4.4 Review Book Chapter

Genomic Approaches to Deconstruct Pluripotency

Journal

Publisher

ANNUAL REVIEWS
DOI: 10.1146/annurev-genom-082410-101506

Keywords

transcription regulation; epigenetics; histone modifications; DNA methylation; pluripotent stem cells

Funding

  1. NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [RC2HL102815, U01HL100001] Funding Source: NIH RePORTER
  2. NATIONAL INSTITUTE OF DENTAL &CRANIOFACIAL RESEARCH [RL1DE019021] Funding Source: NIH RePORTER
  3. NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK059279, R01DK070055] Funding Source: NIH RePORTER
  4. Howard Hughes Medical Institute Funding Source: Medline
  5. NHLBI NIH HHS [U01-HL-100001, RC2 HL102815, U01 HL100001, RC2-HL102815] Funding Source: Medline
  6. NIDCR NIH HHS [RL1DE019021, RL1 DE019021] Funding Source: Medline
  7. NIDDK NIH HHS [R01 DK059279, R01-DK70055, R01 DK070055, R01-DK59279] Funding Source: Medline

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Embryonic stem cells (ESCs) first derived from the inner cell mass of blastocyst-stage embryos have the unique capacity of indefinite self-renewal and potential to differentiate into all somatic cell types. Similar developmental potency can be achieved by reprogramming differentiated somatic cells into induced pluripotent stem cells (iPSCs). Both types of pluripotent stem cells provide great potential for fundamental studies of tissue differentiation, and hold promise for disease modeling, drug development, and regenerative medicine. Although much has been learned about the molecular mechanisms that underlie pluripotency in such cells, our understanding remains incomplete. A comprehensive understanding of ESCs and iPSCs requires the deconstruction of complex transcription regulatory networks, epigenetic mechanisms, and biochemical interactions critical for the maintenance of self-renewal and pluripotency. in this review, we will discuss recent advances gleaned from application of global omics techniques to dissect the molecular mechanisms that define the pluripotent state.

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