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

10.2K
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...
10.2K
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

3.2K
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...
3.2K
Fixing Double-strand Breaks02:04

Fixing Double-strand Breaks

15.3K
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...
15.3K
Fixing Double-strand Breaks02:04

Fixing Double-strand Breaks

4.5K
4.5K
Nucleotide Excision Repair01:38

Nucleotide Excision Repair

5.4K
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...
5.4K
Nucleotide Excision Repair01:08

Nucleotide Excision Repair

41.2K
Overview
41.2K

You might also read

Related Articles

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

Sort by
Same author

Bridging the gap in OA therapeutics: Bioengineered strategies to target osteoclast-chondrocyte crosstalk.

Bioengineering & translational medicine·2026
Same author

A Noachian hydrosphere component in the 4.1-Ga Martian meteorite Teghaza 001.

Science advances·2026
Same author

Dexmedetomidine may alleviate severe acute pancreatitis-associated lung injury by targeting the AIM2 inflammasome in endothelial cells.

BMC anesthesiology·2026
Same author

Determination of HU override for gold fiducial markers in proton therapy.

Journal of applied clinical medical physics·2026
Same author

A Rare Case of Lower Gastrointestinal Bleeding: Appendiceal Dieulafoy's Lesion.

Digestive diseases and sciences·2026
Same author

CELF family of RNA-binding proteins: roles in disease biology and potential for therapeutic intervention.

Cell communication and signaling : CCS·2026
Same journal

RETRACTED: Kim et al. The Angiogenesis Inhibitor ALS-L1023 from Lemon-Balm Leaves Attenuates High-Fat Diet-Induced Nonalcoholic Fatty Liver Disease Through Regulating the Visceral Adipose-Tissue Function. <i>Int. J. Mol. Sci.</i> 2017, <i>18</i>, 846.

International journal of molecular sciences·2026
Same journal

Correction: Mahmud et al. Thymoquinone Attenuates NF-κβ Signalling Activation in Retinal Pigment Epithelium Cells Under AMD-Mimicking Conditions. <i>Int. J. Mol. Sci.</i> 2025, <i>26</i>, 11473.

International journal of molecular sciences·2026
Same journal

Correction: Borovikov et al. The Twisting and Untwisting of Actin and Tropomyosin Filaments Are Involved in the Molecular Mechanisms of Muscle Contraction, and Their Disruption Can Result in Muscle Disorders. <i>Int. J. Mol. Sci</i>. 2025, <i>26</i>, 6705.

International journal of molecular sciences·2026
Same journal

Correction: Molagoda et al. Flavonoid Glycosides from <i>Ziziphus jujuba</i> var. <i>inermis</i> (Bunge) Rehder Seeds Inhibit α-Melanocyte-Stimulating Hormone-Mediated Melanogenesis. <i>Int. J. Mol. Sci.</i> 2021, <i>22</i>, 7701.

International journal of molecular sciences·2026
Same journal

Correction: Guo et al. Integrated Transcriptomic and Metabolomic Analysis Reveals the Molecular Regulatory Mechanism of Flavonoid Biosynthesis in Maize Roots Under Lead Stress. <i>Int. J. Mol. Sci.</i> 2024, <i>25</i>, 6050.

International journal of molecular sciences·2026
Same journal

Correction: Chang et al. Improvement of Carbon Tetrachloride-Induced Acute Hepatic Failure by Transplantation of Induced Pluripotent Stem Cells Without Reprogramming Factor c-Myc. <i>Int. J. Mol. Sci.</i> 2012, <i>13</i>, 3598-3617.

International journal of molecular sciences·2026
See all related articles

Related Experiment Video

Updated: Feb 24, 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

10.8K

FANCD2 and DNA Damage.

Manoj Nepal1,2, Raymond Che3,4, Chi Ma5

  • 1Cancer Biology Program, University of Hawaii Cancer Center, Honolulu, HI 96813, USA. Mnepal@cc.hawaii.edu.

International Journal of Molecular Sciences
|August 22, 2017
PubMed
Summary
This summary is machine-generated.

Fanconi Anemia (FA) is a genetic disease linked to cancer and birth defects. The FANCD2 protein is key to cellular DNA damage response, making it a critical focus for FA research.

Keywords:
DNA damage repairFANCD2Fanconi anemiacancer and agingcheckpoint

More Related Videos

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

3.7K
Characterizing DNA Repair Processes at Transient and Long-lasting Double-strand DNA Breaks by Immunofluorescence Microscopy
08:31

Characterizing DNA Repair Processes at Transient and Long-lasting Double-strand DNA Breaks by Immunofluorescence Microscopy

Published on: June 8, 2018

9.7K

Related Experiment Videos

Last Updated: Feb 24, 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

10.8K
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

3.7K
Characterizing DNA Repair Processes at Transient and Long-lasting Double-strand DNA Breaks by Immunofluorescence Microscopy
08:31

Characterizing DNA Repair Processes at Transient and Long-lasting Double-strand DNA Breaks by Immunofluorescence Microscopy

Published on: June 8, 2018

9.7K

Area of Science:

  • Genetics
  • Molecular Biology
  • Cancer Research

Background:

  • Fanconi Anemia (FA) is a rare genetic disorder.
  • FA is characterized by cancer predisposition and congenital defects.
  • The molecular underpinnings of FA are under intense investigation.

Purpose of the Study:

  • To provide an updated review on the Fanconi Anemia group D2 (FANCD2) protein.
  • To highlight the crucial roles of FANCD2 in cellular DNA damage response.
  • To consolidate recent findings on FANCD2 in the context of FA.

Main Methods:

  • Literature review of recent and relevant studies.
  • Analysis of FANCD2's function in cellular pathways.
  • Focus on FANCD2's role in DNA damage response mechanisms.

Main Results:

  • FANCD2 is central to Fanconi Anemia signaling pathways.
  • FANCD2 plays essential roles in cellular life.
  • FANCD2 is particularly important for DNA damage repair.
  • Recent studies underscore FANCD2's significance in maintaining genomic stability.

Conclusions:

  • FANCD2 is a critical mediator of the DNA damage response in Fanconi Anemia.
  • Understanding FANCD2 function is key to unraveling FA pathogenesis.
  • Further research into FANCD2 pathways may offer therapeutic insights for FA and cancer.