Relevant bibliographies by topics / Quiescence cellulaire

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Quiescence cellulaire'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 January 2025

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Journal articles on the topic "Quiescence cellulaire"

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Yao, Guang. "Modelling mammalian cellular quiescence." Interface Focus 4, no. 3 (2014): 20130074. http://dx.doi.org/10.1098/rsfs.2013.0074.

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Cellular quiescence is a reversible non-proliferating state. The reactivation of ‘sleep-like’ quiescent cells (e.g. fibroblasts, lymphocytes and stem cells) into proliferation is crucial for tissue repair and regeneration and a key to the growth, development and health of higher multicellular organisms, such as mammals. Quiescence has been a primarily phenotypic description (i.e. non-permanent cell cycle arrest) and poorly studied. However, contrary to the earlier thinking that quiescence is simply a passive and dormant state lacking proliferating activities, recent studies have revealed that
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Mohammad, Karamat, Jennifer Anne Baratang Junio, Tala Tafakori, Emmanuel Orfanos, and Vladimir I. Titorenko. "Mechanisms that Link Chronological Aging to Cellular Quiescence in Budding Yeast." International Journal of Molecular Sciences 21, no. 13 (2020): 4717. http://dx.doi.org/10.3390/ijms21134717.

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After Saccharomyces cerevisiae cells cultured in a medium with glucose consume glucose, the sub-populations of quiescent and non-quiescent cells develop in the budding yeast culture. An age-related chronology of quiescent and non-quiescent yeast cells within this culture is discussed here. We also describe various hallmarks of quiescent and non-quiescent yeast cells. A complex aging-associated program underlies cellular quiescence in budding yeast. This quiescence program includes a cascade of consecutive cellular events orchestrated by an intricate signaling network. We examine here how calor
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Fujimaki, Kotaro, Ruoyan Li, Hengyu Chen, et al. "Graded regulation of cellular quiescence depth between proliferation and senescence by a lysosomal dimmer switch." Proceedings of the National Academy of Sciences 116, no. 45 (2019): 22624–34. http://dx.doi.org/10.1073/pnas.1915905116.

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The reactivation of quiescent cells to proliferate is fundamental to tissue repair and homeostasis in the body. Often referred to as the G0 state, quiescence is, however, not a uniform state but with graded depth. Shallow quiescent cells exhibit a higher tendency to revert to proliferation than deep quiescent cells, while deep quiescent cells are still fully reversible under physiological conditions, distinct from senescent cells. Cellular mechanisms underlying the control of quiescence depth and the connection between quiescence and senescence are poorly characterized, representing a missing
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Laporte, Damien, Anne Lebaudy, Annelise Sahin, et al. "Metabolic status rather than cell cycle signals control quiescence entry and exit." Journal of Cell Biology 192, no. 6 (2011): 949–57. http://dx.doi.org/10.1083/jcb.201009028.

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Quiescence is defined as a temporary arrest of proliferation, yet it likely encompasses various cellular situations. Our knowledge about this widespread cellular state remains limited. In particular, little is known about the molecular determinants that orchestrate quiescence establishment and exit. Here we show that upon carbon source exhaustion, budding yeast can enter quiescence from all cell cycle phases. Moreover, using cellular structures that are candidate markers for quiescence, we found that the first steps of quiescence exit can be triggered independently of cell growth and prolifera
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Miles, Shawna, Li Hong Li, Zephan Melville, and Linda L. Breeden. "Ssd1 and the cell wall integrity pathway promote entry, maintenance, and recovery from quiescence in budding yeast." Molecular Biology of the Cell 30, no. 17 (2019): 2205–17. http://dx.doi.org/10.1091/mbc.e19-04-0190.

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Wild Saccharomyces cerevisiae strains are typically diploid. When faced with glucose and nitrogen limitation they can undergo meiosis and sporulate. Diploids can also enter a protective, nondividing cellular state or quiescence. The ability to enter quiescence is highly reproducible but shows broad natural variation. Some wild diploids can only enter cellular quiescence, which indicates that there are conditions in which sporulation is lost or selected against. Others only sporulate, but if sporulation is disabled by heterozygosity at the IME1 locus, those diploids can enter quiescence. W303 h
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Yao, Guang. "Quiescence-Origin Senescence: A New Paradigm in Cellular Aging." Biomedicines 12, no. 8 (2024): 1837. http://dx.doi.org/10.3390/biomedicines12081837.

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Cellular senescence, traditionally viewed as a consequence of proliferating and growing cells overwhelmed by extensive stresses and damage, has long been recognized as a critical cellular aging mechanism. Recent research, however, has revealed a novel pathway termed “quiescence-origin senescence”, where cells directly transition into senescence from the quiescent state, bypassing cell proliferation and growth. This opinion paper presents a framework conceptualizing a continuum between quiescence and senescence with quiescence deepening as a precursor to senescence entry. We explore the trigger
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Laurent, Marc, Lina Cordeddu, Yasaman Zahedi, and Karl Ekwall. "LEO1 Is Required for Efficient Entry into Quiescence, Control of H3K9 Methylation and Gene Expression in Human Fibroblasts." Biomolecules 13, no. 11 (2023): 1662. http://dx.doi.org/10.3390/biom13111662.

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(1) Background: The LEO1 (Left open reading frame 1) protein is a conserved subunit of the PAF1C complex (RNA polymerase II-associated factor 1 complex). PAF1C has well-established mechanistic functions in elongation of transcription and RNA processing. We previously showed, in fission yeast, that LEO1 controls histone H3K9 methylation levels by affecting the turnover of histone H3 in chromatin, and that it is essential for the proper regulation of gene expression during cellular quiescence. Human fibroblasts enter a reversible quiescence state upon serum deprivation in the growth media. Here
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Jia, Wen-Huan, An-Qi Li, Jing-Yi Feng, et al. "DEK terminates diapause by activation of quiescent cells in the crustacean Artemia." Biochemical Journal 476, no. 12 (2019): 1753–69. http://dx.doi.org/10.1042/bcj20190169.

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Abstract To cope with harsh environments, the Artemia shrimp produces gastrula embryos in diapause, a state of obligate dormancy, having cellular quiescence and suppressed metabolism. The mechanism behind these cellular events remains largely unknown. Here, we study the regulation of cell quiescence using diapause embryos of Artemia. We found that Artemia DEK (Ar-DEK), a nuclear factor protein, was down-regulated in the quiescent cells of diapause embryos and enriched in the activated cells of post-diapause embryos. Knockdown of Ar-DEK induced the production of diapause embryos whereas the con
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Arif, Tasleem. "Lysosomes and Their Role in Regulating the Metabolism of Hematopoietic Stem Cells." Biology 11, no. 10 (2022): 1410. http://dx.doi.org/10.3390/biology11101410.

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Hematopoietic stem cells (HSCs) have the capacity to renew blood cells at all stages of life and are largely quiescent at a steady state. It is essential to understand the processes that govern quiescence in HSCs to enhance bone marrow transplantation. It is hypothesized that in their quiescent state, HSCs primarily use glycolysis for energy production rather than mitochondrial oxidative phosphorylation (OXPHOS). In addition, the HSC switch from quiescence to activation occurs along a continuous developmental path that is driven by metabolism. Specifying the metabolic regulation pathway of HSC
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Martinez, Ivan, Karen E. Hayes, Jamie A. Barr, et al. "An Exportin-1–dependent microRNA biogenesis pathway during human cell quiescence." Proceedings of the National Academy of Sciences 114, no. 25 (2017): E4961—E4970. http://dx.doi.org/10.1073/pnas.1618732114.

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The reversible state of proliferative arrest known as “cellular quiescence” plays an important role in tissue homeostasis and stem cell biology. By analyzing the expression of miRNAs and miRNA-processing factors during quiescence in primary human fibroblasts, we identified a group of miRNAs that are induced during quiescence despite markedly reduced expression of Exportin-5, a protein required for canonical miRNA biogenesis. The biogenesis of these quiescence-induced miRNAs is independent of Exportin-5 and depends instead on Exportin-1. Moreover, these quiescence-induced primary miRNAs (pri-mi
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Dissertations / Theses on the topic "Quiescence cellulaire"

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Alshehri, Mohammed. "Characterisation of transcriptional properties of the hid1Δ and hid3Δ mutants of Schizosaccharomyces pombe". Thesis, Bordeaux, 2015. http://www.theses.fr/2015BORD0141/document.

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Schizosaccharomyces pombe devient de plus en plus un système modèle pour étudier la régulation de l'expression des gènes et des protéines dans les processus impliqués dans le développement de cancers et de maladies génétiques. Ces travaux peuvent servir à étudier les propriétés putatives de la protéine humaine HID1 à empêcher des tumeurs de se former. J'ai utilisé la technique RNAseq pour révéler les changements d'expression des gènes sur les cellules de S. pombe dont sont absentes trois gènes orthologues du gène humain HID1: hid1+, hid2+ et hid3+. Des mutants ont été créés par remplacement de
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Dembélé, Laurent. "Développement de modèles d'étude in vitro des stades hépitiques de Plasmodium incluant l'hypnozoïte." Paris 6, 2012. http://www.theses.fr/2012PA066815.

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Froehlich, Jeanne. "Caractérisation de Fam65b, un nouvel effecteur de FoxO1 dans la régulation de la quiescence." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCB075/document.

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Le comportement et le devenir des lymphocytes T (LT) est conditionné par l’intégration de nombreux signaux solubles et cellulaires. Lorsque les LT ne sont pas stimulés, les facteurs de transcription FoxO orchestrent un réseau moléculaire important participant au maintien de la quiescence et à la capacité migratoire des LT. Longtemps considéré comme un état par défaut, le maintien des LT dans cet état quiescent est hautement régulé par un ensemble de signaux parmi lesquels la signalisation via le récepteur à l’interleukine 7 (IL7) et le récepteur à l’antigène (TCR) activé par des molécules du c
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Lossaint, Gérald. "Mécanismes orchestrant la sortie du cycle cellulaire opérant en G2." Thesis, Montpellier 2, 2010. http://www.theses.fr/2010MON20040/document.

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La dérégulation du système de surveillance qui bloque la prolifération lorsque l'intégrité du génome est compromise fait partie intégrante de la cancérogenèse. Nous cherchons à décortiquer les mécanismes qui, en phase G2, orchestrent l'arrêt du cycle cellulaire, irréversible, en présence des lésions de l'ADN (sénescence) ou réversible (quiescence), en absence de signaux mitogéniques ou confluence. L'objectif du premier volet fut d'élucider les rôles respectifs de l'inhibiteur de CDK (CKI) p21Waf1 et des kinases Chk1 et Chk2 dans l'arrêt en G2 dû au stress génotoxique menant à la sénescence. No
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Ostyn, Pauline. "Facteurs inflammatoires et contrôle de la quiescence/activation des cellules souches tumorales de mélanome." Thesis, Lille 2, 2016. http://www.theses.fr/2016LIL2S013/document.

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Une tumeur est composée de plusieurs sous populations cellulaires. L’une d’entre elles, celle des cellules souches tumorales, est à l’origine du développement des tumeurs. Une des propriétés majeures de ces cellules est la capacité d’entrer dans un état de quiescence. De ce fait, elles sont résistantes aux thérapies anticancéreuses conventionnelles qui visent les cellules cyclantes et peuvent ainsi persister pendant de nombreuses années. Ce phénomène est appelé dormance tumorale. L’activation de ces cellules souches tumorales quiescentes conduit à la récidive de la maladie. Le passage de l’éta
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Koning, Leanne de. "Facteurs d'assemblage de la chromatine et organisation de l'hétérochromatine du normal au pathologique." Paris 6, 2009. https://tel.archives-ouvertes.fr/tel-00814265.

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Dans le cancer, des défauts affectant l’organisation d’ADN en chromatine sont fréquents. Le complexe CAF-1 intervient dans l’assemblage en chromatine lors de la réplication et la réparation et est sous-exprimé en quiescence. CAF-1 interagit avec les protéines HP1, dont il existe trois isoformes humaines (HP1,  et ) et qui sont impliquées dans la répression des gènes et la mitose. Cette thèse adresse deux questions : Est-ce que l’expression de HP1 est régulée en fonction de la prolifération et de la tumorigénèse ? Je montre que l’expression de HP1, mais pas HP1 ou , est dépendante de la p
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Than, Trong Emmanuel. "Le rôle de la signalisation Notch3 dans le maintien des cellules souches neurales du télencéphale adulte Neural stem cell quiescence and stemness are molecularly distinct outputs of the Notch3 signaling cascade in the vertebrate adult brain her4-expressing neural stem cells are maintained through population asymmetry and embedded into a hierarchy of progenitors responsible for their life-long expansion Radial Glia and Neural Progenitors in the Adult Zebrafish Central Nervous System." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS541.

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Un certain nombre de régions du cerveau des vertébrés, y compris chez l’homme, continuent d’être le siège de l’ajout de nouveaux neurones à l’âge adulte. Ces nouveaux neurones sont produits à partir de cellules spécialisées, appelées cellules souches neurales (CSN). Celles-ci sont capables de s’auto-renouveler et sont principalement trouvées dans un état d’arrêt transitoire du cycle cellulaire que l’on appelle quiescence. A l’heure actuelle, les mécanismes cellulaires et moléculaires permettant aux CSN de trouver un équilibre entre maintien et différentiation, ainsi que les règles générales go
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De, Koning Leanne. "Facteurs d'assemblage de la chromatine et organisation de l'hétérochromatine du normal au pathologique." Phd thesis, Université Pierre et Marie Curie - Paris VI, 2009. http://tel.archives-ouvertes.fr/tel-00814265.

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Dans les cellules cancéreuses, des défauts affectant l'organisation d'ADN en chromatine sont fréquemment observés. L'étude de facteurs impliqués dans cette organisation est donc essentielle pour mieux appréhender leur implication dans la tumorigénèse. Un facteur particulièrement intéressant dans ce contexte est le facteur d'assemblage de la chromatine, le complexe CAF-1 (Chromatin Assembly Factor 1). CAF-1 est impliqué dans l'assemblage en chromatine de l'ADN lors de la réplication et la réparation de l'ADN. Deux sous-unités de CAF-1 sont sous-exprimés dans les cellules non-proliférantes (quie
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Polo, Sophie. "Facteurs d'assemblage de la chromatine, prolifération cellulaire et maintien de l'intégrité du génome." Paris 6, 2006. http://www.theses.fr/2006PA066126.

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Martinet-Corbineau, Clémence. "Rôle du gène H19 dans les cellules souches musculaires." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCB004/document.

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Le gène H19, soumis à l’empreinte parentale, est fortement exprimé durant le développement embryonnaire, cependant, son expression est réprimée après la naissance dans l’ensemble des tissus à l’exception du muscle squelettique, et plus particulièrement des cellules souches musculaires : les cellules satellites. L’objectif de ma thèse a été de déterminer le rôle du gène H19 dans la mise en place et dans la fonction de ces cellules souches durant la myogénèse adulte. En utilisant un modèle murin présentant une délétion du gène H19, les souris H19∆3, notre laboratoire avait montré que le gène H19
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Books on the topic "Quiescence cellulaire"

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Lacorazza, H. Daniel, ed. Cellular Quiescence. Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7371-2.

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Lacorazza, H. Daniel. Cellular Quiescence: Methods and Protocols. Springer New York, 2017.

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Lacorazza, H. Daniel. Cellular Quiescence: Methods and Protocols. Springer New York, 2018.

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Pitzalis, Costantino, Frances Humby, and Michael P. Seed. Synovial pathology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0052.

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Synovial pathology is seen in a variety of disease states, including rheumatoid arthritis (RA), osteoarthritis (OA), psoriatic arthritis, and systemic lupus erythmatosus (SLE). This chapter highlights recent advances that characterize the cellular composition of these tissues according to surface markers and chemokine and cytokine expression, and describes synovial functional status and response to therapeutics. In RA, after initiation, pannus migrates over and under cartilage, and into subchondral bone, in a destructive process. Cartilage-pannus junction (CPJ) is characterized as invasive or
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Book chapters on the topic "Quiescence cellulaire"

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So, Wai-Kin, and Tom H. Cheung. "Molecular Regulation of Cellular Quiescence: A Perspective from Adult Stem Cells and Its Niches." In Cellular Quiescence. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7371-2_1.

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Rodriguez, Christine N., and Hoang Nguyen. "Identifying Quiescent Stem Cells in Hair Follicles." In Cellular Quiescence. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7371-2_10.

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Brun, Caroline E., Yu Xin Wang, and Michael A. Rudnicki. "Single EDL Myofiber Isolation for Analyses of Quiescent and Activated Muscle Stem Cells." In Cellular Quiescence. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7371-2_11.

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Yang, Kai, and Hongbo Chi. "Investigating Cellular Quiescence of T Lymphocytes and Antigen-Induced Exit from Quiescence." In Cellular Quiescence. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7371-2_12.

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Park, Chun Shik, and H. Daniel Lacorazza. "Retroviral Transduction of Quiescent Murine Hematopoietic Stem Cells." In Cellular Quiescence. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7371-2_13.

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Jalbert, Emilie, and Eric M. Pietras. "Analysis of Murine Hematopoietic Stem Cell Proliferation During Inflammation." In Cellular Quiescence. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7371-2_14.

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Buschhaus, Johanna M., Kathryn E. Luker, and Gary D. Luker. "A Facile, In Vitro 384-Well Plate System to Model Disseminated Tumor Cells in the Bone Marrow Microenvironment." In Cellular Quiescence. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7371-2_15.

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Srivastava, Surabhi, Hardik P. Gala, Rakesh K. Mishra, and Jyotsna Dhawan. "Distinguishing States of Arrest: Genome-Wide Descriptions of Cellular Quiescence Using ChIP-Seq and RNA-Seq Analysis." In Cellular Quiescence. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7371-2_16.

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Bierhoff, Holger. "Analysis of lncRNA-Protein Interactions by RNA-Protein Pull-Down Assays and RNA Immunoprecipitation (RIP)." In Cellular Quiescence. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7371-2_17.

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Bukhari, Syed I. A., Samuel S. Truesdell, and Shobha Vasudevan. "Analysis of MicroRNA-Mediated Translation Activation of In Vitro Transcribed Reporters in Quiescent Cells." In Cellular Quiescence. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7371-2_18.

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Conference papers on the topic "Quiescence cellulaire"

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Fessel, Joshua P., Kirk B. Lane, Tom Blackwell, and James D. West. "Oxidative Stress Caused By BMPR2 Mutation Requires Cellular Quiescence." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3394.

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Irwin, Robert J., and Howard A. Blair. "Quantum cellular automata without quiescent states." In SPIE Defense, Security, and Sensing, edited by Eric Donkor, Andrew R. Pirich, and Howard E. Brandt. SPIE, 2011. http://dx.doi.org/10.1117/12.884182.

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Shi, Ying, Jiaofei Cao, Augustine M. K. Choi, and Danielle Morse. "Carbon Monoxide Inhibits Lung Fibrosis By Inducing Cellular Quiescence Via E2F4." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5284.

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Gould, Russell, Karen Chin, Puifai Santisakultam та ін. "Anisotropic Strain Fields Enhance Matrix Remodeling Through Elevated TGF-β Signaling". У ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53805.

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In this work, we demonstrate the unique effect of controlled anisotropic strain on fibroblast behavior in 3D engineered tissue environments. Anisotropy of biaxial strain resulted in increased cellular orientation and collagen fiber alignment. Transforming growth factor beta-1 (TGFβ1) gene expression and pSmad2 nuclear translocation increased with biaxial directionality. Myofibroblastic alpha-smooth muscle actin (α-SMA) decreased with applied strain similar to mechanically unloaded hydrogels. Collectively, these results demonstrate a novel mechanobiological mechanism by which fibroblasts develo
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Yoshida, Go J., and Hideyuki Saya. "Abstract B06: EpCAM functions as a sensor that allows prostate cancer cells to become quiescent in response to lack of growth factors." In Abstracts: AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment; February 26 — March 1, 2014; San Diego, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.chtme14-b06.

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Hau, G., T. B. Nishimura, and N. Iwata. "Distortion analysis of a power heterojunction FET under low quiescent drain current for 3.5 V wide-band CDMA cellular phones." In 1999 IEEE MTT-S International Topical Symposium on Technologies for Wireless Applications (Cat. No. 99TH8390). IEEE, 1999. http://dx.doi.org/10.1109/mtttwa.1999.755125.

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Deng, Xiaobing, and Eileen Friedman. "Abstract 5087: Mirk/Dyrk1B kinase mediates survival of quiescent tumor cells and is downstream of the cellular energy sensor AMPK." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5087.

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Sewell-Loftin, M. K., and W. David Merryman. "The Role of SRC in Strain- and Ligand- Dependent Phenotypic Modulation of Mouse Embryonic Fibroblasts." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53604.

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Connective tissue fibrosis represents a significant portion of mortality and morbidity in our society. These diseases include many illnesses such as heart valve disease, atherosclerosis, macular degeneration, and cirrhosis, meaning that millions of lives are affected by these conditions each year. Fibrotic tissues form when quiescent fibroblasts activate becoming myofibroblasts, the phenotype of active tissue construction and fibrosis. During this process, the cells produce smooth muscle α-actin (αSMA), a contractile element considered to be the hallmark of cellular activation [1]. Following t
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Gupta, Vijay K., and Charles D. Eggleton. "A Numerical Method for Coupling Nano-Scale Molecular Binding With Mesoscale Cellular Deformation." In ASME 2009 International Mechanical Engineering Congress and Exposition. ASMEDC, 2009. http://dx.doi.org/10.1115/imece2009-13296.

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Cell adhesion plays a pivotal role in diverse biological processes, including inflammation and thrombosis. Changes in cell adhesion can be the defining event in a wide range of diseases, including cancer, osteoporosis, atherosclerosis, and arthritis. Cells are exposed constantly to hemodynamic/hydrodynamic forces and the balance between the dispersive hydrodynamic forces and the adhesive forces generated by the interactions of membrane-bound receptors and their ligands determines cell adhesion. The ultimate objective of our work is to develop software that can simulate the adhesion of cells co
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de Agostini, A., J. Marcum, and R. Rosenberg. "THE BINDING OF ANTITHROMBIN TO CAPILLARY ENDOTHELIAL CELLS GROWN IN VITRO." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643343.

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Cloned endothelial cells from rat epididymal fat pads synthesize anticoagulantly active heparan sulfate proteoglycans containing the disaccharide, GlcA→ AMN-3,6-O-SO3, which is a marker for the antithrombin-binding domain of heparin. To demonstrate that antithrombin (AT) binds to cell surface heparan sulfate, a binding assay employing 125I-AT and cell monolayers has been developed. Post-confluent endothelial cells (7 days) were incubated with radiolabeled AT for 1 h at 4° and washed with PBS. Bound radioactivity was quantitated after solubilizing whole cells. Under these conditions, ∼1% (2174±
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