Evidence map›Paper›PMID 8884601›Full record

ArticleJournal of muscle research and cell motility1996

Quantitative analysis of low molecular weight G-actin-binding proteins, cofilin, ADF and profilin, expressed in developing and degenerating chicken skeletal muscles.

R Nagaoka, N Minami, K Hayakawa, H Abe, T Obinata

Abstract read
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In one paragraph

Article in Journal of muscle research and cell motility, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. The Mechanisms of Thin Filament Assembly and Length Regulation in Muscles.International journal of molecular sciences · 2022
    Review
  3. Article
  4. Functions of cofilin in cell locomotion and invasion.Nature reviews. Molecular cell biology · 2013
    Review
  5. Review
  6. 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 2 institutions in 1 country.

R NagaokaDepartment of Biology, Faculty of Science, Chiba University, Japan.
N Minami
K Hayakawa
H Abe
T Obinata
Chiba University · JPNational Center of Neurology and Psychiatry · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A large amount of G-actin is pooled in the cytoplasm of young embryonic skeletal muscle and, although its concentration is reduced as muscle develops, the total amount of actin in muscle cells increases remarkably. Three G-actin-binding proteins, cofilin, ADF and profilin, are known to be involved in creating the G-actin pool in the embryonic muscle. To better understand how they are responsible for the regulation of assembly and disassembly of actin in developing and degenerating muscles, we measured the amounts of the three G-actin-binding proteins by means of quantitative immunoblotting and compared them with that of G-actin. The sum of the amounts of the three actin-binding proteins was insufficient at early developmental stages but sufficient at later stages to account for the pool of G-actin in young muscle cells. It decreased in parallel with the decrease in the G-actin pool as muscle developed. Expression of thymosin beta 4, which is known to be extremely important for G-actin-sequestering in a variety of non-muscle cells, was detected at a considerable level in young embryonic but not in adult skeletal muscles according to Northern and Western blotting. In degenerating denervated and dystrophic muscles, cofilin and profilin, but not ADF, were significantly increased in amount. From these results, we conclude that the G-actin pool in young embryonic skeletal muscle is mainly due to cofilin, ADF, profilin and thymosin beta 4, but thymosin beta 4 as well as ADF becomes less important as muscle develops. Cofilin and profilin may also be involved in the redistribution of actin during myofibrillogenesis and in the process of actin disassembly in degenerating muscles.

Indexed as

Actin Depolymerizing FactorsAgingAnimalsBlotting, NorthernBlotting, WesternBrain ChemistryChick EmbryoChickensContractile ProteinsDestrinElectrophoresis, Polyacrylamide GelKineticsMicrofilament ProteinsMolecular WeightMuscle DenervationMusclesActin Depolymerizing FactorsContractile ProteinsDestrinMicrofilament ProteinsNerve Tissue ProteinsProfilinsThymosinThymosin beta(4)

Identifiers

PMID8884601
OpenAlexW2024575044

What OpenQuestion holds

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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.