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Journal articles on the topic 'Quiescence cellulaire'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 January 2025

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1

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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2

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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3

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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5

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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6

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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7

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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9

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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10

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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11

Aguanno, Salvatore, Claudia Petrelli, Sara Di Siena, Luciana De Angelis, Manuela Pellegrini, and Fabio Naro. "A Three-Dimensional Culture Model of Reversibly Quiescent Myogenic Cells." Stem Cells International 2019 (November 11, 2019): 1–12. http://dx.doi.org/10.1155/2019/7548160.

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Satellite cells (SC) are the stem cells of skeletal muscles. They are quiescent in adult animals but resume proliferation to allow muscle hypertrophy or regeneration after injury. The mechanisms balancing quiescence, self-renewal, and differentiation of SC are difficult to analyze in vivo owing to their complexity and in vitro because the staminal character of SC is lost when they are removed from the niche and is not adequately reproduced in the culture models currently available. To overcome these difficulties, we set up a culture model of the myogenic C2C12 cell line in suspension. When C2C

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12

Chen, Danica. "MITOCHONDRIAL METABOLIC CHECKPOINT, STEM CELL AGING AND REJUVENATION." Innovation in Aging 6, Supplement_1 (2022): 287. http://dx.doi.org/10.1093/geroni/igac059.1143.

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Abstract Cell cycle checkpoints are surveillance mechanisms in eukaryotic cells that monitor the condition of the cell, repair cellular damages, and allow the cell to progress through the various phases of the cell cycle when conditions become favorable. Recent advances in stem cell biology highlight a mitochondrial metabolic checkpoint that is essential for stem cells to return to the quiescent state. As quiescent stem cells enter the cell cycle, mitochondrial biogenesis is induced and mitochondrial stress is increased. Mitochondrial unfolded protein response and mitochondrial oxidative stres

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13

Gu, Zhu Chao, Edwin Wu, Carolin Sailer, et al. "Ubiquitin orchestrates proteasome dynamics between proliferation and quiescence in yeast." Molecular Biology of the Cell 28, no. 19 (2017): 2479–91. http://dx.doi.org/10.1091/mbc.e17-03-0162.

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Proteasomes are essential for protein degradation in proliferating cells. Little is known about proteasome functions in quiescent cells. In nondividing yeast, a eukaryotic model of quiescence, proteasomes are depleted from the nucleus and accumulate in motile cytosolic granules termed proteasome storage granules (PSGs). PSGs enhance resistance to genotoxic stress and confer fitness during aging. Upon exit from quiescence PSGs dissolve, and proteasomes are rapidly delivered into the nucleus. To identify key players in PSG organization, we performed high-throughput imaging of green fluorescent p

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14

Itaman, Sheed, Grigori Enikolopov, and Oleg V. Podgorny. "Detection of De Novo Dividing Stem Cells In Situ through Double Nucleotide Analogue Labeling." Cells 11, no. 24 (2022): 4001. http://dx.doi.org/10.3390/cells11244001.

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Tissue-specific somatic stem cells are characterized by their ability to reside in a state of prolonged reversible cell cycle arrest, referred to as quiescence. Maintenance of a balance between cell quiescence and division is critical for tissue homeostasis at the cellular level and is dynamically regulated by numerous extrinsic and intrinsic factors. Analysis of the activation of quiescent stem cells has been challenging because of a lack of methods for direct detection of de novo dividing cells. Here, we present and experimentally verify a novel method based on double labeling with thymidine

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15

Chen, Danica. "The Mitochondrial Metabolic Checkpoint and Reversing Stem Cell Aging." Blood 128, no. 22 (2016): SCI—34—SCI—34. http://dx.doi.org/10.1182/blood.v128.22.sci-34.sci-34.

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Abstract Cell cycle checkpoints are surveillance mechanisms in eukaryotic cells that monitor the condition of the cell, repair cellular damages, and allow the cell to progress through the various phases of the cell cycle when conditions become favorable. Recent advances in hematopoietic stem cell (HSC) biology highlight a mitochondrial metabolic checkpoint that is essential for HSCs to return to the quiescent state. As quiescent HSCs enter the cell cycle, mitochondrial biogenesis is induced, which is associated with increased mitochondrial protein folding stress and mitochondrial oxidative str

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16

Wang, Yuehong, Yuman Yu, Weijun Yang, et al. "SETD4 Confers Cancer Stem Cell Chemoresistance in Nonsmall Cell Lung Cancer Patients via the Epigenetic Regulation of Cellular Quiescence." Stem Cells International 2023 (May 27, 2023): 1–19. http://dx.doi.org/10.1155/2023/7367854.

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Increasing evidence indicates that quiescent cancer stem cells (CSCs) are a root cause of chemoresistance. SET domain-containing protein 4 (SETD4) epigenetically regulates cell quiescence in breast cancer stem cells (BCSCs), and SETD4-positive BCSCs are chemoradioresistant. However, the role of SETD4 in chemoresistance, tumor progression, and prognosis in nonsmall cell lung cancer (NSCLC) patients is unclear. Here, SETD4-positive cells were identified as quiescent lung cancer stem cells (qLCSCs) since they expressed high levels of ALDH1 and CD133 and low levels of Ki67. SETD4 expression was si

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17

Chen, Xin, Ali Momin, Siyi Wanggou, et al. "STEM-27. MECHANOSENSITIVE BRAIN TUMOR CELLS CONSTRUCT BLOOD-TUMOR BARRIER TO MASK CHEMOSENSITIVITY." Neuro-Oncology 24, Supplement_7 (2022): vii37. http://dx.doi.org/10.1093/neuonc/noac209.144.

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Abstract Two major obstacles in brain cancer treatment are the blood-tumor barrier (BTB) and quiescent tumor cells. Here we show that Sox2+ tumor cells directly project cellular processes to ensheathe capillaries in medulloblastoma (MB), a process that depends on the mechanosensitive ion channel Piezo2. MB develops a tissue stiffness gradient as a function of distance to capillaries. Sox2+ tumor cells perceive substrate stiffness to sustain local intracellular calcium, actomyosin tension, and adhesion to promote cellular process growth and cell surface sequestration of β-Catenin. Piezo2 knocko

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18

Laporte, Damien, Fabien Courtout, Bénédicte Salin, Johanna Ceschin, and Isabelle Sagot. "An array of nuclear microtubules reorganizes the budding yeast nucleus during quiescence." Journal of Cell Biology 203, no. 4 (2013): 585–94. http://dx.doi.org/10.1083/jcb.201306075.

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The microtubule cytoskeleton is a highly dynamic network. In dividing cells, its complex architecture not only influences cell shape and movement but is also crucial for chromosome segregation. Curiously, nothing is known about the behavior of this cellular machinery in quiescent cells. Here we show that, upon quiescence entry, the Saccharomyces cerevisiae microtubule cytoskeleton is drastically remodeled. Indeed, while cytoplasmic microtubules vanish, the spindle pole body (SPB) assembles a long and stable monopolar array of nuclear microtubules that spans the entire nucleus. Consequently, th

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19

Datta, S. "Control of proliferation activation in quiescent neuroblasts of the Drosophila central nervous system." Development 121, no. 4 (1995): 1173–82. http://dx.doi.org/10.1242/dev.121.4.1173.

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Stem cell proliferation is controlled through cell cycle arrest and activation. In the central nervous system of Drosophila melanogaster, neuroblast quiescence and activation takes place in defined spatial and temporal patterns. Two genes have been identified that regulate the pattern of neuroblast quiescence and proliferation. ana, which has been previously described by Ebens and coworkers (Ebens, A., Garren, H., Cheyette, B. N. R. and Zipursky, S. L. (1993). Cell 74, 15–28), encodes a secreted glial glycoprotein that inhibits premature neuroblast proliferation. We previously showed that trol

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20

Sagot, Isabelle, Benoît Pinson, Bénédicte Salin, and Bertrand Daignan-Fornier. "Actin Bodies in Yeast Quiescent Cells: An Immediately Available Actin Reserve?" Molecular Biology of the Cell 17, no. 11 (2006): 4645–55. http://dx.doi.org/10.1091/mbc.e06-04-0282.

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Most eukaryotic cells spend most of their life in a quiescent state, poised to respond to specific signals to proliferate. In Saccharomyces cerevisiae, entry into and exit from quiescence are dependent only on the availability of nutrients in the environment. The transition from quiescence to proliferation requires not only drastic metabolic changes but also a complete remodeling of various cellular structures. Here, we describe an actin cytoskeleton organization specific of the yeast quiescent state. When cells cease to divide, actin is reorganized into structures that we named “actin bodies.

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Robinson, Dr Ruth, Ms Emily Gaizley, Dr Elitza Deltcheva, Dr Sam Marguerat, Dr Jason Wray, and Prof Tariq Enver. "MITOCHONDRIAL MEMBRANE POTENTIAL IS A FUNCTIONALLY RELEVANT AXIS OF NON-GENETIC CELLULAR HETEROGENEITY IN GLIOBLASTOMA." Neuro-Oncology 26, Supplement_7 (2024): vii8. http://dx.doi.org/10.1093/neuonc/noae158.029.

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Abstract AIMS Glioma stem cells (GSCs) are believed to underpin treatment resistance in glioblastoma by virtue of their self- renewal capabilities and presumed transcriptional plasticity. Understanding how cell state diversity is established and maintained is crucial to make therapeutic gains. We have previously shown mitochondrial membrane potential (MMP) to be a functionally relevant source of extrinsic noise in embryonic and haematopoietic stem cells. This study evaluates cellular MMP as an axis of variability in GSCs. METHOD MMP was measured by ﬂow cytometry in patient-derived GSC lines us

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22

Suda, Toshio. "Purine Metabolism and Hematopoietic Stem and Progenitor Stem Cells Under Stress." Blood 132, Supplement 1 (2018): SCI—19—SCI—19. http://dx.doi.org/10.1182/blood-2018-99-109515.

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Abstract Hematopoietic stem cells (HSCs) play a key role in the lifelong maintenance of hematopoiesis through self-renewal and multi-lineage differentiation. Adult HSCs reside within a specialized microenvironment of the bone marrow (BM), called "niche", in which they are maintained in a quiescent state in cell cycle. Most of HSCs within BM show quiescence under the hypoxic niche. Since the loss of HSC quiescence leads to the exhaustion or aging of stem cells through excess cell division, the regulation of quiescence in HSCs is essential for hematopoietic homeostasis. On the other hand, cellul

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23

Roche, Benjamin, Benoit Arcangioli, and Robert Martienssen. "Transcriptional reprogramming in cellular quiescence." RNA Biology 14, no. 7 (2017): 843–53. http://dx.doi.org/10.1080/15476286.2017.1327510.

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24

Saffert, Ryan T., and Robert F. Kalejta. "Human Cytomegalovirus Gene Expression Is Silenced by Daxx-Mediated Intrinsic Immune Defense in Model Latent Infections Established In Vitro." Journal of Virology 81, no. 17 (2007): 9109–20. http://dx.doi.org/10.1128/jvi.00827-07.

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ABSTRACT In addition to productive lytic infections, herpesviruses such as human cytomegalovirus (HCMV) establish a reservoir of latently infected cells that permit lifelong colonization of the host. When latency is established, the viral immediate-early (IE) genes that initiate the lytic replication cycle are not expressed. HCMV IE gene expression at the start of a lytic infection is facilitated by the viral pp71 protein, which is delivered to cells by infectious viral particles. pp71 neutralizes the Daxx-mediated cellular intrinsic immune defense that silences IE gene expression by generatin

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Mapfumo, Kudzanayi Z., Jane C. Pagan’a, Victor Ogesa Juma, Nikos I. Kavallaris, and Anotida Madzvamuse. "A Model for the Proliferation–Quiescence Transition in Human Cells." Mathematics 10, no. 14 (2022): 2426. http://dx.doi.org/10.3390/math10142426.

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The process of revitalising quiescent cells in order for them to proliferate plays a pivotal role in the repair of worn-out tissues as well as for tissue homeostasis. This process is also crucial in the growth, development and well-being of higher multi-cellular organisms such as mammals. Deregulation of proliferation-quiescence transition is related to many diseases, such as cancer. Recent studies have revealed that this proliferation–quiescence process is regulated tightly by the Rb−E2F bistable switch mechanism. Based on experimental observations, in this study, we formulate a mathematical

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26

McMahon, Robert, and Derek Walsh. "Efficient Quiescent Infection of Normal Human Diploid Fibroblasts with Wild-Type Herpes Simplex Virus Type 1." Journal of Virology 82, no. 20 (2008): 10218–30. http://dx.doi.org/10.1128/jvi.00859-08.

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ABSTRACT Quiescent infection of cultured cells with herpes simplex virus type 1 (HSV-1) provides an important, amenable means of studying the molecular mechanics of a nonproductive state that mimics key aspects of in vivo latency. To date, establishing high-multiplicity nonproductive infection of human cells with wild-type HSV-1 has proven challenging. Here, we describe simple culture conditions that established a cell state in normal human diploid fibroblasts that supported efficient quiescent infection using wild-type virus and exhibited many important properties of the in vivo latent state.

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Pugh, G. E., P. J. Coates, E. B. Lane, Y. Raymond, and R. A. Quinlan. "Distinct nuclear assembly pathways for lamins A and C lead to their increase during quiescence in Swiss 3T3 cells." Journal of Cell Science 110, no. 19 (1997): 2483–93. http://dx.doi.org/10.1242/jcs.110.19.2483.

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The expression of A-type lamins coincides with cell differentiation and as A-type lamins specifically interact with chromatin, a role in the regulation of differential gene expression has been suggested for A-type lamins. Using the mouse Swiss 3T3 cell line as a model, the change in two A-type lamins, lamins A and C, during cellular quiescence has been investigated. This well established model system mimics the first stages of differentiation when cells exit the cell cycle. In fact, quiescence in Swiss 3T3 cells was accompanied by a significant increase (2.6-fold) in lamin A protein levels and

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Padmanabhan, R., T. H. Howard, and B. H. Howard. "Specific growth inhibitory sequences in genomic DNA from quiescent human embryo fibroblasts." Molecular and Cellular Biology 7, no. 5 (1987): 1894–99. http://dx.doi.org/10.1128/mcb.7.5.1894-1899.1987.

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We used HeLa cells as recipients in a gene transfer assay to characterize DNA sequences that negatively regulate mammalian cell growth. In this assay, genomic DNA from quiescent human embryo fibroblasts was more inhibitory for HeLa replication than was DNA from either Escherichia coli or HeLa cells. Surprisingly, growth inhibitory activity depended on the growth state of the cells from which genomic DNA was prepared; it was strongest in DNA prepared from serum-deprived, quiescent embryo fibroblasts. This latter observation implies a role for DNA modification(s) in regulating the activity of th

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Padmanabhan, R., T. H. Howard, and B. H. Howard. "Specific growth inhibitory sequences in genomic DNA from quiescent human embryo fibroblasts." Molecular and Cellular Biology 7, no. 5 (1987): 1894–99. http://dx.doi.org/10.1128/mcb.7.5.1894.

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We used HeLa cells as recipients in a gene transfer assay to characterize DNA sequences that negatively regulate mammalian cell growth. In this assay, genomic DNA from quiescent human embryo fibroblasts was more inhibitory for HeLa replication than was DNA from either Escherichia coli or HeLa cells. Surprisingly, growth inhibitory activity depended on the growth state of the cells from which genomic DNA was prepared; it was strongest in DNA prepared from serum-deprived, quiescent embryo fibroblasts. This latter observation implies a role for DNA modification(s) in regulating the activity of th

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30

Coller, Hilary A., Liyun Sang, and James M. Roberts. "A New Description of Cellular Quiescence." PLoS Biology 4, no. 3 (2006): e83. http://dx.doi.org/10.1371/journal.pbio.0040083.

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Marescal, Océane, and Iain M. Cheeseman. "Cellular Mechanisms and Regulation of Quiescence." Developmental Cell 55, no. 3 (2020): 259–71. http://dx.doi.org/10.1016/j.devcel.2020.09.029.

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Yanagida, Mitsuhiro. "Cellular quiescence: are controlling genes conserved?" Trends in Cell Biology 19, no. 12 (2009): 705–15. http://dx.doi.org/10.1016/j.tcb.2009.09.006.

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PALOMARES-RIUS, JUAN E., JOHN T. JONES, PETER J. COCK, PABLO CASTILLO, and VIVIAN C. BLOK. "Activation of hatching in diapaused and quiescent Globodera pallida." Parasitology 140, no. 4 (2012): 445–54. http://dx.doi.org/10.1017/s0031182012001874.

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SUMMARYThe potato cyst nematodes (PCN) Globodera pallida and G. rostochiensis are major pests of potatoes. The G. pallida (and G. rostochiensis) life cycle includes both diapause and quiescent stages. Nematodes in dormancy (diapause or quiescent) are adapted for long-term survival and are more resistant to nematicides. This study analysed the mechanisms underlying diapause and quiescence. The effects of several compounds (8Br-cGMP, oxotremorine and atropine) on the activation of hatching were studied. The measurements of some morphometric parameters in diapaused and quiescent eggs after exposu

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Alder, Jonathan K., Robert W. Georgantas, Xiaobing Yu, and Curt I. Civin. "KLF4 as a Mediator of Quiescence in Hematopoietic Stem/Progenitor Cells." Blood 104, no. 11 (2004): 4146. http://dx.doi.org/10.1182/blood.v104.11.4146.4146.

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Abstract At any given time, only a very small fraction of the hematopoietic stem cells (HSCs) in an organism are actively dividing; the vast majority of these cells remain in a quiescent state. HSCs can escape this quiescent state to self-renew and give rise to progenitor cells (HPCs), which expand rapidly to form all of the mature progeny cells of the lympho-hematopoietic system. Despite the centrality of quiescence in hematopoiesis, the mechanisms by which quiescence is regulated are largely unknown. Several studies have shown that p21CIP/WAF1 is required for cell cycle arrest of HSCs, and d

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Arenas, Alicia, Daniel Lainez, Cristina Serrano del Castillo, et al. "Inhibition of the Hedgehog Pathway Decreases the Quiescent CD34+CD38- Population in Acute Myeloid Leukemia." Blood 132, Supplement 1 (2018): 1509. http://dx.doi.org/10.1182/blood-2018-99-118636.

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Abstract Introduction Acute myeloid leukemia (AML) is a clonal disease with a reduced life expectancy due to a high relapse rate. One explanation is that leukemic stem cells (LSC) evade the action of conventional chemotherapy due to their quiescent state. Several mechanisms have been proposed that regulate their quiescence, however, by analogy with normal hematopoietic stem cells, a key role may be carried out by the signaling pathways Notch and Hedgehog (Hh). The objectives of this study are to analyze the role of Notch and Hh pathways in the quiescence of LSC and to verify if the pharmacolog

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Roche, B., B. Arcangioli, and R. A. Martienssen. "RNA interference is essential for cellular quiescence." Science 354, no. 6313 (2016): aah5651. http://dx.doi.org/10.1126/science.aah5651.

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Brien, Gerard L., and Adrian P. Bracken. "The PCL1-p53 axis promotes cellular quiescence." Cell Cycle 15, no. 3 (2016): 305–6. http://dx.doi.org/10.1080/15384101.2015.1124701.

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Holt, S. E., W. E. Wright, and J. W. Shay. "Regulation of telomerase activity in immortal cell lines." Molecular and Cellular Biology 16, no. 6 (1996): 2932–39. http://dx.doi.org/10.1128/mcb.16.6.2932.

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Telomerase is a ribonucleoprotein whose activity has been detected in germ line cells, immortal cells, and most cancer cells. Except in stem cells, which have a low level of telomerase activity, its activity is absent from normal somatic tissues. Understanding the regulation of telomerase activity is critical for the development of potential tools for the diagnosis and treatment of cancer. Using the telomeric repeat amplification protocol, we found that immortal, telomerase-positive, pseudodiploid human cells (HT1080 and HL60 cells) sorted by flow repressed in quiescent cells. This was true wh

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Zahedi, Yasaman, Mickael Durand-Dubief, and Karl Ekwall. "High-Throughput Flow Cytometry Combined with Genetic Analysis Brings New Insights into the Understanding of Chromatin Regulation of Cellular Quiescence." International Journal of Molecular Sciences 21, no. 23 (2020): 9022. http://dx.doi.org/10.3390/ijms21239022.

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Cellular quiescence is a reversible differentiation state when cells are changing the gene expression program to reduce metabolic functions and adapt to a new cellular environment. When fission yeast cells are deprived of nitrogen in the absence of any mating partner, cells can reversibly arrest in a differentiated G0-like cellular state, called quiescence. This change is accompanied by a marked alteration of nuclear organization and a global reduction of transcription. Using high-throughput flow cytometry combined with genetic analysis, we describe the results of a comprehensive screen for ge

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Pascetti, Erica M., Sebastian Restrepo-Cruz, Muskan Floren, Chelsea A. Saito-Reis, Victoria D. Balise, and Jennifer M. Gillette. "Tetraspanin CD82 Regulates Hematopoietic Stem and Progenitor Cell Quiescence and Regeneration." Blood 138, Supplement 1 (2021): 3264. http://dx.doi.org/10.1182/blood-2021-153266.

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Abstract The significant cellular demand of the hematopoietic system is maintained by a rare pool of tissue-specific, hematopoietic stem and progenitor cells (HSPCs) that are primarily found in a quiescent state. Upon hemopoietic stresses, such as significant bleeding, overwhelming infection, and myelosuppressive therapy, HSPCs undergo rapid cell cycle activation, but ultimately must return to quiescence to prevent exhaustion of the hematopoietic system. Emerging evidence from our laboratory suggests that the tetraspanin CD82 plays a critical role in the regulation of HSPC quiescence and activ

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Torres-Barrera, Patricia, Dafne Moreno-Lorenzana, José Antonio Alvarado-Moreno, et al. "Cell Contact with Endothelial Cells Favors the In Vitro Maintenance of Human Chronic Myeloid Leukemia Stem and Progenitor Cells." International Journal of Molecular Sciences 23, no. 18 (2022): 10326. http://dx.doi.org/10.3390/ijms231810326.

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Chronic Myeloid Leukemia (CML) originates in a leukemic stem cell that resides in the bone marrow microenvironment, where they coexist with cellular and non-cellular elements. The vascular microenvironment has been identified as an important element in CML development since an increase in the vascularization has been suggested to be related with poor prognosis; also, using murine models, it has been reported that bone marrow endothelium can regulate the quiescence and proliferation of leukemic stem and progenitor cells. This observation, however, has not been evaluated in primary human cells.

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An, Sugyun, Si-Young Cho, Junsoo Kang, et al. "Inhibition of 3-phosphoinositide–dependent protein kinase 1 (PDK1) can revert cellular senescence in human dermal fibroblasts." Proceedings of the National Academy of Sciences 117, no. 49 (2020): 31535–46. http://dx.doi.org/10.1073/pnas.1920338117.

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Cellular senescence is defined as a stable, persistent arrest of cell proliferation. Here, we examine whether senescent cells can lose senescence hallmarks and reenter a reversible state of cell-cycle arrest (quiescence). We constructed a molecular regulatory network of cellular senescence based on previous experimental evidence. To infer the regulatory logic of the network, we performed phosphoprotein array experiments with normal human dermal fibroblasts and used the data to optimize the regulatory relationships between molecules with an evolutionary algorithm. From ensemble analysis of netw

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Boulais, Philip E., and Paul S. Frenette. "Making sense of hematopoietic stem cell niches." Blood 125, no. 17 (2015): 2621–29. http://dx.doi.org/10.1182/blood-2014-09-570192.

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Abstract The hematopoietic stem cell (HSC) niche commonly refers to the pairing of hematopoietic and mesenchymal cell populations that regulate HSC self-renewal, differentiation, and proliferation. Anatomic localization of the niche is a dynamic unit from the developmental stage that allows proliferating HSCs to expand before they reach the bone marrow where they adopt a quiescent phenotype that protects their integrity and functions. Recent studies have sought to clarify the complexity behind the HSC niche by assessing the contributions of specific cell populations to HSC maintenance. In part

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Keroack, Caroline D., and Manoj T. Duraisingh. "Molecular mechanisms of cellular quiescence in apicomplexan parasites." Current Opinion in Microbiology 70 (December 2022): 102223. http://dx.doi.org/10.1016/j.mib.2022.102223.

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Liu, Helen, Adam S. Adler, Eran Segal, and Howard Y. Chang. "A Transcriptional Program Mediating Entry into Cellular Quiescence." PLoS Genetics 3, no. 6 (2007): e91. http://dx.doi.org/10.1371/journal.pgen.0030091.

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Sajiki, K., M. Hatanaka, T. Nakamura, et al. "Genetic control of cellular quiescence in S. pombe." Journal of Cell Science 122, no. 9 (2009): 1418–29. http://dx.doi.org/10.1242/jcs.046466.

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Raheja, Radhika, and Roopali Gandhi. "FXR1: Linking cellular quiescence, immune genes and cancer." Cell Cycle 15, no. 20 (2016): 2695–96. http://dx.doi.org/10.1080/15384101.2016.1215692.

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van Velthoven, Cindy T. J., and Thomas A. Rando. "Stem Cell Quiescence: Dynamism, Restraint, and Cellular Idling." Cell Stem Cell 24, no. 2 (2019): 213–25. http://dx.doi.org/10.1016/j.stem.2019.01.001.

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Kuneš, Pavel, Zdeňka Holubcová, and Jan Krejsek. "Occurrence and Significance of the Nuclear Transcription Factor Krüppel-Like Factor 4 (KLF4) in the Vessel Wall." Acta Medica (Hradec Kralove, Czech Republic) 52, no. 4 (2009): 135–39. http://dx.doi.org/10.14712/18059694.2016.119.

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Practically all mammalian cells including human can switch, according to micro- or macroenvironmental conditions, from states of cellular quiescence to inflammatory activation and vice versa. Along with recent knowledge, cellular quiescence is not a passive, but a highly active state with broad engagement of the cell synthetic and secretory machinery. Inflammatory activation is a beneficial process in cases of infection; however, if its control fails, it may degrade into autoimmune diseases or cancer growth. Control over cellular quiescence is exerted predominantly by a set of zincfinger trans

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Rojas-Sutterlin, Shanti, André Haman, and Trang Hoang. "Hematopoietic Stem Cells Have an Intrinsic Expansion Limit." Blood 120, no. 21 (2012): 4749. http://dx.doi.org/10.1182/blood.v120.21.4749.4749.

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Abstract Abstract 4749 Hematopoietic stem cell (HSC) transplantation is the first successful cellular therapy and remains the only treatment providing long-term cure in acute myeloblastic leukemia. At the apex of the hematopoietic system, quiescent HSCs are spared by chemotherapeutic treatments that target proliferating cells and therefore can regenerate the entire blood system of a patient after drug exposure. Nevertheless, the consequence of repeated chemotherapy regimen on HSC function remains to be clarified. We previously showed that Scl/Tal1 gene dosage regulates HSC quiescence and funct

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