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

Long-patch Base Excision Repair01:02

Long-patch Base Excision Repair

7.0K
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:
7.0K
Spreading of Chromatin Modifications02:25

Spreading of Chromatin Modifications

8.2K
The histone proteins in the nucleosomes are post-translationally modified (PTM) to increase or decrease access to DNA. The commonly observed PTMs are methylation, acetylation, phosphorylation, and ubiquitination of lysine amino acids in the histone H3 tail region. These histone modifications have specific meaning for the cell. Hence, they are called "histone code". The protein complex involved in histone modification is termed as "reader-writer" complex.
Writers
The writer...
8.2K
DNA Damage can Stall the Cell Cycle02:37

DNA Damage can Stall the Cell Cycle

9.0K
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...
9.0K
Abnormal Proliferation02:23

Abnormal Proliferation

4.5K
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...
4.5K
Chromatin Structure Regulates pre-mRNA Processing02:41

Chromatin Structure Regulates pre-mRNA Processing

6.9K
In eukaryotic cells, nascent mRNA transcripts need to undergo many post-transcriptional modifications to reach the cell cytoplasm and translate into functional proteins. For a long time, transcription and pre-mRNA processing were considered two independent events that occur sequentially in the cell. However, it has now been well established that transcription and pre-mRNA processing are two simultaneous processes that are precisely regulated inside the cell.
The chromatin structure, especially...
6.9K
Restarting Stalled Replication Forks02:37

Restarting Stalled Replication Forks

5.8K
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,...
5.8K

You might also read

Related Articles

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

Sort by
Same author

Updated ENIGMA recommendations for reporting germline variants in cancer susceptibility genes and their translation into twenty languages.

Journal of medical genetics·2026
Same author

Does artificial intelligence need companionship to assist in drug discovery? The Kirsten rat sarcoma virus study.

BJR artificial intelligence·2026
Same author

A stress-induced PI3P complex controls autophagy in erythroid precursors.

iScience·2026
Same author

ISL1: A Novel Neuroendocrine Subtype in Small Cell Lung Cancer Predicts Durable Response to Lurbinectedin.

Molecular cancer therapeutics·2026
Same author

Different plasma exosome isolation methods generated distinct microRNA and protein profiles in healthy controls and patients with advanced prostate and lung cancer.

BMC cancer·2025
Same author

Cancer-associated fibroblasts confer ALK inhibitor resistance in <i>EML4-ALK</i>-driven lung cancer by concurrent integrin and MET signaling.

Science signaling·2025

Related Experiment Video

Updated: Jun 7, 2025

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

10.2K

SART1 modulates poly-(ADP-ribose) chain accumulation and PARP1 chromatin localization.

Samuele Lodovichi1,2,3, Thales C Nepomuceno1, Nicholas T Woods4

  • 1Department of Cancer Epidemiology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA.

Iscience
|November 21, 2024
PubMed
Summary

Scientists discovered SART1, a protein that regulates Poly (ADP-ribose) polymerase 1 (PARP1) activity. Silencing SART1 increases PARP1 activity and PARP inhibitor sensitivity, suggesting SART1 as a potential therapeutic target for cancer treatment.

Keywords:
Cell biologyMolecular biologyOmics

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

4.2K
Author Spotlight: Quantitative Detection of DNA Protein Crosslinks and Their Post-Translational Modifications
10:12

Author Spotlight: Quantitative Detection of DNA Protein Crosslinks and Their Post-Translational Modifications

Published on: April 21, 2023

2.7K

Related Experiment Videos

Last Updated: Jun 7, 2025

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

10.2K
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

4.2K
Author Spotlight: Quantitative Detection of DNA Protein Crosslinks and Their Post-Translational Modifications
10:12

Author Spotlight: Quantitative Detection of DNA Protein Crosslinks and Their Post-Translational Modifications

Published on: April 21, 2023

2.7K

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • Poly (ADP-ribose) polymerase inhibitors (PARPis) are crucial for treating cancers with homologous recombination deficiencies, particularly those with BRCA1/BRCA2 mutations.
  • Understanding and overcoming resistance to PARPis necessitates the identification of novel modulators of PARP1 activity.

Purpose of the Study:

  • To identify novel regulators of Poly (ADP-ribose) polymerase 1 (PARP1) activity by integrating data from multiple omics-scale screens.
  • To investigate the role of the identified regulator, SART1, in PARP1 activity, DNA damage response, and sensitivity to PARP inhibitors.

Main Methods:

  • Integrated data from three omics-scale screens to identify PARP1 activity modulators.
  • Utilized gene silencing techniques to assess the impact of SART1 on poly-ADP ribosylation and PARP1 chromatin association.
  • Investigated SART1 recruitment to chromatin post-DNA damage and its functional domains (N-terminus, RGG/RG box).

Main Results:

  • Identified SART1 as a novel regulator of PARP1; SART1 silencing increases poly-ADP ribosylation and chromatin-bound PARP1.
  • SART1 is recruited to chromatin after DNA damage, limiting PARP1 retention and activity; its N-terminus is sufficient for this regulation.
  • SART1 silencing enhances sensitivity to ionizing radiation (IR) regardless of BRCA1 status and to PARPis specifically in BRCA1-deficient cells.

Conclusions:

  • SART1 acts as a negative regulator of PARP1 activity on chromatin, particularly following DNA damage.
  • The findings suggest SART1's potential clinical utility in enhancing the efficacy of PARP inhibitors, especially in BRCA1-mutated cancers.
  • SART1 represents a promising therapeutic target for improving cancer treatment strategies involving PARPis.