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

Methods of Nuclear Reprogramming01:24

Methods of Nuclear Reprogramming

1.8K
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...
1.8K
Somatic to iPS Cell Reprogramming01:29

Somatic to iPS Cell Reprogramming

2.2K
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...
2.2K
Abnormal Proliferation02:23

Abnormal Proliferation

4.5K
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.5K
Chromatin Modification in iPS Cells01:32

Chromatin Modification in iPS Cells

1.7K
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...
1.7K
Induced Pluripotent Stem Cells01:06

Induced Pluripotent Stem Cells

4.1K
Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
Somatic...
4.1K
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

7.5K
The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
7.5K

You might also read

Related Articles

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

Sort by
Same author

Oncogene inactivation-induced senescence facilitates tumor relapse.

Nature communications·2026
Same author

DNA methylation signatures distinguish extranodal NK/T-cell lymphoma and EBV-positive nodal T/NK-cell lymphoma and identify prognostic subgroups.

Leukemia·2026
Same author

Genomic loss of MLH1/PMS2 loci defines a mismatch repair deficient subgroup in monomorphic epitheliotropic intestinal T-cell lymphoma.

Blood cancer journal·2026
Same author

Feasibility and safety of rapid glofitamab ramp-up.

Leukemia·2026
Same author

Rapid and Reproducible Karyotyping with Long Read Sequencing in AML Patients.

Blood advances·2026
Same author

Nodular lymphocyte-predominant Hodgkin lymphoma controversy and insights: a global NLPHL one working group summit report.

Leukemia·2026

Related Experiment Video

Updated: Jul 11, 2025

A High Resolution Method to Monitor Phosphorylation-dependent Activation of IRF3
11:44

A High Resolution Method to Monitor Phosphorylation-dependent Activation of IRF3

Published on: January 24, 2016

12.0K

Transcriptional reprogramming by mutated IRF4 in lymphoma.

Nikolai Schleussner1,2,3, Pierre Cauchy4,5,6,7, Vedran Franke8

  • 1Max-Delbrück-Center for Molecular Medicine in the Helmholtz Association (MDC), Biology of Malignant Lymphomas, 13125, Berlin, Germany.

Nature Communications
|November 7, 2023
PubMed
Summary

A specific mutation in Interferon Regulatory Factor 4 (IRF4) alters its DNA binding in lymphomas. This IRF4 mutation causes a switch in gene regulation, impacting B cell identity and disease progression.

More Related Videos

Native Polyacrylamide Gel Electrophoresis Immunoblot Analysis of Endogenous IRF5 Dimerization
08:57

Native Polyacrylamide Gel Electrophoresis Immunoblot Analysis of Endogenous IRF5 Dimerization

Published on: October 6, 2019

10.0K
Generation of Induced Pluripotent Stem Cells from Human Melanoma Tumor-infiltrating Lymphocytes
10:03

Generation of Induced Pluripotent Stem Cells from Human Melanoma Tumor-infiltrating Lymphocytes

Published on: November 11, 2016

9.9K

Related Experiment Videos

Last Updated: Jul 11, 2025

A High Resolution Method to Monitor Phosphorylation-dependent Activation of IRF3
11:44

A High Resolution Method to Monitor Phosphorylation-dependent Activation of IRF3

Published on: January 24, 2016

12.0K
Native Polyacrylamide Gel Electrophoresis Immunoblot Analysis of Endogenous IRF5 Dimerization
08:57

Native Polyacrylamide Gel Electrophoresis Immunoblot Analysis of Endogenous IRF5 Dimerization

Published on: October 6, 2019

10.0K
Generation of Induced Pluripotent Stem Cells from Human Melanoma Tumor-infiltrating Lymphocytes
10:03

Generation of Induced Pluripotent Stem Cells from Human Melanoma Tumor-infiltrating Lymphocytes

Published on: November 11, 2016

9.9K

Area of Science:

  • Molecular Biology
  • Genetics
  • Immunology

Background:

  • Mutations in transcription factors (TFs) can alter their DNA binding and interactions.
  • The impact of TF mutations on composite element (CE) binding and TF interactions remains unclear.
  • Perturbed B cell identity in lymphomas, like classic Hodgkin lymphoma, involves altered TF function.

Purpose of the Study:

  • To investigate the mechanism of TF alteration in human lymphomas due to mutations.
  • To understand how a specific mutation in Interferon Regulatory Factor 4 (IRF4) affects its DNA binding and function.
  • To elucidate the role of IRF4 mutations in lymphoma pathogenesis and gene regulation.

Main Methods:

  • Analysis of a recurrent somatic missense mutation (c.295T>C, p.Cys99Arg; p.C99R) in the IRF4 DNA-binding domain.
  • Assessment of IRF4 DNA-binding specificity to canonical and non-canonical motifs and composite elements (CEs).
  • Evaluation of IRF4 function in plasma cell induction and regulation of disease-specific genes.

Main Results:

  • The IRF4-C99R mutation alters DNA binding, causing loss of binding to canonical IRF motifs.
  • IRF4-C99R exhibits neomorphic gain-of-binding to canonical and non-canonical IRF CEs.
  • IRF4-C99R blocks IRF4-dependent plasma cell induction and up-regulates disease-specific genes via an AP-1-IRF-CE (AICE) dependent manner.

Conclusions:

  • A single mutation in IRF4 can cause a complex switch in TF specificity and gene regulation.
  • The study explains how IRF4 mutations contribute to lymphoma development by altering TF function.
  • Targeting neomorphic DNA-binding activities of mutant TFs presents a potential therapeutic strategy.