A molecular basis for human embryonic stem cell pluripotency. Review uri icon

Overview

MeSH

  • Animals
  • Forecasting
  • Humans
  • Transforming Growth Factor beta
  • Wnt Proteins

MeSH Major

  • Embryonic Stem Cells
  • Pluripotent Stem Cells
  • Signal Transduction

abstract

  • Embryonic stem cells (ESCs) are able to generate a wide array of differentiated cell fates while maintaining self-renewal. Understanding the biology of these choices may be central to the use of human embryonic stem cells (HESCs), both as a model for early human development as well as a resource for cell based therapies. Efforts to dissect the molecular mechanisms that mediate stem cell identity are underway, and in this review we summarize recent progress in defining the markers and pathways involved in these decisions. We discuss recent efforts to assess the molecular signature of pluripotent HESCs and highlight work demonstrating a set of genes, including representatives from the FGF, TGFbeta, and Wnt signaling pathways, that consistently mark the undifferentiated state. In addition, we describe experiments in which signaling of HESCs is augmented by chemical probing with small molecule compounds. Using these compounds, we have demonstrated an important role for Wnt signaling in HESC pluripotency and shown a requirement for TGFbeta signaling in the maintenance of the undifferentiated state. These experiments have revealed some molecular aspects of the pluripotent state and demonstrated clear differences between mouse and human ESCs in the maintenance of this identity.

publication date

  • 2005

has subject area

  • Animals
  • Embryonic Stem Cells
  • Forecasting
  • Humans
  • Pluripotent Stem Cells
  • Signal Transduction
  • Transforming Growth Factor beta
  • Wnt Proteins

Research

keywords

  • Journal Article
  • Review

Identity

Language

  • eng

Digital Object Identifier (DOI)

  • 10.1385/SCR:1:2:111

PubMed ID

  • 17142845

Additional Document Info

start page

  • 111

end page

  • 118

volume

  • 1

number

  • 2