Evidence map›Paper›PMID 9382868›Full record

ArticleThe Journal of cell biology1997

Growth and muscle defects in mice lacking adult myosin heavy chain genes.

L J Acakpo-Satchivi, W Edelmann, C Sartorius, B D Lu, P A Wahr, S C Watkins, J M Metzger, L Leinwand, R Kucherlapati

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of cell biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

37 citing papers in PubMed, 89 citations in OpenAlex.

  1. Article
  2. Homologous mutations in human β, embryonic, and perinatal muscle myosins have divergent effects on molecular power generation.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  9. Review
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  11. Driving an Oxidative Phenotype ProtectsFrontiers in physiology · 2021
    Article
  12. Article
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  14. Defective sarcomere organization and reduced larval locomotion and fish survival in slow muscle heavy chain 1 (smyhc1) mutants.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  15. Article
  16. Sarcopenia: Aging-Related Loss of Muscle Mass and Function.Physiological reviews · 2019 · on this map
    Review
  17. Article
  18. Article
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  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

9 authors at 4 institutions in 1 country.

L J Acakpo-SatchiviDepartment of Molecular Genetics, Albert Einstein College of Medicine, New York 10461, USA.
W Edelmann
C Sartorius
B D Lu
P A Wahr
S C Watkins
J M Metzger
L Leinwand
R Kucherlapati
University of Pittsburgh · USUniversity of Colorado Boulder · USAlbert Einstein College of Medicine · USUniversity of Michigan–Ann Arbor · US

Funding

WORD PROCESSORP30CA013330 · NCI · YESHIVA UNIVERSITY · PI THOMAS E ROHAN · 1985 to 2026
$111.2M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007288 · NIGMS · YESHIVA UNIVERSITY · PI AKABAS, MYLES H. · 1985 to 2022
$35.6M
MYOSIN GENE DIVERSITY AND FUNCTIONR01GM029090 · NIGMS · YESHIVA UNIVERSITY · PI Leslie Anne Leinwand · 1985 to 2026
$12.3M
MINORITY PREDOCTORAL FELLOWSHIP PROGRAM--NIGMSF31HG000064 · NHGRI · YESHIVA UNIVERSITY · PI ACAKPO-SATCHIVI, LESLIE J · 1991 to 1995
–
MYOSIN GENES AND MOUSE SKELETAL MUSCLEF32AR008443 · NIAMS · UNIVERSITY OF COLORADO DENVER · PI SARTORIUS, CAROL ANN · 1996 to 1999
–
NCI NIH HHS P30 CA013330NHGRI NIH HHS F31 HG000064NIAMS NIH HHS 1F32AR08443NIAMS NIH HHS F32 AR008443NIGMS NIH HHS GM29090NIGMS NIH HHS R01 GM029090NIGMS NIH HHS T32 GM007288NIGMS NIH HHS T32GM07288
6 · The paper itself

Abstract

The three adult fast myosin heavy chains (MyHCs) constitute the vast majority of the myosin in adult skeletal musculature, and are >92% identical. We describe mice carrying null mutations in each of two predominant adult fast MyHC genes, IIb and IId/x. Both null strains exhibit growth and muscle defects, but the defects are different between the two strains and do not correlate with the abundance or distribution of each gene product. For example, despite the fact that MyHC-IIb accounts for >70% of the myosin in skeletal muscle and shows the broadest distribution of expression, the phenotypes of IIb null mutants are generally milder than in the MyHC-IId/x null strain. In addition, in a muscle which expresses both IIb and IId/x MyHC in wild-type mice, the histological defects are completely different for null expression of the two genes. Most striking is that while both null strains exhibit physiological defects in isolated muscles, the defects are distinct. Muscle from IIb null mice has significantly reduced ability to generate force while IId null mouse muscle generates normal amounts of force, but has altered kinetic properties. Many of the phenotypes demonstrated by these mice are typical in human muscle disease and should provide insight into their etiology.

Indexed as

Mice, Mutant StrainsAge FactorsAnimalsBody WeightGrowth DisordersKyphosisMiceMice, Inbred C57BLMuscle ContractionMuscle Fibers, Fast-TwitchMuscle, SkeletalMuscle WeaknessMuscular DiseasesMutagenesis, Site-DirectedMyosin Heavy ChainsMyosin Heavy Chains

Identifiers

PMID9382868
PMCPMC2140209
OpenAlexW2005411659

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.