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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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DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

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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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DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

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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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Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

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Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
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Negative Regulator Molecules01:23

Negative Regulator Molecules

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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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Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

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The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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Related Experiment Video

Updated: Apr 27, 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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[Abnormal p53-HDM2 interaction in hematological malignancy].

Yoko Tabe, Kensuke Kojima

    Nihon Rinsho. Japanese Journal of Clinical Medicine
    |July 15, 2014
    PubMed
    Summary

    Targeting the p53-HDM2 interaction with small-molecule inhibitors reactivates the tumor suppressor p53 (protein 53). This strategy shows promise for treating hematological malignancies by inducing cancer cell death.

    Area of Science:

    • Oncology
    • Molecular Biology
    • Biochemistry

    Background:

    • The tumor suppressor protein p53 (protein 53) is crucial for cell survival and death.
    • p53 gene mutations occur in ~50% of human cancers.
    • In hematological malignancies with wild-type p53, p53 is often inhibited by human double minute 2 (HDM2).

    Purpose of the Study:

    • To review the biology of the p53-HDM2 interaction.
    • To explore the anti-tumor effects of HDM2 inhibitors in hematological malignancies.

    Main Methods:

    • Focuses on the mechanism of HDM2 as a p53-specific E3 ubiquitin ligase.
    • Discusses small-molecule antagonists that disrupt the p53-HDM2 interaction by binding to HDM2's p53-binding pocket.

    Main Results:

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    Purification of Ubiquitinated p53 Proteins from Mammalian Cells
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    • HDM2 inhibitors prevent p53 degradation by blocking HDM2 activity.
    • Stabilization of p53 leads to its activation.

    Conclusions:

    • Activated p53 induces cell cycle arrest, growth inhibition, and apoptosis in hematological malignant cells.
    • Disrupting the p53-HDM2 interaction is a viable therapeutic strategy for hematological cancers harboring wild-type p53.