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Journal articles on the topic 'Stem cell quiescence'

Author: Grafiati

Published: 2 June 2025

Last updated: 31 July 2025

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1

Otsuki, L., and A. H. Brand. "Cell cycle heterogeneity directs the timing of neural stem cell activation from quiescence." Science 360, no. 6384 (2018): 99–102. http://dx.doi.org/10.1126/science.aan8795.

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Quiescent stem cells in adult tissues can be activated for homeostasis or repair. Neural stem cells (NSCs) in Drosophila are reactivated from quiescence in response to nutrition by the insulin signaling pathway. It is widely accepted that quiescent stem cells are arrested in G0. In this study, however, we demonstrate that quiescent NSCs (qNSCs) are arrested in either G2 or G0. G2-G0 heterogeneity directs NSC behavior: G2 qNSCs reactivate before G0 qNSCs. In addition, we show that the evolutionarily conserved pseudokinase Tribbles (Trbl) induces G2 NSCs to enter quiescence by promoting degradat

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2

Mohammad, Karamat, Paméla Dakik, Younes Medkour, Darya Mitrofanova, and Vladimir I. Titorenko. "Quiescence Entry, Maintenance, and Exit in Adult Stem Cells." International Journal of Molecular Sciences 20, no. 9 (2019): 2158. http://dx.doi.org/10.3390/ijms20092158.

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Cells of unicellular and multicellular eukaryotes can respond to certain environmental cues by arresting the cell cycle and entering a reversible state of quiescence. Quiescent cells do not divide, but can re-enter the cell cycle and resume proliferation if exposed to some signals from the environment. Quiescent cells in mammals and humans include adult stem cells. These cells exhibit improved stress resistance and enhanced survival ability. In response to certain extrinsic signals, adult stem cells can self-renew by dividing asymmetrically. Such asymmetric divisions not only allow the mainten

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3

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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4

Purnell, B. A. "Translating stem cell quiescence." Science 351, no. 6274 (2016): 677–78. http://dx.doi.org/10.1126/science.351.6274.677-b.

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5

Liu, Yan, Yasuhiko Miyata, Goro Sashida, et al. "Genetic Uncoupling of the Regulation of Hematopoietic Stem Cell Quiescence and Self-Renewal." Blood 108, no. 11 (2006): 1347. http://dx.doi.org/10.1182/blood.v108.11.1347.1347.

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Abstract It is usually stated that HSCs must choose to either self-renew or to differentiate and lose some of their multi potentiality. Recently, we demonstrated that MEF, an ETS family of transcription factor, played an important role in regulating HSC quiescence, illustrating a third choice for the HSC, namely to make an “active” choice and remain quiescent, without undergoing either self-renewal, or differentiation. MEF null HSCs are more quiescent than normal HSCs. In addition, MEF null mice exhibit greater numbers of hematopoietic stem cells and show resistance to chemotherapy and radiati

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6

Liu, Yan, Shannon E. Elf, Yasuhiko Miyata, et al. "Regulation of Hematopoietic Stem Cell Quiescence - A Novel Role for p53." Blood 110, no. 11 (2007): 92. http://dx.doi.org/10.1182/blood.v110.11.92.92.

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Abstract Although the p53 tumor suppressor can elicit cell-cycle arrest or apoptosis in hematopoietic cells upon DNA damage, its function during steady-state hematopoiesis is largely unknown. We demonstrated that the Ets transcription factor MEF/ELF4 regulates both HSC proliferation/self-renewal and quiescence, as Mef null mice exhibit greater numbers of hematopoietic stem cells and the Mef null HSCs are more quiescent than normal. As such, the hematopoietic compartment of Mef null mice shows significant resistance to chemotherapy and radiation (Lacorazza et al., Cancer Cell, 2006). In this st

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7

Ghaffari, Saghi. "Regulation of Hematopoietic Stem Cell Mitochondrial Metabolism." Blood 128, no. 22 (2016): SCI—33—SCI—33. http://dx.doi.org/10.1182/blood.v128.22.sci-33.sci-33.

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Abstract Hematopoietic stem cells (HSCs) like most, if not all, adult stem cells are primarily quiescent but have the potential to become highly active on demand. HSC quiescence is maintained by glycolytic metabolism and low levels of reactive oxygen species (ROS), which indicate that mitochondria are relatively inactive in quiescent HSC. However, HSC cycling - and exit of quiescence state - require a swift metabolic switch from glycolysis to mitochondrial oxidative phosphorylation. To improve our understanding of mechanisms that integrate energy metabolism with HSC homeostasis, my laboratory

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8

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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9

VanHook, Annalisa M. "Inflammation induces stem cell quiescence." Science Signaling 12, no. 605 (2019): eaaz9665. http://dx.doi.org/10.1126/scisignal.aaz9665.

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10

Sorrentino, Brian P. "Scl and stem cell quiescence." Blood 115, no. 4 (2010): 751–52. http://dx.doi.org/10.1182/blood-2009-11-251264.

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11

Li, Ling, and Ravi Bhatia. "Stem Cell Quiescence: Figure 1." Clinical Cancer Research 17, no. 15 (2011): 4936–41. http://dx.doi.org/10.1158/1078-0432.ccr-10-1499.

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12

Zhou, Shaopu, Lifang Han, and Zhenguo Wu. "A Long Journey before Cycling: Regulation of Quiescence Exit in Adult Muscle Satellite Cells." International Journal of Molecular Sciences 23, no. 3 (2022): 1748. http://dx.doi.org/10.3390/ijms23031748.

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Skeletal muscle harbors a pool of stem cells called muscle satellite cells (MuSCs) that are mainly responsible for its robust regenerative capacities. Adult satellite cells are mitotically quiescent in uninjured muscles under homeostasis, but they exit quiescence upon injury to re-enter the cell cycle to proliferate. While most of the expanded satellites cells differentiate and fuse to form new myofibers, some undergo self-renewal to replenish the stem cell pool. Specifically, quiescence exit describes the initial transition of MuSCs from quiescence to the first cell cycle, which takes much lo

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13

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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14

Tipping, Alex J., Cristina Pina, Anders Castor, et al. "High GATA-2 expression inhibits human hematopoietic stem and progenitor cell function by effects on cell cycle." Blood 113, no. 12 (2009): 2661–72. http://dx.doi.org/10.1182/blood-2008-06-161117.

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Abstract Evidence suggests the transcription factor GATA-2 is a critical regulator of murine hematopoietic stem cells. Here, we explore the relation between GATA-2 and cell proliferation and show that inducing GATA-2 increases quiescence (G0 residency) of murine and human hematopoietic cells. In human cord blood, quiescent fractions (CD34+CD38−HoechstloPyronin Ylo) express more GATA-2 than cycling counterparts. Enforcing GATA-2 expression increased quiescence of cord blood cells, reducing proliferation and performance in long-term culture-initiating cell and colony-forming cell (CFC) assays. G

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15

Higuchi, Yusuke, Jia-Ling Teo, Daniel Yi, and Michael Kahn. "Safely Targeting Cancer, the Wound That Never Heals, Utilizing CBP/Beta-Catenin Antagonists." Cancers 17, no. 9 (2025): 1503. https://doi.org/10.3390/cancers17091503.

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Stem cells, both normal somatic (SSC) and cancer stem cells (CSC) exist in minimally two states, i.e., quiescent and activated. Regulation of these two states, including their reliance on different metabolic processes, i.e., FAO and glycolysis in quiescent versus activated stem cells respectively, involves the analysis of a complex array of factors (nutrient and oxygen levels, adhesion molecules, cytokines, etc.) to initiate the epigenetic changes to either depart or enter quiescence. Quiescence is a critical feature of SSC that is required to maintain the genomic integrity of the stem cell po

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16

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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17

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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18

Hidayat, Moulid, Moulid Hidayat, and Nurwidya Fariz. "Peran FBXW7 pada Stem Cell Normal dan Cancer Stem Cell." Unram Medical Journal 5, no. 2 (2016): 44. http://dx.doi.org/10.29303/jku.v5i2.195.

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F-box and WD40 repeat domain-containing 7 (FBXW7) adalah protein F-box yang merupakan komponen sistem ubiquitin proteasome yang berhubungan dengan beberapa protein onkogenik penting seperti Notch, c-Myc, cyclin E and c-Jun dalam mengatur proses pertumbuhan dan perkembangan sel, metabolism sel, diferensiasi dan apoptosis. Beberapa studi terkini menunjukkan bahwa FBXW7 berperan dalam perkembangan beberapa stem cell, mencakup proses self-renewal, multipotensi, diferensiasi, dan survival. Cancer stem cell (CSC) diketahui merupakan salah satu penyebab resistensi tumor terhadap berbagai kemoterapi,

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19

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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20

Liu, Lu, Ayaka Inoki, Kelly Fan, et al. "ER-associated degradation preserves hematopoietic stem cell quiescence and self-renewal by restricting mTOR activity." Blood 136, no. 26 (2020): 2975–86. http://dx.doi.org/10.1182/blood.2020007975.

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Abstract Hematopoietic stem cells (HSC) self-renew to sustain stem cell pools and differentiate to generate all types of blood cells. HSCs remain in quiescence to sustain their long-term self-renewal potential. It remains unclear whether protein quality control is required for stem cells in quiescence when RNA content, protein synthesis, and metabolic activities are profoundly reduced. Here, we report that protein quality control via endoplasmic reticulum-associated degradation (ERAD) governs the function of quiescent HSCs. The Sel1L/Hrd1 ERAD genes are enriched in the quiescent and inactive H

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21

Cheung, Tom H., and Thomas A. Rando. "Molecular regulation of stem cell quiescence." Nature Reviews Molecular Cell Biology 14, no. 6 (2013): 329–40. http://dx.doi.org/10.1038/nrm3591.

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22

Liu, Yan, Shannon E. Elf, Yasuhiko Miyata, et al. "p53 Regulates Hematopoietic Stem Cell Quiescence." Cell Stem Cell 4, no. 1 (2009): 37–48. http://dx.doi.org/10.1016/j.stem.2008.11.006.

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23

Li, June. "Quiescence regulators for hematopoietic stem cell." Experimental Hematology 39, no. 5 (2011): 511–20. http://dx.doi.org/10.1016/j.exphem.2011.01.008.

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24

Watt, Fiona M., and Kim B. Jensen. "Epidermal stem cell diversity and quiescence." EMBO Molecular Medicine 1, no. 5 (2009): 260–67. http://dx.doi.org/10.1002/emmm.200900033.

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25

Pelletier, Alexandre, Arnaud Carrier, Yongmei Zhao, et al. "Epigenetic and Transcriptomic Programming of HSC Quiescence Signaling in Large for Gestational Age Neonates." International Journal of Molecular Sciences 23, no. 13 (2022): 7323. http://dx.doi.org/10.3390/ijms23137323.

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Excessive fetal growth is associated with DNA methylation alterations in human hematopoietic stem and progenitor cells (HSPC), but their functional impact remains elusive. We implemented an integrative analysis combining single-cell epigenomics, single-cell transcriptomics, and in vitro analyses to functionally link DNA methylation changes to putative alterations of HSPC functions. We showed in hematopoietic stem cells (HSC) from large for gestational age neonates that both DNA hypermethylation and chromatin rearrangements target a specific network of transcription factors known to sustain ste

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26

Singh, Balraj, and Anthony Lucci. "Abstract 5280: A strategic framework for modeling abnormal quiescence that drives cancer evolution, and for preclinical development of therapies to prevent recurrence and metastasis in high-risk patients." Cancer Research 85, no. 8_Supplement_1 (2025): 5280. https://doi.org/10.1158/1538-7445.am2025-5280.

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Abstract Our goal is to develop a cell culture model of cancer cells that persist under all challenges including therapies, mostly in quiescence, and evolve further to cause recurrence. The rationale for the choice of model as cell culture is that it is ideal of evaluating therapeutic strategies that may inhibit highly abnormal but adaptable cells. Body imposes a variety of bottlenecks ranging from different components of immunity to metabolic challenges to enforce quiescence and influence cancer evolution. As it is not possible to replicate all such bottlenecks in cell culture, our approach i

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Vannini, Nicola, Mukul Girotra, Olaia M. Naveiras, et al. "Mitochondrial Activity Determines Hematopoietic Stem Cell Fate Decisions." Blood 124, no. 21 (2014): 4327. http://dx.doi.org/10.1182/blood.v124.21.4327.4327.

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Abstract A tight control of hematopoietic stem cell (HSC) quiescence, self-renewal and differentiation is crucial for lifelong blood production. The mechanisms behind this control are still poorly understood. Here we show that mitochondrial activity determines HSC fate decisions. A low mitochondrial membrane potential (Δψm) predicts long-term multi-lineage blood reconstitution capability, as we show for freshly isolated and in vitro-cultured HSCs. However, as in vivo both quiescent and cycling HSCs have comparable Δψm distributions, a low Δψm is not per se related to quiescence but is also fou

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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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Lala-Tabbert, Neena, Hamood AlSudais, François Marchildon, Dechen Fu, and Nadine Wiper-Bergeron. "CCAAT/enhancer-binding protein beta promotes muscle stem cell quiescence through regulation of quiescence-associated genes." STEM CELLS 39, no. 3 (2020): 345–57. http://dx.doi.org/10.1002/stem.3319.

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30

Dong, Jian, Yuan-Bo Pan, Xin-Rong Wu, et al. "A neuronal molecular switch through cell-cell contact that regulates quiescent neural stem cells." Science Advances 5, no. 2 (2019): eaav4416. http://dx.doi.org/10.1126/sciadv.aav4416.

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The quiescence of radial neural stem cells (rNSCs) in adult brain is regulated by environmental stimuli. However, little is known about how the neurogenic niche couples the external signal to regulate activation and transition of quiescent rNSCs. Here, we reveal that long-term excitation of hippocampal dentate granule cells (GCs) upon voluntary running leads to activation of adult rNSCs in the subgranular zone and thereby generation of newborn neurons. Unexpectedly, the role of these excited GC neurons in NSCs depends on direct GC-rNSC interaction in the local niche, which is through down-regu

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Sauer, Karsten. "IP3 3-Kinase B Controls Hematopoietic Stem Cell Homeostasis and Prevents Lethal Hematopoietic Failure in Mice." Blood 124, no. 21 (2014): 250. http://dx.doi.org/10.1182/blood.v124.21.250.250.

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Tight regulation of hematopoietic stem cell (HSC) homeostasis ensures life-long hematopoiesis and prevents blood cancers. The mechanisms balancing HSC quiescence with expansion and differentiation into hematopoietic progenitors are incompletely understood. Here, we identify inositoltrisphosphate (IP3) 3-kinase B (Itpkb) as a novel essential regulator of HSC quiescence and function. Young Itpkb-/- mice accumulated phenotypic HSC which were less quiescent and proliferated more than wildtype controls. Itpkb-/- HSC downregulated quiescence and stemness associated mRNAs, but upregulated activation,

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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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Woolthuis, Carolien M., Annet Z. Vos, Gerwin Huls, Joost TM de Wolf, Jan J. Schuringa, and Edo Vellenga. "Loss of Stem Cell Quiescence and Impaired Stem Cell Function of CD34+/CD38low Cells One Year Following Autologous Stem Cell Transplantation." Blood 118, no. 21 (2011): 1893. http://dx.doi.org/10.1182/blood.v118.21.1893.1893.

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Abstract Abstract 1893 Autologous stem cell transplantation (ASCT) allows the application of high-dose chemotherapy and is included in the standard treatment regimens for multiple myeloma and relapsing lymphoma. The application of ASCT has considerably improved treatment outcome but in 30–50% of the patients the underlying malignant disorder relapses. In that case treatment options are limited, in part due to a diminished capacity of the transplanted bone marrow to tolerate chemotherapy. The transplanted bone marrow seems to be more vulnerable to chemotoxic stress. This is supported by our rec

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Shiroshita, Kohei, Hiroshi Kobayashi, Shinichiro Okamoto, Keisuke Kataoka, and Keiyo Takubo. "Reverting to Quiescence Preserves Hematopoietic Stem Cells Following Genome Editing." Blood 138, Supplement 1 (2021): 3977. http://dx.doi.org/10.1182/blood-2021-149520.

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Abstract Hematopoietic stem cells (HSCs) in steady-state are quiescent in cell cycle. CRISPR-Cas9 genome editing has revolutionized the HSC research and therapeutic application of HSCs for hematological diseases. Although these methods and clinical results are promising, keeping HSC function after highly efficient genome editing is still challenging because HSCs gradually lose their repopulation capacity following cell cycle activation. Preserving the function of HSCs after genome editing is an urgent issue. In this study, we interrogated the culture method following genome editing to reverse

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Kandasamy, Mahesh, Bernadette Lehner, Sabrina Kraus, et al. "TGF-beta signalling in the adult neurogenic niche promotes stem cell quiescence as well as generation of new neurons." J Cell Mol Med 18, no. 7 (2014): 1444–59. https://doi.org/10.1111/jcmm.12298.

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Members of the transforming growth factor (TGF)-b family govern a wide range of mechanisms in brain development and in the adult, in particular neuronal/glial differentiation and survival, but also cell cycle regulation and neural stem cell maintenance. This clearly created some discrepancies in the field with some studies favouring neuronal differentiation/survival of progenitors and others favouring cell cycle exit and neural stem cell quiescence/maintenance. Here, we provide a unifying hypothesis claiming that through its regulation of neural progenitor cell (NPC) proliferati

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Radak, Mehran, and Hossein Fallahi. "The Epigenetic Regulation of Quiescent in Stem Cells." Global Medical Genetics 10, no. 04 (2023): 339–44. http://dx.doi.org/10.1055/s-0043-1777072.

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AbstractThis review article discusses the epigenetic regulation of quiescent stem cells. Quiescent stem cells are a rare population of stem cells that remain in a state of cell cycle arrest until activated to proliferate and differentiate. The molecular signature of quiescent stem cells is characterized by unique epigenetic modifications, including histone modifications and deoxyribonucleic acid (DNA) methylation. These modifications play critical roles in regulating stem cell behavior, including maintenance of quiescence, proliferation, and differentiation. The article specifically focuses on

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Rezazadeh, Sarallah. "Stem cell exhaustion and its role in healthy aging." Open Access Government 46, no. 1 (2025): 0–61. https://doi.org/10.56367/oag-046-11950.

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Stem cell exhaustion and its role in healthy aging Scientist Sarallah Rezazadeh from the Icahn School of Medicine explores the molecular mechanisms behind adult stem cells as we age. Stem cell exhaustion is the gradual decline in the function and regenerative potential of adult stem cells over time. In various tissues, the upkeep of homeostasis and the capacity to regenerate after injury depend on tissue-specific adult stem cells. These stem cells typically follow tissue-specific differentiation patterns. Their ability to alternate between states of rest (quiescence) and active proliferation i

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Zelentsova, Katya, Ziv Talmi, Ghada Abboud-Jarrous, et al. "Protein S Regulates Neural Stem Cell Quiescence and Neurogenesis." STEM CELLS 35, no. 3 (2016): 679–93. http://dx.doi.org/10.1002/stem.2522.

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Sirin, Olga, Orla M. Conneely, and Margaret A. Goodell. "Enforced Nr4a2 expression Drives HSCs into Quiescence." Blood 112, no. 11 (2008): 1326. http://dx.doi.org/10.1182/blood.v112.11.1326.1326.

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Abstract Hematopoietic stem cells (HSCs) are used as a paradigm for understanding somatic stem cell biology, yet the factors that regulate their self-renewal and differentiation are poorly understood. Our lab has recently discovered that within the hematopoietic lineage, Nr4a2 expression is restricted to the stem and progenitor cell compartment. Furthermore, we have observed a dramatic decrease in its expression when the bone marrow cells are exposed to 5-fluorouracil which forces quiescent HSCs into cycle. We therefore hypothesize that Nr4a2 may be involved in maintaining stem cell quiescence

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Lu, Zhanping, Anna L. F. V. Assumpção, Aaron D. Viny, Ross L. Levine, and Xuan Pan. "YY1 Controls Hematopoietic Stem Cell Quiescence By Repressing Cohesin Expression." Blood 132, Supplement 1 (2018): 3831. http://dx.doi.org/10.1182/blood-2018-99-118679.

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Abstract Hematopoietic stem cells (HSCs) are undifferentiated, self-renewing, pluripotent cells that have the capacity to differentiate into all mature lineage-specific cells in adult blood. Adult HSCs can remain in a quiescent state for a prolonged time, and quiescence is a fundamental characteristic of HSCs in adult bone marrow. Thus, the cell cycle must be precisely regulated. Yin Yang 1 (YY1) is a multifunctional transcription factor and Polycomb Group Protein (PcG) that is important for embryonic development, adult hematopoiesis, cell proliferation and maintaining higher-order chromosomal

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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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Gan, Boyi, and Ronald DePinho. "mTORC1 signaling governs hematopoietic stem cell quiescence." Cell Cycle 8, no. 7 (2009): 1003–6. http://dx.doi.org/10.4161/cc.8.7.8045.

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Luo, Meng, Jin-Fan Li, Qi Yang, et al. "Stem cell quiescence and its clinical relevance." World Journal of Stem Cells 12, no. 11 (2020): 1307–26. http://dx.doi.org/10.4252/wjsc.v12.i11.1307.

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44

Jayapal, Senthil Raja, and Philipp Kaldis. "Cyclin E1 regulates hematopoietic stem cell quiescence." Cell Cycle 12, no. 23 (2013): 3588. http://dx.doi.org/10.4161/cc.26974.

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Kunisaki, Yuya, Ingmar Bruns, Christoph Scheiermann, et al. "Arteriolar niches maintain haematopoietic stem cell quiescence." Nature 502, no. 7473 (2013): 637–43. http://dx.doi.org/10.1038/nature12612.

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46

Ding, Rouven, and Christian Berger. "Hippo pathway regulates neural stem cell quiescence." Cell Cycle 15, no. 12 (2016): 1525–26. http://dx.doi.org/10.1080/15384101.2016.1171653.

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47

Basak, Onur, Teresa G. Krieger, Mauro J. Muraro, et al. "Troy+ brain stem cells cycle through quiescence and regulate their number by sensing niche occupancy." Proceedings of the National Academy of Sciences 115, no. 4 (2018): E610—E619. http://dx.doi.org/10.1073/pnas.1715911114.

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The adult mouse subependymal zone provides a niche for mammalian neural stem cells (NSCs). However, the molecular signature, self-renewal potential, and fate behavior of NSCs remain poorly defined. Here we propose a model in which the fate of active NSCs is coupled to the total number of neighboring NSCs in a shared niche. Using knock-in reporter alleles and single-cell RNA sequencing, we show that the Wnt target Tnfrsf19/Troy identifies both active and quiescent NSCs. Quantitative analysis of genetic lineage tracing of individual NSCs under homeostasis or in response to injury reveals rapid e

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Suda, Toshio. "Metabolic Regulation of Hematopoietic Stem Cells During Stress." Blood 120, no. 21 (2012): SCI—42—SCI—42. http://dx.doi.org/10.1182/blood.v120.21.sci-42.sci-42.

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Abstract Abstract SCI-42 Tissue homeostasis over the life of an organism relies on both self-renewal and multipotent differentiation of stem cells. Hematopoietic stem cells (HSCs) are sustained in a specific microenvironment known as the stem cell niche. Adult HSCs are kept quiescent during the cell cycle in the endosteal niche of the bone marrow. Normal HSCs maintain intracellular hypoxia, stabilize the hypoxia-inducible factor-1a (HIF-1a) protein, and generate ATP by anaerobic metabolism. In HIF-1a deficiency, HSCs became metabolically aerobic, lost cell cycle quiescence, and finally became

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Wirick, Matthew J., Allison R. Cale, Isaac T. Smith, et al. "daf-16/FOXO blocks adult cell fate in Caenorhabditis elegans dauer larvae via lin-41/TRIM71." PLOS Genetics 17, no. 11 (2021): e1009881. http://dx.doi.org/10.1371/journal.pgen.1009881.

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Many tissue-specific stem cells maintain the ability to produce multiple cell types during long periods of non-division, or quiescence. FOXO transcription factors promote quiescence and stem cell maintenance, but the mechanisms by which FOXO proteins promote multipotency during quiescence are still emerging. The single FOXO ortholog in C. elegans, daf-16, promotes entry into a quiescent and stress-resistant larval stage called dauer in response to adverse environmental cues. During dauer, stem and progenitor cells maintain or re-establish multipotency to allow normal development to resume afte

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Jiang, Linjia, Xue Han, Jin Wang та ін. "SHP-1 regulates hematopoietic stem cell quiescence by coordinating TGF-β signaling". Journal of Experimental Medicine 215, № 5 (2018): 1337–47. http://dx.doi.org/10.1084/jem.20171477.

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Cell cycle quiescence is critical for hematopoietic stem cell (HSC) maintenance. TGF-β signaling in bone marrow niche has been identified in regulating HSC quiescence; however, the intrinsic regulatory mechanisms remain unclear. This study reports that Shp-1 knockout HSCs have attenuated quiescence and impaired long-term self-renewal. SHP-1–activated HSCs are surrounded by megakaryocytes, which regulate HSC quiescence by producing TGF-β1. Mechanistically, SHP-1 interacts with the immunoreceptor tyrosine-based inhibition motif on TGF-β receptor 1 and is critical for TGF-β signaling activation i

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