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Related Concept Videos

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 daughter...
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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...
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

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Negative Regulator Molecules

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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 hydroxylase and factor...
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Interactions Between Signaling Pathways

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Updated: Jun 8, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

p53 impairs endothelial function by transcriptionally repressing Kruppel-Like Factor 2.

Ajay Kumar1, Cuk-Seong Kim, Timothy A Hoffman

  • 1University of Pittsburgh Medical Center, Pittsburgh, PA 15213, USA. Kumara@upmc.edu

Arteriosclerosis, Thrombosis, and Vascular Biology
|October 16, 2010
PubMed
Summary

The tumor suppressor p53 reduces Kruppel-Like Factor 2 (KLF2) expression, contributing to endothelial dysfunction. Restoring KLF2 levels can reverse p53-induced vascular problems.

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Purification of Ubiquitinated p53 Proteins from Mammalian Cells
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Purification of Ubiquitinated p53 Proteins from Mammalian Cells

Published on: March 21, 2022

Area of Science:

  • Vascular Biology
  • Molecular Biology
  • Oncology

Background:

  • Endothelial Kruppel-Like Factor 2 (KLF2) is crucial for vascular homeostasis, maintaining anti-inflammatory and antithrombotic properties.
  • The tumor suppressor p53 promotes endothelial dysfunction by inducing inflammatory gene expression and impairing vasodilation.

Purpose of the Study:

  • To investigate if p53 suppresses KLF2 expression.
  • To determine if p53-mediated KLF2 downregulation contributes to p53-induced endothelial dysfunction.

Main Methods:

  • Assessed p53's effect on KLF2 transcription and its binding to the KLF2 promoter.
  • Examined p53's impact on KLF2 target genes involved in vascular function.
  • Investigated the role of KLF2 in p53-induced changes in endothelial cells and vascular responses.

Main Results:

  • p53 inhibited KLF2 transcription via histone deacetylase-dependent mechanisms and direct binding to the KLF2 promoter.
  • p53 overexpression suppressed beneficial endothelial genes (eNOS, thrombomodulin) and increased detrimental ones (PAI-1, endothelin-1).
  • KLF2 knockdown mimicked and exacerbated p53-induced endothelial dysfunction, including increased coagulation and impaired vasodilation; KLF2 restoration rescued these effects.

Conclusions:

  • p53 negatively regulates endothelial KLF2 expression through a novel mechanism.
  • Downregulation of KLF2 is a key mediator of p53-induced endothelial dysfunction, impacting vascular homeostasis.