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

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...
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...
Overview of DNA Repair02:25

Overview of DNA Repair

In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
Chemically...
Nucleotide Excision Repair01:38

Nucleotide Excision Repair

DNA Distortion and Damage
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
Nucleotide Excision Repair01:08

Nucleotide Excision Repair

Overview
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.

You might also read

Related Articles

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

Sort by
Same author

The role of 1400 plasma metabolites in gastric cancer: A bidirectional Mendelian randomization study and metabolic pathway analysis.

Medicine·2024
Same author

Airborne Acoustic Vortex End Effector-based Contactless, Multi-mode, Programmable Control of Object Surfing.

Advanced materials technologies·2024
Same author

Effect of frozen storage duration on temporal dominance of sensations (TDS), chemical investigations and moisture distribution of roasted chicken wings.

Food chemistry·2024
Same author

Authenticating the Geographical Origin of Jingbai Pear in Northern China by Multiple Stable Isotope and Elemental Analysis.

Foods (Basel, Switzerland)·2024
Same author

Interaction between young fecal transplantation and perfluorobutanesulfonate endocrine disrupting toxicity in aged recipients: An estrobolome perspective.

Environment international·2024
Same author

Lower-dose vs high-dose oral bisphenol S action of lipid metabolism in liver of male SD rat via mediating different SREBP isoforms.

Environmental pollution (Barking, Essex : 1987)·2024
Same journal

Investigating transcription factor dynamics in health and disease using FRAP.

FEBS letters·2026
Same journal

Regulation of CFTR stability at the plasma membrane-Mechanisms and therapeutic opportunities in cystic fibrosis.

FEBS letters·2026
Same journal

Identification of a Shiga toxin A-derived peptide internalized into Gb3 receptor-bearing cells via interaction with the Shiga toxin B subunit.

FEBS letters·2026
Same journal

The dual role of lectins in cancer-immunotherapy tools and therapeutic targets.

FEBS letters·2026
Same journal

Decoding the dynamic extracellular matrix in cancer-3D models and bioscaffolds rewire the rules of tumor progression.

FEBS letters·2026
Same journal

Extending the classical sequence-structure-function paradigm through protein dynamics and context-dependent behavior.

FEBS letters·2026
See all related articles

Related Experiment Video

Updated: Jun 17, 2026

Laser Microirradiation to Study In Vivo Cellular Responses to Simple and Complex DNA Damage
10:44

Laser Microirradiation to Study In Vivo Cellular Responses to Simple and Complex DNA Damage

Published on: January 31, 2018

Sharp-1 modulates the cellular response to DNA damage.

Jian-Jun Liu1, Teng-Kai Chung, Jiali Li

  • 1Department of Physiology, National University of Singapore, Singapore, Singapore.

FEBS Letters
|December 17, 2009
PubMed
Summary
This summary is machine-generated.

The transcription factor Sharp-1 induces cell cycle arrest and reduces apoptosis, suggesting a role in DNA damage response. Its inappropriate expression may link to cancer development.

More Related Videos

Laser Micro-Irradiation to Study DNA Recruitment During S Phase
07:11

Laser Micro-Irradiation to Study DNA Recruitment During S Phase

Published on: April 16, 2021

Two- and Three-Dimensional Live Cell Imaging of DNA Damage Response Proteins
10:24

Two- and Three-Dimensional Live Cell Imaging of DNA Damage Response Proteins

Published on: September 28, 2012

Related Experiment Videos

Last Updated: Jun 17, 2026

Laser Microirradiation to Study In Vivo Cellular Responses to Simple and Complex DNA Damage
10:44

Laser Microirradiation to Study In Vivo Cellular Responses to Simple and Complex DNA Damage

Published on: January 31, 2018

Laser Micro-Irradiation to Study DNA Recruitment During S Phase
07:11

Laser Micro-Irradiation to Study DNA Recruitment During S Phase

Published on: April 16, 2021

Two- and Three-Dimensional Live Cell Imaging of DNA Damage Response Proteins
10:24

Two- and Three-Dimensional Live Cell Imaging of DNA Damage Response Proteins

Published on: September 28, 2012

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • DNA damage checkpoints are crucial for maintaining genome stability.
  • The transcription factor Sharp-1's role in DNA damage response is not well understood.

Purpose of the Study:

  • To investigate the function of the transcription factor Sharp-1 in the DNA damage response.
  • To explore the effects of Sharp-1 overexpression on cell cycle progression and apoptosis.

Main Methods:

  • Inducible overexpression of Sharp-1 in cells.
  • Analysis of cell cycle progression (S and G2/M phases).
  • Measurement of Brca1 and GADD45alpha gene expression.
  • Assessment of apoptosis in response to chemotherapeutic drugs.
  • Evaluation of p53 expression and activity.

Main Results:

  • Sharp-1 overexpression caused S and G2/M cell cycle arrest.
  • Brca1 and GADD45alpha expression were upregulated by Sharp-1.
  • Endogenous Sharp-1 mRNA levels increased upon treatment with DNA-damaging agents.
  • Sharp-1 overexpressing cells showed reduced apoptosis and lower p53 activity when treated with chemotherapy drugs.

Conclusions:

  • Sharp-1 plays a novel role in cell cycle arrest and DNA damage-induced apoptosis.
  • Inappropriate Sharp-1 expression may be implicated in tumorigenesis.