Related Experiment Video

Updated: May 4, 2026

Live Cell Imaging of the TGF- β/Smad3 Signaling Pathway In Vitro and In Vivo Using an Adenovirus Reporter System
11:06

Live Cell Imaging of the TGF- β/Smad3 Signaling Pathway In Vitro and In Vivo Using an Adenovirus Reporter System

Published on: July 30, 2018

8.7K

Links between tumor suppressors: p53 is required for TGF-beta gene responses by cooperating with Smads

Michelangelo Cordenonsi1, Sirio Dupont, Silvia Maretto

  • 1Department of Histology, Microbiology, and Medical Biotechnologies, Section of Histology and Embryology, University of Padua, viale Colombo 3, 35121 Padua, Italy.

Cell
|May 7, 2003
PubMed

Insights

The p53 tumor suppressor protein is crucial for cellular responses to transforming growth factor-beta (TGF-β) signals. This discovery reveals a vital link between p53 and TGF-β pathways in vertebrate development and tumor suppression.

Area of Science:

  • Cell Biology
  • Developmental Biology
  • Molecular Oncology

Background:

  • The p53 tumor suppressor family regulates cell proliferation, apoptosis, and differentiation.
  • The interaction between p53 functions and extracellular growth factor signaling, particularly TGF-β, remains largely uncharacterized.

Purpose of the Study:

  • To investigate the intersection of p53 family member activity with transforming growth factor-beta (TGF-β) signaling pathways.
  • To elucidate the role of p53 in TGF-β-mediated cellular responses during embryonic development and in mammalian cells.

Main Methods:

  • Utilized Xenopus embryonic development models to assess p53's role in TGF-β target gene activation and mesoderm differentiation.
  • Employed mammalian cell culture systems to examine TGF-β-induced p21(WAF1) transcription in p53-deficient cells.
  • Investigated the physical interaction between p53 and Smad proteins and their synergistic transcriptional activation of target genes.

Main Results:

  • p53 family members are essential for key cellular responses to TGF-β signals.
  • p53 promotes TGF-β target gene activation and mesoderm differentiation in Xenopus embryos.
  • Full TGF-β-induced transcription of p21(WAF1) in mammalian cells requires p53, and p53-deficient cells show impaired cytostatic responses.
  • Smad and p53 complexes synergistically activate transcription by binding to separate elements, with p53 interacting with Smad2 in a TGF-β-dependent manner.

Conclusions:

  • This study uncovers a significant, previously unrecognized link between the p53 tumor suppressor pathway and TGF-β signaling in vertebrates.
  • The findings highlight the critical role of p53 in mediating TGF-β responses, impacting cell proliferation, differentiation, and tumor suppression.

More Related Videos

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells06:54

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

13.1K
Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence04:56

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence

Published on: December 30, 2025

371

Related Concept Videos

Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
32.1K
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
8.5K
Abnormal Proliferation02:23

Abnormal Proliferation

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...
4.0K
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

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...
4.7K
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
2.4K
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

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...
7.2K