Evidence map›Paper›PMID 8603924›Full record

ArticleThe Journal of cell biology1996

Agrin-induced acetylcholine receptor clustering in mammalian muscle requires tyrosine phosphorylation.

M Ferns, M Deiner, Z Hall

Abstract read
In one paragraph

Article in The Journal of cell biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
–field-weighted citation impact
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

47 citing papers in PubMed.

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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

3 authors.

M FernsDepartment of Physiology, University of California at San Francisco, 94143-0444, USA.
M Deiner
Z Hall

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Agrin is thought to be the nerve-derived factor that initiates acetylcholine receptor (AChR) clustering at the developing neuromuscularjunction. We have investigated the signaling pathway in mouse C2 myotubes and report that agrin induces a rapid but transient tyrosine phosphorylation of the AChR beta subunit. As the beta-subunit tyrosine phosphorylation occurs before the formation of AChR clusters, it may serve as a precursor step in the clustering mechanism. Consistent with this, we observed that tyrosine phosphorylation of the beta subunit correlated precisely with the presence or absence of clustering under several experimental conditions. Moreover, two tyrosine kinase inhibitors, herbimycin and staurosporine, that blocked beta-subunit phosphorylation also blocked agrin-induced clustering. Surprisingly, the inhibitors also dispersed preformed AChR clusters, suggesting that the tyrosine phosphorylation of other proteins may be required for the maintenance of receptor clusters. These findings indicate that in mammalian muscle, agrin-induced AChR clustering occurs through a mechanism that requires tyrosine phosphorylation and may involve tyrosine phosphorylation of the AChR itself.

Indexed as

Signal TransductionAgrinAlkaloidsAnimalsBenzoquinonesCells, CulturedEnzyme InhibitorsLactams, MacrocyclicMiceMusclesPhosphoproteinsPhosphorylationPhosphotyrosineProtein-Tyrosine KinasesQuinonesReceptor AggregationAgrinAlkaloidsBenzoquinonesEnzyme InhibitorsherbimycinLactams, MacrocyclicPhosphoproteinsPhosphotyrosineProtein-Tyrosine KinasesQuinonesReceptors, CholinergicRifabutinStaurosporine

Identifiers

PMID8603924
PMCPMC2120739

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Registered trials

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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.