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

The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal01:22

Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal

Erythropoietin-producing hepatocellular carcinoma receptor (Eph) and its ligand, Eph receptor-interacting protein (Ephrin) were first discovered in the human carcinoma cell line, hence the name. Ephrin-Eph interaction guides cells to reach their appropriate location in adult tissues. They also play an essential role in the immune system by helping in immune cell migration, adhesion, and activation. Based on their structure and function, Eph is divided into two classes — EphA and EphB.
NF-kB-dependent Signaling Pathway02:26

NF-kB-dependent Signaling Pathway

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 heterodimer of NF-κB...
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR activation may...
B Cell Activation and Differentiation01:24

B Cell Activation and Differentiation

The adaptive immune response, a sophisticated defense mechanism, relies on the activation and differentiation of B lymphocytes, or B cells. These processes enable our bodies to mount a tailored response against specific pathogens such as bacteria, free virus particles, toxins, and parasites.
When naive B cells encounter a specific antigen that can bind to the B cell receptor (BCR) on their surface, they undergo sensitization to respond to the antigen's presence. Sensitization begins with...
Inhibitors of Viral Protein Synthesis01:30

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...

You might also read

Related Articles

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

Sort by
Same author

Extracellular release of cytotoxic aggregates from HSV-1-replicating SH-SY5Y cells: involvement of alpha-synuclein and poly-ubiquitin conjugates.

Experimental cell research·2026
Same author

The atypical IκB factor IκBδ enhances CD8 T cell accumulation and effector functions in solid tumors.

bioRxiv : the preprint server for biology·2026
Same author

HBV Envelope Protein-Bearing Vesicles Show Preferential Uptake in Hepatocyte-Derived Cells.

International journal of molecular sciences·2026
Same author

Cytomegalovirus-encoded immediate early 1 protein perturbs neural progenitor proliferation via interfering with host PML-DISC1 interaction.

The Journal of biological chemistry·2026
Same author

Overcoming Normalcy Bias in Acute Myocardial Infarction: A Case Report of Generative AI as a Behavioral Catalyst for Emergency Care Seeking.

Cureus·2026
Same author

Nogo-A-cleaved amino-terminal fragment but not Nogo-B regulates STAT3 activation.

Biochemical and biophysical research communications·2025

Related Experiment Video

Updated: Jun 27, 2026

Isolation and Quantification of Epstein-Barr Virus from the P3HR1 Cell Line
09:14

Isolation and Quantification of Epstein-Barr Virus from the P3HR1 Cell Line

Published on: September 28, 2022

Epstein-Barr virus-derived EBNA2 regulates STAT3 activation.

Ryuta Muromoto1, Osamu Ikeda, Kanako Okabe

  • 1Department of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Kita-Ku Kita 12 Nishi 6, Sapporo 060-0812, Japan.

Biochemical and Biophysical Research Communications
|November 27, 2008
PubMed
Summary

The Epstein-Barr virus (EBV) protein EBNA2 enhances STAT3 activity by influencing DNA binding. EBNA2 and LMP1 cooperate to activate STAT3, highlighting EBNA2's role as a coactivator.

More Related Videos

An Efficient and Simple Method to Establish NK and T Cell Lines from Patients with Chronic Active Epstein-Barr Virus Infection
09:43

An Efficient and Simple Method to Establish NK and T Cell Lines from Patients with Chronic Active Epstein-Barr Virus Infection

Published on: March 30, 2018

Separation of Immune Cell Subpopulations in Peripheral Blood Samples from Children with Infectious Mononucleosis
08:44

Separation of Immune Cell Subpopulations in Peripheral Blood Samples from Children with Infectious Mononucleosis

Published on: September 7, 2022

Related Experiment Videos

Last Updated: Jun 27, 2026

Isolation and Quantification of Epstein-Barr Virus from the P3HR1 Cell Line
09:14

Isolation and Quantification of Epstein-Barr Virus from the P3HR1 Cell Line

Published on: September 28, 2022

An Efficient and Simple Method to Establish NK and T Cell Lines from Patients with Chronic Active Epstein-Barr Virus Infection
09:43

An Efficient and Simple Method to Establish NK and T Cell Lines from Patients with Chronic Active Epstein-Barr Virus Infection

Published on: March 30, 2018

Separation of Immune Cell Subpopulations in Peripheral Blood Samples from Children with Infectious Mononucleosis
08:44

Separation of Immune Cell Subpopulations in Peripheral Blood Samples from Children with Infectious Mononucleosis

Published on: September 7, 2022

Area of Science:

  • Molecular Biology
  • Virology
  • Cellular Biology

Background:

  • Epstein-Barr virus (EBV) is a human herpesvirus associated with various cancers.
  • EBV-encoded nuclear antigen 2 (EBNA2) is a key viral protein for EBV-driven cell transformation.
  • Signal transducer and activator of transcription 3 (STAT3) is crucial in cytokine signaling and cellular processes.

Purpose of the Study:

  • To investigate the interaction between EBV's EBNA2 and STAT3.
  • To determine how EBNA2 affects STAT3 transcriptional activity.
  • To explore the cooperative effect of EBNA2 and LMP1 on STAT3 activation.

Main Methods:

  • Co-immunoprecipitation assays to detect protein interactions.
  • Reporter assays to measure transcriptional activity.
  • Analysis of STAT3 DNA-binding influenced by EBNA2.

Main Results:

  • EBNA2 directly interacts with STAT3.
  • EBNA2 enhances STAT3 transcriptional activity by modulating its DNA-binding.
  • EBNA2 and LMP1 exhibit cooperative activation of STAT3.

Conclusions:

  • EBNA2 functions as a transcriptional coactivator for STAT3.
  • This interaction provides a mechanism for EBV-induced cellular transformation.
  • The interplay between EBNA2, LMP1, and STAT3 is critical for EBV pathogenesis.