Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

5.4K
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...
5.4K
Negative Regulator Molecules01:23

Negative Regulator Molecules

39.0K
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.
39.0K
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

10.4K
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...
10.4K
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

3.4K
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...
3.4K
Restarting Stalled Replication Forks02:37

Restarting Stalled Replication Forks

6.6K
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,...
6.6K
Conservative Site-specific Recombination and Phase Variation02:53

Conservative Site-specific Recombination and Phase Variation

7.4K
Because the DNA segments are cut and reorganized in a direction-specific manner, site-specific recombination has emerged as an efficient genetic engineering technique. Flippase and Cyclization recombinases or Flp and Cre, respectively, are two members of the tyrosine recombinase family derived from bacteriophages, that are used to mediate site-specific DNA insertions, deletions, and targeted expression of proteins in mammalian cell lines.
The recognition sites for Cre recombinase called LoxP...
7.4K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Correction: The EHMT2-MBLAC2 axis suppresses ribosomal DNA transcription in response to nucleolar DNA damage.

Cell death & disease·2026
Same author

Real-world operational characteristics of perovskite photovoltaics.

BMC chemistry·2026
Same author

Autistic traits in children with ADHD: preliminary evidence for a subgroup with elevated rule-breaking and aggressive behaviors.

BMC psychiatry·2026
Same author

Prognostic value of pretreatment neutrophil-to-lymphocyte ratio in breast cancer patients receiving neoadjuvant chemotherapy: a systematic review and meta-analysis.

Frontiers in oncology·2026
Same author

JOSD1-mediated stabilization of SUFU controls pancreatic cancer progression.

Cell death & disease·2026
Same author

Large Exchange Bias Effect in Geometrically Frustrated Spin Glass Through High-Density Coherent Chemical Interfaces.

Advanced materials (Deerfield Beach, Fla.)·2026

Related Experiment Video

Updated: Apr 7, 2026

Identifying the Effects of BRCA1 Mutations on Homologous Recombination using Cells that Express Endogenous Wild-type BRCA1
08:53

Identifying the Effects of BRCA1 Mutations on Homologous Recombination using Cells that Express Endogenous Wild-type BRCA1

Published on: February 17, 2011

15.2K

p53 suppresses hyper-recombination by modulating BRCA1 function.

Chao Dong1, Fengmei Zhang1, Yue Luo1

  • 1Department of Environment and Health, School of public health, Shandong University, Jinan, Shandong Province 250012, China.

DNA Repair
|July 12, 2015
PubMed
Summary

The tumor suppressor p53 inhibits homologous recombination (HR) DNA repair, working with BRCA1 through transcriptional regulation. P53 also independently suppresses HR, maintaining genetic stability and potentially rescuing BRCA1 deficiency.

Keywords:
BRCA1Chromosomal stabilityHomologous recombinationHyper-recombinationp53

More Related Videos

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

10.2K
Visualization of DNA Repair Proteins Interaction by Immunofluorescence
07:55

Visualization of DNA Repair Proteins Interaction by Immunofluorescence

Published on: June 26, 2020

11.4K

Related Experiment Videos

Last Updated: Apr 7, 2026

Identifying the Effects of BRCA1 Mutations on Homologous Recombination using Cells that Express Endogenous Wild-type BRCA1
08:53

Identifying the Effects of BRCA1 Mutations on Homologous Recombination using Cells that Express Endogenous Wild-type BRCA1

Published on: February 17, 2011

15.2K
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

10.2K
Visualization of DNA Repair Proteins Interaction by Immunofluorescence
07:55

Visualization of DNA Repair Proteins Interaction by Immunofluorescence

Published on: June 26, 2020

11.4K

Area of Science:

  • Molecular Biology
  • Cancer Research
  • DNA Damage Repair

Background:

  • p53 and BRCA1 are crucial tumor suppressors involved in DNA repair, cell cycle arrest, and apoptosis.
  • Their association is implicated in regulating genes for cell replication and DNA repair pathways.
  • The precise molecular mechanisms linking p53 and BRCA1 in DNA repair remain unclear.

Purpose of the Study:

  • To investigate the functional relationship between p53 and BRCA1 in DNA repair mechanisms.
  • To determine if p53 influences homologous recombination (HR) repair pathways.
  • To elucidate the roles of p53 and BRCA1 in maintaining genomic stability.

Main Methods:

  • Utilized a pDR-GFP plasmid recombination substrate in MCF7 breast cancer cells.
  • Employed HPV-E6 induced p53 inactivation and p53 knockdown assays.
  • Investigated protein complex formation between p53 and BRCA1.

Main Results:

  • p53 suppressed Rad51-mediated hyper-recombinational repair via transcriptional regulation, inhibiting BRCA1 over-function.
  • Defective p53-induced hyper-recombination correlated with radioresistance and chromosomal instability.
  • p53 loss rescued BRCA1 deficiency by restoring HR and chromosomal stability, indicating p53's independent HR-inhibitory role.

Conclusions:

  • p53 inhibits recombination through both BRCA1-dependent and -independent pathways.
  • A functional link exists between p53 suppression and BRCA1 promotion in regulating HR activity at transcriptional and possibly post-transcriptional levels.
  • p53 plays a critical role in maintaining genetic stability by inhibiting hyper-recombination.