Regulation of Stem Cell Systems by PI3K/Akt Signaling

doi:https://doi.org/10.1007/978-1-60327-227-8_26

Book Chapter10.1007/978-1-60327-227-8_26

Regulation of Stem Cell Systems by PI3K/Akt Signaling

Tohru Kimura,Toru Nakano-2009-01-01-Humana Press eBooks

14

TL;DRAbstract

Stem cells can replenish their own population while supplying the cells necessary to maintain tissue homeostasis. Pluripotent stem cells, which have broader developmental potency than tissue stem cells, are derived from the same source in mice and humans. In this review, we summarize the functions of phosphoinositide-3 kinase (PI3K) and its downstream serine/threonine kinase Akt in a variety of stem cell systems. Primordial germ cells (PGCs), which are embryonic germ cell precursors, are unique in that they acquire pluripotency under cultural and pathological conditions. PGCs lacking Pten, which encodes a phosphatase that antagonizes PI3K signaling, give rise to early-onset testicular teratomas in vivo and augment the derivation of pluripotent embryonic germ (EG) cells in vitro. Transient activation of Akt sufficiently recapitulates the effects of Pten deficiency on EG cell derivation. Enhanced EG cell derivation is brought about by the Akt-mediated inhibition of the tumor suppressor p

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Stem cells can replenish their own population while supplying the cells necessary to maintain tissue homeostasis. Pluripotent stem cells, which have broader developmental potency than tissue stem cells, are derived from the same source in mice and humans. In this review, we summarize the functions of phosphoinositide-3 kinase (PI3K) and its downstream serine/threonine kinase Akt in a variety of stem cell systems. Primordial germ cells (PGCs), which are embryonic germ cell precursors, are unique in that they acquire pluripotency under cultural and pathological conditions. PGCs lacking Pten, which encodes a phosphatase that antagonizes PI3K signaling, give rise to early-onset testicular teratomas in vivo and augment the derivation of pluripotent embryonic germ (EG) cells in vitro. Transient activation of Akt sufficiently recapitulates the effects of Pten deficiency on EG cell derivation. Enhanced EG cell derivation is brought about by the Akt-mediated inhibition of the tumor suppressor p

Keywords

PI3K/AKT/mTOR pathwayCell biologyProtein kinase BBiologyStem cellInduced pluripotent stem cellEmbryonic stem cellPTEN

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