Evidence map›Paper›PMID 23065386›Full record

ReviewMolecular neurobiology2013

Nuclear lamins in the brain - new insights into function and regulation.

Hea-Jin Jung, John M Lee, Shao H Yang, Stephen G Young, Loren G Fong

Abstract readReview
In one paragraph

Review in Molecular neurobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

23 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Lamin B1 as a key modulator of the developing and aging brain.Frontiers in cellular neuroscience · 2023
    Review
  4. Article
  5. Article
  6. Article
  7. Increased expression of LAP2β eliminates nuclear membrane ruptures in nuclear lamin-deficient neurons and fibroblasts.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. An absence of lamin B1 in migrating neurons causes nuclear membrane ruptures and cell death.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Defects of Lipid Synthesis Are Linked to the Age-Dependent Demyelination Caused by Lamin B1 Overexpression.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  20. 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

5 authors at 2 institutions in 1 country.

Hea-Jin JungMolecular Biology Institute, University of California-Los Angeles, Los Angeles, CA 90095, USA.
John M Lee
Shao H Yang
Stephen G Young
Loren G Fong
University of California, Los Angeles · USCharles R. Drew University of Medicine and Science · US

Funding

New Therapeutic Approaches for Hutchinson-Gilford Progeria SyndromeR01HL086683 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI FONG, LOREN GI · 2007 to 2011
$2.2M
CaaX Protein Processing and Human DiseaseR01AG035626 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI YOUNG, STEPHEN G. · 2009 to 2013
$2.0M
Protein Prenylation and ProgeriaR01HL089781 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI FONG, LOREN GI · 2009 to 2013
$1.9M
Hutchinson Gilford Progeria Syndrome and AtherosclerosisR01HL076839 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI YOUNG, STEPHEN G. · 2005 to 2009
$1.9M
NHLBI NIH HHS HL089781NHLBI NIH HHS HL76839NHLBI NIH HHS HL86683NHLBI NIH HHS R01 HL076839NHLBI NIH HHS R01 HL086683NHLBI NIH HHS R01 HL089781NIA NIH HHS AG035626-09NIA NIH HHS R01 AG035626
6 · The paper itself

Abstract

The nuclear lamina is an intermediate filament meshwork composed largely of four nuclear lamins - lamins A and C (A-type lamins) and lamins B1 and B2 (B-type lamins). Located immediately adjacent to the inner nuclear membrane, the nuclear lamina provides a structural scaffolding for the cell nucleus. It also interacts with both nuclear membrane proteins and the chromatin and is thought to participate in many important functions within the cell nucleus. Defects in A-type lamins cause cardiomyopathy, muscular dystrophy, peripheral neuropathy, lipodystrophy, and progeroid disorders. In contrast, the only bona fide link between the B-type lamins and human disease is a rare demyelinating disease of the central nervous system - adult-onset autosomal-dominant leukoencephalopathy, caused by a duplication of the gene for lamin B1. However, this leukoencephalopathy is not the only association between the brain and B-type nuclear lamins. Studies of conventional and tissue-specific knockout mice have demonstrated that B-type lamins play essential roles in neuronal migration in the developing brain and in neuronal survival. The importance of A-type lamin expression in the brain is unclear, but it is intriguing that the adult brain preferentially expresses lamin C rather than lamin A, very likely due to microRNA-mediated removal of prelamin A transcripts. Here, we review recent studies on nuclear lamins, focusing on the function and regulation of the nuclear lamins in the central nervous system.

Indexed as

AnimalsBrainCell NucleusDiseaseHumansLaminsMammalsMicroRNAsLaminsMicroRNAs

Identifiers

PMID23065386
PMCPMC3538886
OpenAlexW2018275041

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.