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Related Concept Videos

Cooperative Binding of Transcription Regulators02:13

Cooperative Binding of Transcription Regulators

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Transcriptional regulators bind to specific cis-regulatory sequences in the DNA to regulate gene transcription. These cis-regulatory sequences are very short, usually less than ten nucleotide pairs in length. The short length means that there is a high probability of the exact same sequence randomly occurring throughout the genome.  Since regulators can also bind to groups of similar sequences, this further increases the chances of random binding. Transcriptional regulators form...
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Cooperative Binding of Transcription Regulators02:13

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Transcription Factors02:16

Transcription Factors

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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...
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Transcription Elongation Factors02:35

Transcription Elongation Factors

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Transcription elongation is a dynamic process that alters depending upon the sequence heterogeneity of the DNA being transcribed. Hence, it is not surprising that the elongation complex's composition also varies along the way while transcribing a gene.
The transcription elongation is regulated via pausing of RNA polymerase on several occasions during transcription. In bacteria, these halts are necessary because the transcription of DNA into mRNA is coupled to the translation of that mRNA...
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General Transcription Factors01:30

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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...
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Related Experiment Video

Updated: Feb 1, 2026

Hemogenic Reprogramming of Human Fibroblasts by Enforced Expression of Transcription Factors
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Hemogenic Reprogramming of Human Fibroblasts by Enforced Expression of Transcription Factors

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Cooperative Transcription Factor Induction Mediates Hemogenic Reprogramming.

Andreia M Gomes1, Ilia Kurochkin2, Betty Chang3

  • 1Department of Cell, Developmental and Regenerative Biology, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, Box 1496, New York, NY 10029, USA; Black Family Stem Cell Institute, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, Box 1496, New York, NY 10029, USA; Doctoral Programme in Experimental Biology and Biomedicine, University of Coimbra, Largo Marquês do Pombal 3004-517, Coimbra, Portugal; Centre for Neuroscience and Cell Biology, University of Coimbra, Largo Marquês do Pombal 3004-517, Coimbra, Portugal.

Cell Reports
|December 6, 2018
PubMed
Summary

Human fibroblasts can be reprogrammed into hemogenic cells using specific transcription factors, mimicking developmental hematopoiesis. This breakthrough offers potential for generating hematopoietic stem and progenitor cells (HSPCs) for clinical use.

Keywords:
FOSGATA2GFI1Bcooperative bindingdirect cell reprogramminghematopoietic stem cellhematopoietic transcription factorhemogenic endotheliumhemogenic reprogramminghuman endothelial-to-hematopoietic transition

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Reprogramming Mouse Embryonic Fibroblasts with Transcription Factors to Induce a Hemogenic Program
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Assessing Cardiomyocyte Subtypes Following Transcription Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts
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Area of Science:

  • Developmental biology
  • Stem cell biology
  • Molecular genetics

Background:

  • Hematopoietic stem and progenitor cells (HSPCs) originate from endothelial cells via endothelial-to-hematopoietic transition (EHT).
  • The genetic underpinnings of human HSPC development are not fully understood.
  • Previous work demonstrated fibroblast reprogramming to hemogenic precursors in mice.

Purpose of the Study:

  • To investigate the reprogramming of human fibroblasts into hemogenic cells.
  • To elucidate the genetic program governing human HSPC emergence.
  • To assess the potential of reprogrammed cells for therapeutic applications.

Main Methods:

  • Reprogramming human fibroblasts using specific transcription factors.
  • Analysis of transcriptional programs during endothelial-to-hematopoietic transition (EHT).
  • Functional assays including hematopoietic progeny generation and in vivo repopulation studies in immunodeficient mice.
  • Investigating the roles of GATA2 and GFI1B in cooperative binding and gene regulation.

Main Results:

  • Human fibroblasts successfully reprogrammed into hemogenic cells exhibiting EHT transcriptional dynamics.
  • Induced cells generated hematopoietic progeny and displayed HSPC surface markers.
  • Reprogrammed cells repopulated immunodeficient mice for up to 3 months.
  • GATA2 and GFI1B were found to interact and co-occupy regulatory targets, driving fibroblast gene silencing and hemogenic program activation, with GATA2 showing dominant early activity.

Conclusions:

  • Identified key transcription factors capable of reprogramming human fibroblasts into functional hemogenic cells.
  • Elucidated the molecular mechanisms involving GATA2 and GFI1B in controlling the hemogenic program.
  • Demonstrated the potential of these reprogrammed cells for generating hematopoietic stem cells for clinical applications.