Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Somatic to iPS Cell Reprogramming01:29

Somatic to iPS Cell Reprogramming

2.0K
Reprogramming alters the gene expression in somatic cells, transforming them into induced pluripotent stem (iPS) cells over several generations. Scientists can reprogram cells by introducing genes for four transcription factors—Oct4, Sox2, Klf4, and c-Myc (OSKM) by viral or non-viral methods. These factors are also known as Yamanaka factors after Shinya Yamanaka, who first generated iPS cells using mouse skin cells. Yamanaka was awarded the Nobel Prize in Physiology or Medicine in 2012...
2.0K
Methods of Nuclear Reprogramming01:24

Methods of Nuclear Reprogramming

1.4K
Nuclear reprogramming is a process of transforming one cell type into an unrelated cell type by epigenetic changes that alter the cell’s original gene expression pattern. Such epigenetic changes force cells to express a different set of genes, which play a significant role in inducing transformation into other cell types. Nuclear reprogramming offers applications in reproductive cloning for livestock propagation and regenerative medicine — developing patient-specific cells for...
1.4K
Forced Transdifferentiation01:28

Forced Transdifferentiation

1.5K
Transdifferentiation, also known as lineage reprogramming, was first discovered by Selman and Kafatos in 1974 in silkmoths. They observed that the moths’ cuticle-producing cells transformed into salt-producing cells. Many such cases of natural transdifferentiation occur in organisms. In humans, pancreatic alpha cells can become beta cells. In newts, the loss of the eye’s lens causes the pigmented epithelial cells to transdifferentiate into the lens cells.
Artificial...
1.5K
Chromatin Modification in iPS Cells01:32

Chromatin Modification in iPS Cells

1.5K
Chromatin modification alters gene expression; therefore, scientists can add histone-modifying enzymes, histone variants, and chromatin remodeling complexes to somatic cells to aid reprogramming into pluripotent stem (iPS) cells.
Compact chromatin makes reprogramming difficult. Enzymes, such as histone demethylases and acetyltransferases, are often added during reprogramming to loosen the chromatin, making the DNA more accessible to transcription factors. Molecules that inhibit histone...
1.5K
Introduction to Nuclear Reprogramming01:14

Introduction to Nuclear Reprogramming

1.3K
Nuclear reprogramming is the process of switching gene expression of one cell type to that of another cell type, usually from a differentiated cell state to an undifferentiated cell state. Differentiation occurs during processes such as development and morphogenesis, tissue regeneration, and malignancy. Cells can also be artificially induced to reprogram their gene expression by techniques such as nuclear transfer, induced pluripotency, and cell fusion. Such techniques have many applications in...
1.3K
Maintenance of the ES Cell State01:14

Maintenance of the ES Cell State

1.9K
The cells of the blastocyst inner cell mass only remain pluripotent for a short time. This state of pluripotency and self-renewal can be maintained in embryonic stem (ES) cell culture by adding specific chemicals or growth factors to ensure the cells can continue dividing and later differentiate into different cell types. In some cases, the cells are grown on a feeder layer of differentiated cells, which provides the growth factors and extracellular matrix components necessary for stem cell...
1.9K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Interferon beta drives therapy resistance in a patient-derived model of high-grade serous ovarian cancer.

Molecular oncology·2026
Same author

Multi-Omics Analysis Reveals Chronic Cisplatin Exposure Is Associated with Metabolic Rewiring Toward Glutathione Metabolism to Support Redox Adaptation in High-Grade Serous Ovarian Cancer.

Cancers·2026
Same author

A novel hyperactive <i>BCR::ABL1</i> <sup><i>e6a3</i></sup> variant confers resistance to combined asciminib plus ponatinib therapy.

medRxiv : the preprint server for health sciences·2026
Same author

Efficient Generation of Functional TCRαβ<sup>+</sup> Cytotoxic T Cells from hiPSCs via Small-Molecule Modulation.

bioRxiv : the preprint server for biology·2026
Same author

Soluble Notch agonist enables human ameloblast maturation and enamel-like tissue formation for tooth regeneration.

International journal of oral science·2026
Same author

Bnip3lb-driven mitophagy maintains fate of the embryonic hematopoietic stem cell pool.

Nature communications·2026

Related Experiment Video

Updated: Apr 22, 2026

An Enzyme- and Serum-free Neural Stem Cell Culture Model for EMT Investigation Suited for Drug Discovery
07:43

An Enzyme- and Serum-free Neural Stem Cell Culture Model for EMT Investigation Suited for Drug Discovery

Published on: August 23, 2016

8.8K

The epithelial-mesenchymal transition factor SNAIL paradoxically enhances reprogramming.

Juli J Unternaehrer1, Rui Zhao1, Kitai Kim1

  • 1Division of Pediatric Hematology/Oncology, Stem Cell Transplantation Program, Manton Center for Orphan Disease Research, Howard Hughes Medical Institute, Children's Hospital Boston and Dana Farber Cancer Institute, Harvard University, Cambridge, MA 02138, USA; Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Harvard University, Cambridge, MA 02138, USA; Harvard Stem Cell Institute, Harvard University, Cambridge, MA 02138, USA.

Stem Cell Reports
|October 16, 2014
PubMed
Summary

Scientists discovered that the epithelial-to-mesenchymal transition (EMT) factor SNAI1 unexpectedly enhances induced pluripotent stem cell (iPSC) reprogramming. This finding reveals a novel role for SNAI1 in converting somatic cells to pluripotency.

More Related Videos

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
11:42

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells

Published on: April 7, 2017

8.4K
Induction and Analysis of Epithelial to Mesenchymal Transition
10:37

Induction and Analysis of Epithelial to Mesenchymal Transition

Published on: August 27, 2013

38.0K

Related Experiment Videos

Last Updated: Apr 22, 2026

An Enzyme- and Serum-free Neural Stem Cell Culture Model for EMT Investigation Suited for Drug Discovery
07:43

An Enzyme- and Serum-free Neural Stem Cell Culture Model for EMT Investigation Suited for Drug Discovery

Published on: August 23, 2016

8.8K
Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
11:42

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells

Published on: April 7, 2017

8.4K
Induction and Analysis of Epithelial to Mesenchymal Transition
10:37

Induction and Analysis of Epithelial to Mesenchymal Transition

Published on: August 27, 2013

38.0K

Area of Science:

  • Cell Biology
  • Developmental Biology
  • Stem Cell Research

Background:

  • Reprogramming somatic cells to induced pluripotent stem cells (iPSCs) involves a mesenchymal-to-epithelial transition (MET).
  • The precise molecular mechanisms governing MET during reprogramming remain incompletely understood.

Purpose of the Study:

  • To investigate the role of the epithelial-to-mesenchymal transition (EMT) factor SNAI1 in the MET process during fibroblast reprogramming.
  • To elucidate the impact of SNAI1 modulation on reprogramming efficiency in human and mouse cells.

Main Methods:

  • Knockdown (KD) and overexpression of SNAI1 in human and mouse fibroblasts.
  • Utilizing a SNAI1-YFP reporter mouse model to track SNAI1 expression during reprogramming.
  • Assessing reprogramming efficiency and nuclear localization of SNAI1.
  • Investigating the interaction of SNAI1 with the let-7 promoter and the effect of let-7 microRNA levels.

Main Results:

  • SNAI1 knockdown paradoxically reduced reprogramming efficiency, while SNAI1 overexpression enhanced it.
  • Nuclear localization of SNAI1 was observed during early reprogramming stages.
  • Fibroblasts expressing SNAI1 demonstrated higher reprogramming efficiency.
  • SNAI1 binds to the let-7 promoter, potentially reducing let-7 microRNA expression, which, when enforced early, compromises reprogramming.

Conclusions:

  • The EMT factor SNAI1 plays an unexpected, crucial role in promoting somatic cell reprogramming to pluripotency.
  • SNAI1's function in reprogramming may involve the regulation of let-7 microRNA levels.
  • This study uncovers a novel mechanism influencing the efficiency of induced pluripotent stem cell generation.