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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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The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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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.
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mRNA Stability and Gene Expression

The structure and stability of mRNA molecules regulates gene expression, as mRNAs are a key step in the pathway from gene to protein. In eukaryotes, the half-life of mRNA varies from a few minutes up to several days. mRNA stability is essential in growth and development. The absence of the proteins regulating its stability, such as tristetraprolin in mice, can cause systemic issues, including bone marrow overgrowth, inflammation, and autoimmunity.
Cis-acting Elements involved in mRNA stability

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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

Trim24 targets endogenous p53 for degradation.

Kendra Allton1, Abhinav K Jain, Hans-Martin Herz

  • 1Department of Biochemistry and Molecular Biology, Program in Genes and Development, Graduate School of Biomedical Sciences and Center for Stem Cell and Developmental Biology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.

Proceedings of the National Academy of Sciences of the United States of America
|June 27, 2009
PubMed
Summary

Researchers identified Tripartite-motif protein 24 (Trim24) as a novel negative regulator of the tumor suppressor p53. Trim24 targets p53 for ubiquitylation, offering a potential therapeutic strategy for cancer.

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Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Genetics

Background:

  • The tumor suppressor p53 is crucial for genomic stability, cell cycle arrest, and apoptosis, but is frequently mutated in human cancers.
  • Most p53 research uses cancer cell lines, which may have mutated or dysfunctional p53 regulatory pathways.
  • Understanding p53 regulation in normal cells is essential for cancer research.

Purpose of the Study:

  • To investigate the regulation of endogenous p53 in normal cells.
  • To identify novel p53-interacting proteins and regulatory mechanisms.
  • To explore the therapeutic potential of targeting p53 regulators.

Main Methods:

  • Created a knock-in mouse and stem cell model with a tandem-affinity-purification (TAP) epitope on endogenous Trp-53.
  • Utilized mass spectrometry to identify p53-interacting proteins from purified complexes.
  • Performed in vivo studies in Drosophila and human breast cancer cells to validate findings.

Main Results:

  • Identified Tripartite-motif protein 24 (Trim24) as a novel p53-binding partner.
  • Demonstrated that Trim24 negatively regulates p53 levels through ubiquitylation.
  • Showed that Trim24/bonus pathway negatively regulates p53 in Drosophila, and this link is conserved in human cells, where Trim24 depletion causes p53-dependent apoptosis.

Conclusions:

  • Trim24 is an evolutionarily conserved negative regulator of p53.
  • Trim24-mediated ubiquitylation of p53 impacts tumor suppression.
  • Targeting Trim24 may represent a novel therapeutic strategy to restore p53's tumor-suppressive functions.