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Related Concept Videos

Introduction to Nuclear Reprogramming01:14

Introduction to Nuclear Reprogramming

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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...
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Methods of Nuclear Reprogramming01:24

Methods of Nuclear Reprogramming

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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...
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Treatment Resistant Cancers02:56

Treatment Resistant Cancers

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Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
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Somatic to iPS Cell Reprogramming01:29

Somatic to iPS Cell Reprogramming

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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...
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Forced Transdifferentiation01:28

Forced Transdifferentiation

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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...
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Diversity in Cell Signaling Responses01:22

Diversity in Cell Signaling Responses

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The physiological function of a cell and cellular communication are outcomes of a range of extrinsic signals, intracellular signaling pathways, and cellular responses. No two cell types express the same repertoire of signaling components. Receptors are highly selective for their cognate ligands, but once activated, they can alter multiple cellular processes such as DNA transcription, protein synthesis, and metabolic activity. 
Graded and Abrupt Responses
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Related Experiment Video

Updated: Apr 4, 2026

Application of RNAi and Heat-shock-induced Transcription Factor Expression to Reprogram Germ Cells to Neurons in C. elegans
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Rerouting Resistance: Escaping Restriction Using Alternative Cellular Pathways.

Ailie Marx1, Akram Alian1

  • 1Faculty of Biology, Technion - Israel Institute of Technology, Haifa 320003, Israel.

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|September 6, 2015
PubMed
Summary
This summary is machine-generated.

Pathogens can develop stubborn resistance by rerouting cellular processes when key interactions are blocked. Influenza virus acquired this

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Alternative PathwayHost-Pathogen InteractionReroutingResistance

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Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Pathogens rely on host cell machinery for replication.
  • Cellular redundancies can be exploited by pathogens to overcome blocked interactions.
  • This leads to a novel form of pathogen resistance.

Purpose of the Study:

  • To investigate the mechanisms of pathogen adaptation and resistance.
  • To identify novel resistance strategies employed by viruses.
  • To understand how influenza virus acquires resistance.

Main Methods:

  • Utilizing a mouse model with a deleted vital host factor.
  • Observing influenza virus replication and adaptation.
  • Analyzing host-pathogen interactions at the molecular level.

Main Results:

  • Influenza virus demonstrated an ability to adapt to the absence of a vital host factor.
  • The virus acquired a 'rerouting-resistance' by exploiting cellular redundancies.
  • This adaptation allowed for viral replication despite the genetic modification.

Conclusions:

  • Pathogens can develop adaptable resistance mechanisms by rerouting host cell functions.
  • Influenza virus exemplifies this 'rerouting-resistance' when critical host factors are absent.
  • Understanding these mechanisms is crucial for developing new antiviral strategies.