Evidence map›Paper›PMID 34161290›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2021

Increased expression of LAP2β eliminates nuclear membrane ruptures in nuclear lamin-deficient neurons and fibroblasts.

Natalie Y Chen, Paul H Kim, Yiping Tu, Ye Yang, Patrick J Heizer, Stephen G Young, Loren G Fong

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

15 citing papers in PubMed, 15 citations in OpenAlex.

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  11. Progerin forms an abnormal meshwork and has a dominant-negative effect on the nuclear lamina.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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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

7 authors at 1 institution in 1 country.

Natalie Y ChenDepartment of Medicine, University of California, Los Angeles, CA 90095.ORCID 0000-0002-8961-6244
Paul H KimDepartment of Medicine, University of California, Los Angeles, CA 90095.ORCID 0000-0002-8429-651X
Yiping TuDepartment of Medicine, University of California, Los Angeles, CA 90095.ORCID 0000-0002-4630-9113
Ye YangDepartment of Medicine, University of California, Los Angeles, CA 90095.
Patrick J HeizerDepartment of Medicine, University of California, Los Angeles, CA 90095.
Stephen G YoungDepartment of Medicine, University of California, Los Angeles, CA 90095; sgyoung@mednet.ucla.edu lfong@mednet.ucla.edu.ORCID 0000-0001-7270-3176
Loren G FongDepartment of Medicine, University of California, Los Angeles, CA 90095; sgyoung@mednet.ucla.edu lfong@mednet.ucla.edu.ORCID 0000-0002-4465-5290
University of California, Los Angeles · US

Funding

Women's CancersP30CA016042 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Samuel Wheeler French · 1985 to 2026
$134.5M
Virology CoreP30AI028697 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ANTON, PETER A · 1991 to 2018
$39.9M
Pilot and Feasibility ProgramP30DK041301 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROZENGURT, JUAN ENRIQUE · 1990 to 2019
$18.0M
Training in Molecular, Cellular &Integrative PhysiologyT32GM065823 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TIDBALL, JAMES G · 2003 to 2017
$2.1M
ZMPSTE24, HIV treatment regimens, and atherosclerotic heart diseaseR01HL126551 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI YOUNG, STEPHEN G. · 2014 to 2017
$1.8M
Development of a New Therapeutic Approach for Prelamin A DiseasesR01AG047192 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI FONG, LOREN GI · 2014 to 2018
$1.6M
NCI NIH HHS P30 CA016042NHLBI NIH HHS R01 HL126551NIAID NIH HHS P30 AI028697NIA NIH HHS R01 AG047192NIDDK NIH HHS P30 DK041301NIGMS NIH HHS T32 GM065823
6 · The paper itself

Abstract

Defects or deficiencies in nuclear lamins cause pathology in many cell types, and recent studies have implicated nuclear membrane (NM) ruptures as a cause of cell toxicity. We previously observed NM ruptures and progressive cell death in the developing brain of lamin B1-deficient mouse embryos. We also observed frequent NM ruptures and DNA damage in nuclear lamin-deficient fibroblasts. Factors modulating susceptibility to NM ruptures remain unclear, but we noted low levels of LAP2β, a chromatin-binding inner NM protein, in fibroblasts with NM ruptures. Here, we explored the apparent link between LAP2β and NM ruptures in nuclear lamin-deficient neurons and fibroblasts, and we tested whether manipulating LAP2β expression levels would alter NM rupture frequency. In cortical plate neurons of lamin B1-deficient embryos, we observed a strong correlation between low LAP2β levels and NM ruptures. We also found low LAP2β levels and frequent NM ruptures in neurons of cultured

Indexed as

AnimalsCell DeathCell DifferentiationCerebral CortexDNA-Binding ProteinsDNA DamageEmbryo, MammalianFibroblastsLamin Type ALamin Type BMembrane ProteinsMiceMice, KnockoutNeuronsNuclear EnvelopeOrgan SpecificityDNA-Binding Proteinslamina-associated polypeptide 2Lamin Type ALamin Type BMembrane Proteinslamina-associated polypeptide 2nuclear envelopenuclear laminsnuclear membrane ruptures

Identifiers

PMID34161290
PMCPMC8237679
OpenAlexW3169580824

What OpenQuestion holds

Textmetadata
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.