUM149-PT and SUM159-PT). Three phenotypes were isolated (CD24-/CD44+, CD24+/CD44+, CD24-/CD44-), the latter had not previously been documented in the literature. The phenotypic behavior of CD44-low and CD44-high subpopulations has been characterized by assessing their proportion and analyzing the fluorescence map. Thereby, we observed both a periodic behavior of appearance and disappearance of pool of cells characteristics of each cell lines and a phenotypic re-diversification for each subpopulation. Only the resulting population derived from CD24-/CD44- provided the same balance as the original unsorted population. 3D re-diversification process was observed in tumorspheres from CD24-/CD44+ and CD24+/CD44+. The cells CD24-/CD44did not have that potential but nonetheless outlived anoikis. These behaviors suggest that there is an inter-cell coordination regulating the balance of phenotypic proportions. To discover the social rules regulating inter-phenotypic spatial organization, we have set up a reporter of the endogenous variations of CD24 and CD44 and developed a theoretical model of cell interactions. This work has confirmed our hypothesis that inter-cellular social rules are determining the phenotypic expression at both the uni- and multicellular scales
Libros sobre el tema "Décision de destin cellulaire"
Models of massive parallelism: Analysis of cellular automata and neural networks. Berlin: Springer, 1995.
Buscar texto completoCapítulos de libros sobre el tema "Décision de destin cellulaire"
Bigirimana, Clément, Pierre Nduwingoma y Constantin Ntiranyibagira. "Chapitre 7 : De la décision à l’exécution d’une politique linguistique. Cas de la publicité au Burundi". En Re-penser les politiques linguistiques en Afrique à l’ère de la mondialisation, 197–215. Observatoire européen du plurilinguisme, 2023. http://dx.doi.org/10.3917/oep.bigir.2023.01.0197.
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