Evidence map›Paper›PMID 22127257›Full record

ArticleNucleus (Austin, Tex.)

Are B-type lamins essential in all mammalian cells?

Shao H Yang, Hea-Jin Jung, Catherine Coffinier, Loren G Fong, Stephen G Young

Open access · bronzeAbstract read
In one paragraph

Article in Nucleus (Austin, Tex.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

32 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Nuclear destabilisation - a possible genesis of cancer?Biological reviews of the Cambridge Philosophical Society · 2025
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. 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
  13. Article
  14. Article
  15. Review
  16. Article
  17. 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

5 authors at 3 institutions in 2 countries.

Shao H YangDepartment of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Hea-Jin Jung
Catherine Coffinier
Loren G Fong
Stephen G Young
University of California System · USInstitute of Molecular Biology · BGUniversity of California, Los Angeles · US

Funding

Vascular Biology Training GrantT32HL069766 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LUSIS, ALDONS JAKE · 2002 to 2022
$7.4M
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
CAAX Protein Processing and Cancer TherapyR01CA099506 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI YOUNG, STEPHEN G · 2003 to 2007
$1.7M
STUDY OF PERSISTENT FETAL CIRCULATION IN NEWBORN LAMBF32HL006976 · NHLBI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI WALSH, ROBERT S · 1985 to 1985
–
NCI NIH HHS CA099506-07NCI NIH HHS R01 CA099506NHLBI NIH HHS 2 T32 HL069766:06NHLBI NIH HHS HL086683NHLBI NIH HHS HL089781NHLBI NIH HHS HL76839NHLBI NIH HHS R01 HL076839NHLBI NIH HHS R01 HL086683NHLBI NIH HHS R01 HL089781NHLBI NIH HHS T32 HL069766NIA NIH HHS R01 AG035626
6 · The paper itself

Abstract

The B-type lamins are widely assumed to be essential for mammalian cells. In part, this assumption is based on a highly cited study that found that RNAi-mediated knockdown of lamin B1 or lamin B2 in HeLa cells arrested cell growth and led to apoptosis. Studies indicating that B-type lamins play roles in DNA replication, the formation of the mitotic spindle, chromatin organization and regulation of gene expression have fueled the notion that B-type lamins must be essential. But surprisingly, this idea had never been tested with genetic approaches. Earlier this year, a research group from UCLA reported the development of genetically modified mice that lack expression of both Lmnb1 and Lmnb2 in skin keratinocytes (a cell type that proliferates rapidly and participates in complex developmental programs). They reasoned that if lamins B1 and B2 were truly essential, then keratinocyte-specific lamin B1/lamin B2 knockout mice would exhibit severe pathology. Contrary to expectations, the skin and hair of lamin B1/lamin B2-deficient mice were quite normal, indicating that the B-type lamins are dispensable in some cell types. The same UCLA research group has gone on to show that lamin B1 and lamin B2 are critical for neuronal migration in the developing brain and for neuronal survival.  The absence of either lamin B1 or lamin B2, or the absence of both B-type lamins, results in severe neurodevelopmental abnormalities.

Indexed as

AnimalsApoptosisBrainCell CycleCell MovementCell SurvivalDNA ReplicationGene Expression RegulationGene Knockdown TechniquesHeLa CellsHumansKeratinocytesLamin Type BMiceMice, KnockoutNeuronsLamin Type B

Identifiers

PMID22127257
PMCPMC3324344
OpenAlexW2070067710

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.