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

DNA Damage Can Stall the Cell Cycle

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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.
The Unfolded Protein Response01:37

The Unfolded Protein Response

The ER is the hub of protein synthesis in a cell. It has robust systems to quality control protein folding and also for degradation of terminally misfolded proteins. Under normal conditions, a small proportion of misfolded proteins that cannot be salvaged need to be transported to the cytoplasm by the ER-associated degradation or ERAD pathways. However, if the ERAD cannot handle the misfolded proteins, the cell activates the unfolded protein response or UPR to adjust the protein folding...
Nucleotide Excision Repair01:38

Nucleotide Excision Repair

DNA Distortion and Damage
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...

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Related Experiment Video

Updated: Jun 17, 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

Defects in 18 S or 28 S rRNA processing activate the p53 pathway.

Michael Hölzel1, Mathias Orban, Julia Hochstatter

  • 1Institute of Clinical Molecular Biology and Tumour Genetics, Center of Integrated Protein Science, Munich 85758, Germany. m.holzel@nki.nl

The Journal of Biological Chemistry
|January 9, 2010
PubMed
Summary

Defective ribosome synthesis activates the p53 pathway. This study identifies hUTP18's role in 18S rRNA processing, showing cells independently monitor 18S and 28S rRNA maturation via p53 signaling.

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Purification of Ubiquitinated p53 Proteins from Mammalian Cells
10:55

Purification of Ubiquitinated p53 Proteins from Mammalian Cells

Published on: March 21, 2022

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • The p53 tumor suppressor pathway is crucial for cellular response to stress, including defective ribosome synthesis.
  • Ribosomal protein release from the nucleolus inhibits Hdm2, preventing p53 degradation.
  • The specific mechanisms by which individual rRNA processing defects stabilize p53 were not fully understood.

Purpose of the Study:

  • To investigate how the abrogation of specific rRNA processing pathways contributes to p53 stabilization.
  • To identify novel factors involved in rRNA processing and their link to p53.
  • To elucidate the independent monitoring of small (18S) and large (28S) ribosomal RNA (rRNA) maturation by the p53 pathway.

Main Methods:

  • Selective inhibition of 18S rRNA processing pathways.
  • Knockdown of the novel mammalian rRNA processing factor, hUTP18.
  • Analysis of p53 accumulation and its dependence on ribosomal protein L11.
  • Assessment of 28S rRNA maturation in hUTP18-depleted cells.

Main Results:

  • Selective inhibition of 18S rRNA processing effectively stabilizes p53, similar to 28S rRNA defects.
  • hUTP18 was identified as a novel factor essential for 18S rRNA processing, specifically for cleaving the 5'-external transcribed spacer.
  • hUTP18 depletion did not affect 28S rRNA maturation, indicating independent monitoring of both pathways.
  • p53 stabilization upon hUTP18 knockdown was dependent on the ribosomal protein L11.

Conclusions:

  • The p53 pathway can independently monitor the integrity of both 18S and 28S rRNA synthesis.
  • hUTP18 plays a specific role in 18S rRNA maturation, linking its processing to p53 stabilization.
  • Separate molecular routes likely monitor small and large ribosomal subunit maturation, converging in an L11-dependent pathway for p53 activation.