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Related Concept Videos

Negative Regulator Molecules01:23

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.
Long-patch Base Excision Repair01:02

Long-patch Base Excision Repair

Since the discovery of the two BER pathways, there has been a debate about how a cell chooses one pathway over the other and the factors determining this selection. Numerous in vitro experiments have pointed out multiple determinants for the sub-pathway selection. These are:
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...
Restarting Stalled Replication Forks02:37

Restarting Stalled Replication Forks

DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart, a...
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...

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Related Experiment Video

Updated: Jul 26, 2026

Rapid Analysis of Chromosome Aberrations in Mouse B Lymphocytes by PNA-FISH
07:54

Rapid Analysis of Chromosome Aberrations in Mouse B Lymphocytes by PNA-FISH

Published on: August 19, 2014

p53: only ARF the story.

A C Lloyd

    Nature Cell Biology
    |March 9, 2000
    PubMed
    Summary

    The tumor suppressor proteins p16INK4A and p19 ARF, encoded by the same gene, arrest cell division. Recent findings reveal intricate complexities within their regulatory pathways.

    Area of Science:

    • Molecular Biology
    • Cell Biology
    • Genetics

    Background:

    • The p16INK4A and p19 ARF proteins are key tumor suppressors involved in cell cycle regulation.
    • Both proteins are encoded by the CDKN2A locus, highlighting a shared genetic origin.

    Discussion:

    • Investigating the intricate molecular mechanisms governing the cell-division cycle.
    • Exploring the complex interplay between p16INK4A and p19 ARF pathways.
    • Understanding how these tumor suppressors contribute to cell cycle arrest.

    Key Insights:

    • New research uncovers previously unknown complexities in the pathways regulated by p16INK4A and p19 ARF.
    • These findings deepen our understanding of cell cycle control and tumor suppression.
    • The shared genetic locus adds a layer of complexity to the functional relationship between these proteins.

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    Yeast As a Chassis for Developing Functional Assays to Study Human P53
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    Published on: August 4, 2019

    Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence
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    Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence

    Published on: December 30, 2025

    Related Experiment Videos

    Last Updated: Jul 26, 2026

    Rapid Analysis of Chromosome Aberrations in Mouse B Lymphocytes by PNA-FISH
    07:54

    Rapid Analysis of Chromosome Aberrations in Mouse B Lymphocytes by PNA-FISH

    Published on: August 19, 2014

    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

    Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence
    04:56

    Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence

    Published on: December 30, 2025

    Outlook:

    • Further research into the detailed molecular interactions of p16INK4A and p19 ARF.
    • Potential implications for cancer therapy and understanding tumorigenesis.
    • Elucidating the precise regulatory networks involving these critical tumor suppressors.