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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:
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...
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...
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...
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...

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Related Experiment Video

Updated: Jun 3, 2026

Visualization and Quantitative Analysis of Genotoxin-Induced PARP1/PARP2 Activation in Cells Using a Fluorescent Fusion Protein-Based Reporter
07:53

Visualization and Quantitative Analysis of Genotoxin-Induced PARP1/PARP2 Activation in Cells Using a Fluorescent Fusion Protein-Based Reporter

Published on: April 17, 2026

Deacetylated PCBP1 licenses PARP1 activity for DNA damage repair.

Yuxin Shu1, Jun Zhang2, Linmin Zhou2

  • 1International Cancer Center, Guangdong Key Laboratory of Genome Instability and Human Disease Prevention, Marshall Laboratory of Biomedical Engineering, Department of Biochemistry and Molecular Biology, Shenzhen University Medical School, Shenzhen 518055, China; School of Basic Medical Sciences, Wannan Medical University, Wuhu 241003, China.

Molecular Cell
|June 1, 2026
PubMed
Summary

Poly (ADP-ribose) polymerase 1 (PARP1) is inhibited by poly(rC)-binding protein 1 (PCBP1) under normal conditions. SIRT7-mediated deacetylation of PCBP1 relieves this inhibition, impacting DNA repair and cancer patient survival.

Keywords:
DNA double-strand break repairPARP1PARylationPCBP1SIRT7

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

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Related Experiment Videos

Last Updated: Jun 3, 2026

Visualization and Quantitative Analysis of Genotoxin-Induced PARP1/PARP2 Activation in Cells Using a Fluorescent Fusion Protein-Based Reporter
07:53

Visualization and Quantitative Analysis of Genotoxin-Induced PARP1/PARP2 Activation in Cells Using a Fluorescent Fusion Protein-Based Reporter

Published on: April 17, 2026

Laser Microirradiation to Study In Vivo Cellular Responses to Simple and Complex DNA Damage
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Published on: January 31, 2018

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10:12

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

Published on: April 21, 2023

Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • Poly (ADP-ribose) polymerase 1 (PARP1) is crucial for DNA damage sensing and repair, making its activity a key target for genome stability strategies.
  • Controlling PARP1 activity is essential for developing effective cancer therapies, particularly those aimed at maintaining genomic integrity.

Purpose of the Study:

  • To investigate the regulatory mechanism of PARP1 activity by RNA-binding proteins.
  • To elucidate the role of poly(rC)-binding protein 1 (PCBP1) in modulating PARP1 function.
  • To explore the therapeutic potential of targeting the PCBP1-PARP1 interaction in DNA repair and cancer treatment.

Main Methods:

  • Investigated the interaction between PCBP1 and PARP1 using biochemical assays.
  • Utilized cell and murine models to study the effect of PCBP1 modulation on DNA damage repair.
  • Analyzed patient data to correlate PCBP1 levels with survival outcomes following radiotherapy.
  • Employed gene editing and antagonistic peptides to modulate PCBP1 activity and acetylation.

Main Results:

  • PCBP1 directly interacts with and inhibits PARP1 activity under physiological conditions.
  • Histone deacetylase SIRT7 deacetylates PCBP1 at specific sites (K314, K351), disrupting the PCBP1-PARP1 interaction and activating PARP1.
  • Modulating PCBP1 expression or acetylation impacts DNA repair efficiency in cellular and animal models.
  • Reduced PCBP1 levels are linked to poorer survival rates in cancer patients undergoing radiotherapy.

Conclusions:

  • PCBP1 acts as a physiological inhibitor of PARP1, with its inhibition being relieved during the early DNA damage response.
  • SIRT7-mediated deacetylation of PCBP1 is a key mechanism for regulating PARP1 activation.
  • PCBP1 levels and acetylation status are significant factors in DNA repair efficiency and patient prognosis after radiotherapy.
  • Targeting PCBP1 deacetylation presents a potential therapeutic strategy for enhancing DNA-damaging cancer treatments.