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

Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

3.3K
Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
3.3K
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

9.8K
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...
9.8K
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

7.2K
Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
7.2K
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

10.5K
The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
10.5K
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

8.0K
Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
8.0K
Intracellular Signaling Affects Focal Adhesions01:17

Intracellular Signaling Affects Focal Adhesions

3.5K
Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
3.5K

You might also read

Related Articles

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

Sort by
Same author

Impact of Kidney Function on the Treatment Effect of Multi-Arterial Grafting in CABG Patients.

Journal of Korean medical science·2026
Same author

Serological Susceptibility to Measles Among International Students in South Korea After a Cluster of Cases: A Cross-Sectional Study.

Tropical medicine and infectious disease·2026
Same author

Epigallocatechin-3-gallate Restores X-irradiation-Induced Impairments in Cognitive Function and Hippocampal Neurogenesis by Suppressing the TLR4-NOX3/4 and ROS-NF-κB Pathways in Microglia.

Molecular neurobiology·2025
Same author

Resection arthroplasty for deep shoulder infection in a native shoulder with an intact rotator cuff: a salvage option when reverse shoulder arthroplasty is not feasible.

Archives of orthopaedic and trauma surgery·2025
Same author

Single Versus Multiple Inflow Source for Coronary Artery Bypass Surgery in Ischemic Cardiomyopathy.

Korean circulation journal·2025
Same author

Simulation of organic light-emitting diode-based inkjet printing using a piezoelectric fluid structural interaction model.

Scientific reports·2025

Related Experiment Video

Updated: Jan 19, 2026

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
07:15

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

872

Platelet-activating factor-induced NF-kappaB activation enhances VEGF expression through a decrease in p53 activity.

Hyun-Mi Ko1, Hae Hyun Jung, Kook Heon Seo

  • 1Department of Biological Sciences, The Institute of Basic Sciences, Chonnam National University, Kwangju 500-757, Republic of Korea.

FEBS Letters
|May 11, 2006
PubMed
Summary

The study reveals that nuclear factor-kappaB (NF-kappaB) activity decreases p53 tumor suppressor activity, promoting vascular endothelial growth factor (VEGF) expression. This reciprocal regulation impacts VEGF-driven processes.

More Related Videos

In Vitro Model of Coronary Angiogenesis
08:03

In Vitro Model of Coronary Angiogenesis

Published on: March 10, 2020

8.4K
A Simple Bioassay for the Evaluation of Vascular Endothelial Growth Factors
09:04

A Simple Bioassay for the Evaluation of Vascular Endothelial Growth Factors

Published on: March 15, 2016

10.1K

Related Experiment Videos

Last Updated: Jan 19, 2026

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
07:15

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

872
In Vitro Model of Coronary Angiogenesis
08:03

In Vitro Model of Coronary Angiogenesis

Published on: March 10, 2020

8.4K
A Simple Bioassay for the Evaluation of Vascular Endothelial Growth Factors
09:04

A Simple Bioassay for the Evaluation of Vascular Endothelial Growth Factors

Published on: March 15, 2016

10.1K

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • Vascular Endothelial Growth Factor (VEGF) plays a crucial role in angiogenesis and tumor growth.
  • Nuclear Factor-kappaB (NF-kappaB) is a key transcription factor involved in inflammation and cell survival.
  • The tumor suppressor protein p53 is a critical regulator of cell cycle arrest and apoptosis.

Purpose of the Study:

  • To investigate the interplay between p53 and NF-kappaB in regulating VEGF expression.
  • To elucidate the mechanism by which Platelet-Activating Factor (PAF) influences VEGF production.
  • To understand the cross-regulation between NF-kappaB and p53 signaling pathways.

Main Methods:

  • Transfection of NF-kappaB subunits and p53 into ECV304 cells.
  • Analysis of tumor necrosis factor-alpha and p53 response element (p53RE) promoter activities.
  • Assessment of VEGF expression in response to PAF stimulation.
  • Correlation analysis between p53 activity and VEGF levels.

Main Results:

  • NF-kappaB subunits enhanced tumor necrosis factor-alpha promoter activity, which was inhibited by p53.
  • p53 increased p53RE promoter activity, inhibited by NF-kappaB subunits, demonstrating cross-regulation.
  • PAF-induced increase in VEGF expression correlated with decreased p53 activity.
  • NF-kappaB activation was associated with reduced p53 activity.

Conclusions:

  • NF-kappaB-dependent VEGF expression induced by PAF is mediated by decreased p53 activity.
  • There is a reciprocal regulatory relationship between NF-kappaB and p53.
  • Understanding this cross-talk is crucial for targeting angiogenesis in diseases like cancer.