Related Experiment Video

Updated: May 25, 2026

Reprogramming Mouse Embryonic Fibroblasts with Transcription Factors to Induce a Hemogenic Program
11:00

Reprogramming Mouse Embryonic Fibroblasts with Transcription Factors to Induce a Hemogenic Program

Published on: December 16, 2016

PI3K/Akt-dependent functions of TFII-I transcription factors in mouse embryonic stem cells

Nyam-Osor Chimge1, Aleksandr V Makeyev, Sabine J Waigel

  • 1Department of Reconstructive Sciences, Center for Regenerative Medicine and Skeletal Development, School of Dentistry, University of Connecticut Health Center, 262 Farmington Avenue, Farmington, CT 06030, USA.

Journal of Cellular Biochemistry
|January 26, 2012
PubMed

Insights

Activating PI3K/Akt signaling maintains mouse embryonic stem cell (mESC) pluripotency by downregulating TFII-I factors. Upregulation of TFII-I during differentiation activates developmental genes.

Area of Science:

  • Stem cell biology
  • Molecular biology
  • Epigenetics

Background:

  • Phosphatidylinositol 3-kinase/Akt (PI3K/Akt) signaling pathway activation maintains mouse embryonic stem cell (mESC) pluripotency.
  • This activation leads to the downregulation of Gtf2i and Gtf2ird1, which encode TFII-I family transcription factors.

Purpose of the Study:

  • To investigate the role of Gtf2i and Gtf2ird1 in mESC differentiation.
  • To understand the molecular mechanisms linking PI3K/Akt signaling to gene expression changes during differentiation.

Main Methods:

  • Expression microarray profiling of mESC after PI3K inhibition using LY294002.
  • Genome-wide promoter Chromatin Immunoprecipitation sequencing (ChIP-seq) to map TFII-I binding sites.

Main Results:

  • PI3K inhibition caused significant alterations in the expression of genes encoding chromatin-modifying enzymes.
  • The majority of differentially expressed genes were identified as direct targets of TFII-I transcription factors.
  • TFII-I factors appear to regulate specific subsets of developmental genes.

Conclusions:

  • TFII-I transcription factors play a crucial role in regulating gene expression during mESC differentiation.
  • Upregulation of TFII-I factors promotes the activation of specific developmental genes, contributing to the differentiation process.

More Related Videos

Oct4GiP Reporter Assay to Study Genes that Regulate Mouse Embryonic Stem Cell Maintenance and Self-renewal08:01

Oct4GiP Reporter Assay to Study Genes that Regulate Mouse Embryonic Stem Cell Maintenance and Self-renewal

Published on: May 30, 2012

Generation of Mice Derived from Induced Pluripotent Stem Cells11:56

Generation of Mice Derived from Induced Pluripotent Stem Cells

Published on: November 29, 2012

Related Concept Videos

PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a rapamycin-insensitive companion...
General Transcription Factors01:30

General Transcription Factors

Tissue-specific transcription factors contribute to diverse cellular functions in mammals. For example, the gene for beta globin, a major component of hemoglobin, is present in all cells of the body. However, it is only expressed in red blood cells because the transcription factors that can bind to the promoter sequences of the beta globin gene are only expressed in these cells. Tissue-specific transcription factors also ensure that mutations in these factors may impair only the function of...
Transcription Factors02:16

Transcription Factors

Tissue-specific transcription factors contribute to diverse cellular functions in mammals. For example, the gene for beta globin, a major component of hemoglobin, is present in all cells of the body. However, it is only expressed in red blood cells because the transcription factors that can bind to the promoter sequences of the beta globin gene are only expressed in these cells. Tissue-specific transcription factors also ensure that mutations in these factors may impair only the function of...
Master Transcription Regulators02:23

Master Transcription Regulators

Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a  complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...