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Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

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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...
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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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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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Proteins can undergo many types of post-translational modifications, often in response to changes in their environment. These modifications play an important role in the function and stability of these proteins. Covalently linked molecules include functional groups, such as methyl, acetyl, and phosphate groups, and also small proteins, such as ubiquitin. There are around 200 different types of covalent regulators that have been identified.
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Negative Regulator Molecules01:23

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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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The Intrinsic Apoptotic Pathway01:31

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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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Updated: May 3, 2026

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

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Activating p53Y220C with a mutant-specific small molecule.

Xijun Zhu1, Woong Sub Byun2,3, Dominika Ewa Pieńkowska4

  • 1Department of Chemistry, Stanford University, Stanford, CA, USA.

Nature Communications
|May 1, 2026
PubMed
Summary
This summary is machine-generated.

Scientists developed TRAP-1, a novel compound that reactivates the mutated p53 tumor suppressor protein. This chemical inducer of proximity restores p53 function, offering a new therapeutic strategy for cancer treatment.

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Purification of Ubiquitinated p53 Proteins from Mammalian Cells
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Purification of Ubiquitinated p53 Proteins from Mammalian Cells
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Area of Science:

  • Oncology
  • Molecular Biology
  • Drug Discovery

Background:

  • TP53 is frequently mutated in cancer and difficult to therapeutically target.
  • Restoring tumor suppressor function is a key challenge in cancer therapy.

Purpose of the Study:

  • To discover and characterize a novel small molecule that activates mutant p53.
  • To investigate the potential of chemically induced proximity for cancer therapy.

Main Methods:

  • Discovery of TRanscriptional Activator of p53 (TRAP-1), a small molecule inducer of proximity.
  • Characterization of TRAP-1's mechanism involving ternary complex formation with p53Y220C and BRD4.
  • Assessment of TRAP-1's effect on p53 target gene expression, cellular senescence, and apoptosis in cancer cell lines.

Main Results:

  • TRAP-1 potently activates mutant p53Y220C by forming a ternary complex with BRD4.
  • TRAP-1 treatment leads to upregulation of p53 target genes like CDKN1A.
  • TRAP-1 induces cellular senescence and apoptosis in p53Y220C-expressing cancer cells.

Conclusions:

  • Chemically induced proximity is a viable strategy to restore tumor suppressor function.
  • TRAP-1 demonstrates the potential of this approach for reactivating mutant p53 in cancer therapy.
  • This discovery opens new avenues for developing targeted cancer treatments.