Related Experiment Video

Updated: Jun 15, 2026

Application of Stopped-flow Kinetics Methods to Investigate the Mechanism of Action of a DNA Repair Protein
11:01

Application of Stopped-flow Kinetics Methods to Investigate the Mechanism of Action of a DNA Repair Protein

Published on: March 31, 2010

{Delta}Np73{beta} puts the brakes on DNA repair

Emma Vernersson-Lindahl1, Alea A Mills

  • 1Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA.

Genes & Development
|March 17, 2010
PubMed

Insights

The tumor suppressor p73, a relative of p53, inhibits DNA double-strand break repair pathways. This finding reveals a new mechanism impacting genome stability and cancer prevention.

Area of Science:

  • Molecular biology
  • Genetics
  • Cellular biology

Background:

  • Mammalian cells face millions of daily genomic lesions from metabolic byproducts and environmental factors.
  • Genome maintenance pathways are crucial for preventing mutations linked to aging and cancer.
  • The p53 tumor suppressor, known as the "guardian of the genome," is central to DNA damage repair.

Purpose of the Study:

  • To investigate the role of p73, an older sibling of p53, in DNA damage response pathways.
  • To elucidate the function of p73 in relation to DNA double-strand break resolution.

Main Methods:

  • The study by Wilhelm and colleagues utilized molecular and cellular biology techniques.
  • Experiments focused on analyzing the interaction and function of p73 within DNA repair networks.

Main Results:

  • The research demonstrates that p73 actively inhibits pathways responsible for resolving DNA double-strand breaks.
  • This inhibition by p73 impacts the cell's ability to repair critical DNA damage.

Conclusions:

  • p73 acts as a novel regulator in DNA repair, specifically by suppressing double-strand break resolution.
  • Understanding p73's inhibitory role is essential for comprehending genome stability and its implications in diseases like cancer.

More Related Videos

Proofreading and DNA Repair Assay Using Single Nucleotide Extension and MALDI-TOF Mass Spectrometry Analysis11:08

Proofreading and DNA Repair Assay Using Single Nucleotide Extension and MALDI-TOF Mass Spectrometry Analysis

Published on: June 19, 2018

Assessment of DNA Double Strand Break Repair Activity Using High-throughput and Quantitative Luminescence-Based Reporter Assays05:01

Assessment of DNA Double Strand Break Repair Activity Using High-throughput and Quantitative Luminescence-Based Reporter Assays

Published on: June 14, 2024

Related Concept Videos

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:
Translesion DNA Polymerases02:10

Translesion DNA Polymerases

Translesion (TLS) polymerases rescue stalled DNA polymerases at sites of damaged bases by replacing the replicative polymerase and installing a nucleotide across the damaged site. Doing so, TLS allows additional time for the cell to repair the damage before resuming regular DNA replication.
TLS polymerases are found in all three domains of life - archaea, bacteria, and eukaryotes. Of the different classes of TLS polymerases, members of the Y family are fitted with specialized structures that...
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...
Base Excision Repair01:54

Base Excision Repair

One of the common DNA damages is the chemical alteration of single bases by alkylation, oxidation, or deamination. The altered bases cause mispairing and strand breakage during replication. This type of damage causes minimal change to the DNA double helix structure and can be repaired by the base excision repair (BER) pathways. BER corrects damaged DNA sequences by removing the damaged base and restoring the original base sequence using the complementary strand as a template.
The first step of...
Fixing Double-strand Breaks02:04

Fixing Double-strand Breaks

The double-stranded structure of DNA has two major advantages. First, it serves as a safe repository of genetic information where one strand serves as the back-up in case the other strand is damaged. Second, the double-helical structure can be wrapped around proteins called histones to form nucleosomes, which can then be tightly wound to form chromosomes. This way, DNA chains up to 2 inches long can be contained within microscopic structures in a cell. A double-stranded break not only damages...
Proofreading01:31

Proofreading

Synthesis of new DNA molecules is carried out by the enzyme DNA polymerase, which adds nucleotides on the daughter strand complementary to the template DNA strand. DNA polymerase has a higher affinity to add the correct base and ensures fidelity during DNA replication. Furthermore,  it exhibits proofreading activity during replication, using an exonuclease domain that cuts off incorrect nucleotides from the nascent DNA strand.
Errors During Replication are Corrected by the DNA Polymerase Enzyme