Literature DB >> 29311260

mTOR signaling in stem and progenitor cells.

Delong Meng1,2,3, Anderson R Frank1,2,3, Jenna L Jewell4,2,3.   

Abstract

The mammalian target of rapamycin (mTOR) senses nutrients and growth factors to coordinate cell growth, metabolism and autophagy. Extensive research has mapped the signaling pathways regulated by mTOR that are involved in human diseases, such as cancer, and in diabetes and ageing. Recently, however, new studies have demonstrated important roles for mTOR in promoting the differentiation of adult stem cells, driving the growth and proliferation of stem and progenitor cells, and dictating the differentiation program of multipotent stem cell populations. Here, we review these advances, providing an overview of mTOR signaling and its role in murine and human stem and progenitor cells.
© 2018. Published by The Company of Biologists Ltd.

Entities:  

Keywords:  Amino acids; Metabolism; Signaling; Stem cell; mTOR

Mesh:

Substances:

Year:  2018        PMID: 29311260      PMCID: PMC5825873          DOI: 10.1242/dev.152595

Source DB:  PubMed          Journal:  Development        ISSN: 0950-1991            Impact factor:   6.868


  215 in total

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5.  PtdIns(3,4,5)P3-Dependent Activation of the mTORC2 Kinase Complex.

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6.  Inhibition of pluripotential embryonic stem cell differentiation by purified polypeptides.

Authors:  A G Smith; J K Heath; D D Donaldson; G G Wong; J Moreau; M Stahl; D Rogers
Journal:  Nature       Date:  1988-12-15       Impact factor: 49.962

7.  Targets for cell cycle arrest by the immunosuppressant rapamycin in yeast.

Authors:  J Heitman; N R Movva; M N Hall
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9.  Target of rapamycin in yeast, TOR2, is an essential phosphatidylinositol kinase homolog required for G1 progression.

Authors:  J Kunz; R Henriquez; U Schneider; M Deuter-Reinhard; N R Movva; M N Hall
Journal:  Cell       Date:  1993-05-07       Impact factor: 41.582

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Journal:  Stem Cells Dev       Date:  2016-07-01       Impact factor: 3.272

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8.  The MTOR signaling pathway regulates macrophage differentiation from mouse myeloid progenitors by inhibiting autophagy.

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