Evidence map›Paper›PMID 24563359›Full record

ReviewAdvances in experimental medicine and biology2014

Nuclear lamins and oxidative stress in cell proliferation and longevity.

Takeshi Shimi, Robert D Goldman

Open access · greenAbstract 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 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

31 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Conditioned Medium from HAntioxidants (Basel, Switzerland) · 2022
    Article
  12. Review
  13. Article
  14. Preclinical Advances of Therapies for Laminopathies.Journal of clinical medicine · 2021
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Lamin A/C promotes DNA base excision repair.Nucleic acids research · 2019
    Article
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

2 authors at 1 institution in 1 country.

Takeshi ShimiDepartment of Cell and Molecular Biology, Northwestern University Feinberg School of Medicine, Ward Building 11-145 303 E, Chicago Avenue, Chicago, IL, 60611-3008, USA, takeshi@northwestern.edu.
Robert D Goldman
Northwestern University · US

Funding

INTERMEDIATE FILAMENTS IN NORMAL AND TRANSFORMED CELLSR01CA031760 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI GOLDMAN, ROBERT D · 1985 to 2013
$4.9M
Super-resolution microscopy of nuclear lamin and spindle envelope/matrix functionR01GM106023 · NIGMS · CARNEGIE INSTITUTION OF WASHINGTON, D.C. · PI GOLDMAN, ROBERT D, ZHENG, YIXIAN · 2013 to 2020
$3.5M
NCI NIH HHS R01 CA031760NIGMS NIH HHS R01 GM106023
6 · The paper itself

Abstract

In mammalian cells, the nuclear lamina is composed of a complex fibrillar network associated with the inner membrane of the nuclear envelope. The lamina provides mechanical support for the nucleus and functions as the major determinant of its size and shape. At its innermost aspect it associates with peripheral components of chromatin and thereby contributes to the organization of interphase chromosomes. The A- and B-type lamins are the major structural components of the lamina, and numerous mutations in the A-type lamin gene have been shown to cause many types of human diseases collectively known as the laminopathies. These mutations have also been shown to cause a disruption in the normal interactions between the A and B lamin networks. The impact of these mutations on nuclear functions is related to the roles of lamins in regulating various essential processes including DNA synthesis and damage repair, transcription and the regulation of genes involved in the response to oxidative stress. The major cause of oxidative stress is the production of reactive oxygen species (ROS), which is critically important for cell proliferation and longevity. Moderate increases in ROS act to initiate signaling pathways involved in cell proliferation and differentiation, whereas excessive increases in ROS cause oxidative stress, which in turn induces cell death and/or senescence. In this review, we cover current findings about the role of lamins in regulating cell proliferation and longevity through oxidative stress responses and ROS signaling pathways. We also speculate on the involvement of lamins in tumor cell proliferation through the control of ROS metabolism.

Indexed as

Cell ProliferationLongevityOxidative StressCell NucleusGene ExpressionHumansLaminsProtein Processing, Post-TranslationalProtein StabilityLamins

Identifiers

PMID24563359
PMCPMC4507519
OpenAlexW197228255

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.