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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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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...
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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

Low-level p53 expression changes transactivation rules and reveals superactivating sequences.

Jennifer J Jordan1, Daniel Menendez, Jenia Sharav

  • 1Chromosome Stability Section, Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA.

Proceedings of the National Academy of Sciences of the United States of America
|August 22, 2012
PubMed
Summary
This summary is machine-generated.

Transcriptional activation by tumor suppressor p53 depends on cellular levels and DNA sequence. At low p53 levels, sequence flexibility, not binding affinity, dictates activation, revealing unique target site rules.

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Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • Tumor suppressor p53's transcriptional activation is generally thought to depend on cellular levels.
  • Previous studies indicated p53 target transactivation sensitivity to both p53 amount and DNA sequence.
  • p53 is typically present at low cellular concentrations, with perturbations causing only minor increases.

Purpose of the Study:

  • To investigate transcriptional activation by p53 under limiting cellular p53 levels.
  • To explore the relationship between p53 concentration, DNA sequence, and transactivation.
  • To identify sequence-intrinsic properties governing p53 target recognition at low p53 levels.

Main Methods:

  • Utilized yeast model systems and human cell transfections to examine p53-mediated transactivation.
  • Analyzed the correlation between transactivation, p53 binding affinity, and target sequence torsional flexibility.
  • Performed kinetic and flexibility analyses to understand "supertransactivation" properties.

Main Results:

  • At low p53 levels, the positive correlation between transactivation and binding affinity observed at high levels was absent.
  • Transactivation in yeast systems strongly correlated with the torsional flexibility of p53 target sequences.
  • Certain sequences exhibited "supertransactivation" at low p53 levels due to low binding off rates and high flexibility.

Conclusions:

  • p53 target sequence engagement rules differ significantly at low versus high cellular p53 concentrations.
  • Intrinsic physical properties, particularly torsional flexibility and binding kinetics, are critical determinants of transactivation at limiting p53 levels.
  • These findings offer insights into p53 function, breast cancer-associated p53 mutants, and general transcription factor-DNA interactions.