Evidence map›Paper›PMID 19468071›Full record

ArticleThe Journal of cell biology2009

Rescue of skeletal muscle alpha-actin-null mice by cardiac (fetal) alpha-actin.

Kristen J Nowak, Gianina Ravenscroft, Connie Jackaman, Aleksandra Filipovska, Stefan M Davies, Esther M Lim, Sarah E Squire, Allyson C Potter, Elizabeth Baker, Sophie Clément and 11 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

38 citing papers in PubMed, 74 citations in OpenAlex.

  1. Actin cytoskeletal dynamics in hepatic myofibroblasts and fibrosis.Nature reviews. Gastroenterology & hepatology · 2026
    Review
  2. Review
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  5. Article
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  8. Nemaline myopathies: a current view.Journal of muscle research and cell motility · 2019
    Review
  9. CAP2 deficiency delays myofibril actin cytoskeleton differentiation and disturbs skeletal muscle architecture and function.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  10. Article
  11. Review
  12. Review
  13. Absence of the Drosophila jump muscle actin Act79B is compensated by up-regulation of Act88F.Developmental dynamics : an official publication of the American Association of Anatomists · 2018
    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

21 authors at 9 institutions in 4 countries.

Kristen J NowakCentre for Medical Research, School of Biomedical, Biomolecular, and Chemical Sciences, The University of Western Australia, Perth, Western Australia 6009, Australia. knowak@cyllene.uwa.edu.au
Gianina Ravenscroft
Connie Jackaman
Aleksandra Filipovska
Stefan M Davies
Esther M Lim
Sarah E Squire
Allyson C Potter
Elizabeth Baker
Sophie Clément
Caroline A Sewry
Victoria Fabian
Kelly Crawford
James L Lessard
Lisa M Griffiths
John M Papadimitriou
Yun Shen
Grant Morahan
Anthony J Bakker
Kay E Davies
Nigel G Laing
University of Western Australia · AUHarry Perkins Institute of Medical Research · AUCincinnati Children's Hospital Medical Center · USMedical Research Council · GBRoyal Perth Hospital · AUKing Edward Memorial Hospital · AURobert Jones and Agnes Hunt Orthopaedic Hospital · GBUniversity of Geneva · CHUniversity of Oxford · GB

Funding

Medical Research Council MC_U137761449
6 · The paper itself

Abstract

Skeletal muscle alpha-actin (ACTA1) is the major actin in postnatal skeletal muscle. Mutations of ACTA1 cause mostly fatal congenital myopathies. Cardiac alpha-actin (ACTC) is the major striated actin in adult heart and fetal skeletal muscle. It is unknown why ACTC and ACTA1 expression switch during development. We investigated whether ACTC can replace ACTA1 in postnatal skeletal muscle. Two ACTC transgenic mouse lines were crossed with Acta1 knockout mice (which all die by 9 d after birth). Offspring resulting from the cross with the high expressing line survive to old age, and their skeletal muscles show no gross pathological features. The mice are not impaired on grip strength, rotarod, or locomotor activity. These findings indicate that ACTC is sufficiently similar to ACTA1 to produce adequate function in postnatal skeletal muscle. This raises the prospect that ACTC reactivation might provide a therapy for ACTA1 diseases. In addition, the mouse model will allow analysis of the precise functional differences between ACTA1 and ACTC.

Indexed as

ActinsAnimalsGene Expression ProfilingHeartMiceMice, KnockoutMuscle, SkeletalMyocardiumProtein IsoformsActinsProtein Isoforms

Identifiers

PMID19468071
PMCPMC2711600
OpenAlexW2169099673

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.