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 Experiment Videos

Replication of damaged DNA.

Alan R Lehmann1

  • 1Genome Damage and Stability Centre, University of Sussex, Falmer, Brighton BN1 9RQ, UK. a.r.lehmann@sussex.ac.uk

Cell Cycle (Georgetown, Tex.)
|July 10, 2003
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

Central Nervous System Tumors in Xeroderma Pigmentosum: Five Cases and Review of the Literature.

Movement disorders : official journal of the Movement Disorder Society·2026
Same author

Unusual Disease-Progression in Two Siblings With Xeroderma Pigmentosum Group G.

Clinical genetics·2026
Same author

A Splicing Variant in XPA Results in Delayed Onset of Clinical Features of Xeroderma Pigmentosum.

The Journal of investigative dermatology·2025
Same author

XP-J, a ninth xeroderma pigmentosum complementation group, results from mutations in GTF2H4, encoding TFIIH-p52 subunit.

The Journal of clinical investigation·2025
Same author

TFIIH-p52ΔC defines a ninth xeroderma pigmentosum complementation-group XP-J and restores TFIIH stability to p8-defective trichothiodystrophy.

The Journal of clinical investigation·2025
Same author

Clinical and molecular overlap between nucleotide excision repair (NER) disorders and <i>DYRK1A</i> haploinsufficiency syndrome.

Frontiers in neuroscience·2025
Same journal

Circular RNA circ_0001829 attenuates G2/M arrest to promote hepatocyte proliferation by sponging miR-3095-3p following liver injury.

Cell cycle (Georgetown, Tex.)·2026
Same journal

Identification of PGF+ endothelial cells associated with plaque instability in carotid atherosclerosis by scRNA-seq and RNA-seq analysis.

Cell cycle (Georgetown, Tex.)·2026
Same journal

BMSCs-derived exosomal miR-196a-5p promotes macrophage M2 polarization and osteogenesis in postmenopausal osteoporosis through regulating Rspo2/Wnt/β-catenin signaling.

Cell cycle (Georgetown, Tex.)·2026
Same journal

MicroRNA-6833-3p drives prostate cancer progression and stemness by targeting the NUMB-mediated NOTCH signaling pathway.

Cell cycle (Georgetown, Tex.)·2026
Same journal

OTUD5 promotes AML progression by stabilizing SLC7A11 to suppress ferroptosis.

Cell cycle (Georgetown, Tex.)·2026
Same journal

MITF-Driven melanoma plasticity as a core mechanism of therapy resistance: integrating microenvironmental signaling, mechanotransduction, and metabolic reprogramming.

Cell cycle (Georgetown, Tex.)·2026
See all related articles

Cells use specialized DNA polymerases for translesion synthesis to replicate past DNA damage. These polymerases have open structures and may switch via post-translational modifications.

Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • DNA damage is a continuous cellular event.
  • Cellular replication requires bypassing damaged DNA bases.

Purpose of the Study:

  • To explain the role of specialized DNA polymerases in bypassing DNA damage.
  • To explore the structural and functional characteristics of these polymerases.

Main Methods:

  • Analysis of DNA polymerase structures.
  • Investigation of polymerase localization within replication factories.
  • Review of emerging evidence on polymerase switching mechanisms.

Main Results:

  • Specialized DNA polymerases facilitate translesion synthesis.

Related Experiment Videos

  • These polymerases possess unique open structures for accommodating altered bases.
  • Some translesion polymerases localize to replication factories.
  • Conclusions:

    • Translesion synthesis polymerases are crucial for DNA replication fidelity.
    • Post-translational modifications may regulate the switch between replicative and translesion polymerases.