Evidence map›Paper›PMID 24563357›Full record

ReviewAdvances in experimental medicine and biology2014

DNA damage and lamins.

Susana Gonzalo

Abstract readReview
In one paragraph

Review in Advances in experimental medicine and biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 1 pooled it
10.5field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

62 citing papers in PubMed, 1 synthesis or guideline pooled it, 101 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. DNA damage and repair in cardiomyopathy: mechanisms and therapeutic opportunities.American journal of physiology. Heart and circulatory physiology · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Pathological α-Synuclein Perturbs Nuclear Integrity.bioRxiv : the preprint server for biology · 2025
    Article
  10. International journal of molecular sciences · 2025
    Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Model Systems to Study the Mechanism of Vascular Aging.International journal of molecular sciences · 2023
    Review

2 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Susana GonzaloDepartment of Biochemistry and Molecular Biology, St Louis University School of Medicine, 1100 S Grand Ave, St. Louis, MO, 63104, USA, sgonzalo@slu.edu.
Saint Louis University · US

Funding

MECHANISMS RESPONSIBLE FOR GENOMIC INSTABILITY IN PREMATURE AGING LAMINOPATHIESR01GM094513 · NIGMS · WASHINGTON UNIVERSITY · PI GONZALO HERVAS, SUSANA · 2010 to 2014
$1.4M
NIGMS NIH HHS R01 GM094513
6 · The paper itself

Abstract

The spatial and temporal organization of the genome has emerged as an additional level of regulation of nuclear functions. Structural proteins associated with the nuclear envelope play important roles in the organization of the genome. The nuclear lamina, a polymeric meshwork formed by lamins (A- and B-type) and lamin-associated proteins, is viewed as a scaffold for tethering chromatin and protein complexes regulating a variety of nuclear functions. Alterations in lamins function impact DNA transactions such as transcription, replication, and repair, as well as epigenetic modifications that change chromatin structure. These data, and the association of defective lamins with a whole variety of degenerative disorders, premature aging syndromes, and cancer, provide evidence for these proteins operating as caretakers of the genome. In this chapter, we summarize current knowledge about the function of lamins in the maintenance of genome integrity, with special emphasis on the role of A-type lamins in the maintenance of telomere homeostasis and mechanisms of DNA damage repair. These findings have begun to shed some light onto molecular mechanisms by which alterations in A-type lamins induce genomic instability and contribute to the pathophysiology of aging and aging-related diseases, especially cancer.

Indexed as

DNA DamageDNA RepairGenomic InstabilityHumansLaminsProtein TransportTelomereLamins

Identifiers

PMID24563357
PMCPMC4081481
OpenAlexW2173076959

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.