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FoxOs are critical mediators of hematopoietic stem cell resistance to physiologic oxidative stress.

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TLDR
FoxO proteins play essential roles in the response to physiologic oxidative stress and thereby mediate quiescence and enhanced survival in the HSC compartment, a function that is required for its long-term regenerative potential.
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This article is published in Cell.The article was published on 2007-01-26 and is currently open access. It has received 1511 citations till now. The article focuses on the topics: FOXO Family & Hematopoietic stem cell.

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Citations
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Hand of FATe: lipid metabolism in hematopoietic stem cells.

TL;DR: As these areas evolve, more studies are required to determine the exact contribution of lipids toward HSC maintenance, which will allow newer therapeutic targets to help reduce abnormal hematopoiesis such as myelopoiedis, which contributes to many metabolic diseases.
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Forkhead Box(O) in Control of Reactive Oxygen Species and Genomic Stability to Ensure Healthy Lifespan

TL;DR: Possible connections between FOXO and the DNA damage response in the context of the broader role of connecting lifespan and disease are discussed.
Journal ArticleDOI

Younger for longer: insulin signalling, immunity and ageing.

TL;DR: The evolutionary conservation of the IIS pathway is reviewed and discussed in relation to recent findings on the molecular basis of ageing and the impact and significance of the evolutionary diversification of this pathway are reflected.
Journal Article

FOXO transcription factor activity is partially retained in quiescent CML stem cells and induced by tyrosine kinase inhibitors in CML progenitor cells [published online ahead of print December 1, 2009]. Blood. doi 10.1182/blood-2009-06-226621

TL;DR: It is demonstrated for the first time that TKI-induced G1 arrest in CML progenitor cells is mediated by re-activation of FOXOs, whilst quiescence of CML stem cells is regulated by sustained FOXO activity.
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Metaboloepigenetics: the Emerging Network in Stem Cell Homeostasis Regulation.

TL;DR: This review discusses the possible connections between metabolism and epigenetic regulation of stem cell differentiation and self-renewal, and describes pertinent literature that could explain how altered metabolic state and nutrition can contribute to disease development through epigenetic modifications.
References
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Akt Promotes Cell Survival by Phosphorylating and Inhibiting a Forkhead Transcription Factor

TL;DR: It is demonstrated that Akt also regulates the activity of FKHRL1, a member of the Forkhead family of transcription factors, which triggers apoptosis most likely by inducing the expression of genes that are critical for cell death, such as the Fas ligand gene.
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Prolonged rapamycin treatment inhibits mTORC2 assembly and Akt/PKB.

TL;DR: It is shown that rapamycin inhibits the assembly of mTORC2 and that, in many cell types, prolongedRapamycin treatment reduces the levels of m TORC2 below those needed to maintain Akt/PKB signaling.
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A clonogenic common myeloid progenitor that gives rise to all myeloid lineages

TL;DR: The prospective identification, purification and characterization, using cell-surface markers and flow cytometry, of a complementary clonogenic common myeloid progenitor that gives rise to all myeloids lineages is reported.
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Identification of Clonogenic Common Lymphoid Progenitors in Mouse Bone Marrow

TL;DR: The Lin(-)IL-7R(+)Thy-1(-)Sca-1loc-Kit(lo) population from adult mouse bone marrow possessed a rapid lymphoid-restricted (T, B, and NK) reconstitution capacity in vivo but completely lacked myeloid differentiation potential either in vivo or in vitro.
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