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Introduction to Nuclear Reprogramming

Introduction to Nuclear Reprogramming

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...

Methods of Nuclear Reprogramming

Methods of Nuclear Reprogramming

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 injury repair.

Somatic to iPS Cell Reprogramming

Somatic to iPS Cell Reprogramming

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 for this...

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Updated: Jul 2, 2026

Isolation of Viral Replication Compartment-enriched Sub-nuclear Fractions from Adenovirus-infected Normal Human Cells

Isolation of Viral Replication Compartment-enriched Sub-nuclear Fractions from Adenovirus-infected Normal Human Cells

Published on: November 12, 2015

Epigenetic reprogramming by adenovirus e1a.

Roberto Ferrari¹, Matteo Pellegrini, Gregory A Horwitz

¹Department of Biological Chemistry, University of California, Los Angeles, CA 90095, USA.

Science (New York, N.Y.)

|August 23, 2008

Summary

This summary is machine-generated.

Adenovirus e1a protein reprograms human cells by altering histone acetylation and repressing antiviral responses. This epigenetic reprogramming stimulates cell cycling and promotes cellular transformation.

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Adenovirus-mediated Genetic Removal of Signaling Molecules in Cultured Primary Mouse Embryonic Fibroblasts

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Published on: September 9, 2010

Area of Science:

Epigenetics
Molecular Biology
Virology

Background:

Adenovirus e1a protein is known to induce cell proliferation in quiescent human cells.
The precise molecular mechanisms by which e1a achieves this cellular reprogramming are not fully understood.

Purpose of the Study:

To investigate the role of adenovirus e1a in the epigenetic reprogramming of human cells.
To elucidate the temporal dynamics of e1a interactions with key regulatory proteins and their impact on gene expression.

Main Methods:

Chromatin immunoprecipitation (ChIP) to analyze protein binding and histone modifications at gene promoters.
Western blotting to assess protein levels and histone acetylation.
Gene expression analysis to determine transcriptional changes.

Main Results:

Adenovirus e1a causes global relocalization of retinoblastoma (RB) proteins and p300/CBP histone acetyltransferases.
e1a restricts histone 3 lysine-18 acetylation (H3K18ac) to a limited gene set, stimulating cell cycling and inhibiting antiviral responses.
Temporal binding of e1a to promoters of cell cycle, antiviral, and differentiation genes orchestrates transcriptional changes.

Conclusions:

Adenovirus e1a drives cellular transformation through a defined epigenetic reprogramming process.
The temporal interactions of e1a with p300/CBP and RB proteins are critical for its function.
Understanding these mechanisms provides insights into viral oncogenesis and cellular transformation.