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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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DNA damage accumulation and repair defects in acute myeloid leukemia: implications for pathogenesis, disease progression, and chemotherapy resistance

TL;DR: The current review summarizes the DDR pathways in the context of AML and describes how aberrant DNA damage response can affect AML pathogenesis, disease progression, and resistance to standard chemotherapy, and how defects in DDR pathways may provide a new avenue for personalized therapeutic strategies in AML.
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Interplay of dFOXO and two ETS-family transcription factors determines lifespan in Drosophila melanogaster.

TL;DR: A complex interplay between evolutionarily conserved ETS factors and dFOXO is revealed, the functional significance of which may extend well beyond animal lifespan.
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Dickkopf-1 promotes hematopoietic regeneration via direct and niche-mediated mechanisms.

TL;DR: Deletion of the pro-apoptotic genes Bak and Bax in Osx in osterix cells in mice promotes HSC regeneration and hematopoietic radioprotection following total body irradiation and demonstrates paracrine cross-talk between BM osteolineage cells and endothelial cells in regulating hematopolietic reconstitution following injury.
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Pharmacological Regulation of Oxidative Stress in Stem Cells

TL;DR: The defined roles of oxidative Stress in pluripotent stem cells and hematopoietic stem cells are introduced and the potential applications of pharmacological approaches for regulating oxidative stress in regenerative medicine are discussed.
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The role of autophagy in neonatal tissues: just a response to amino acid starvation?

TL;DR: Autophagy is activated soon after birth in neonatal tissues and is essential for survival because mice deficient in Atg5 or Atg7 autophagy genes die within 1 day after birth, but may have other important functions in Neonatal physiology, including glycogen degradation, programmed cell remodeling and response to oxidative stress.
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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