Evidence map›Paper›PMID 17485447›Full record

ArticleMolecular and cellular biology2007

GA-binding protein is dispensable for neuromuscular synapse formation and synapse-specific gene expression.

Alexander Jaworski, Cynthia L Smith, Steven J Burden

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

14 citing papers in PubMed, 29 citations in OpenAlex.

  1. NMJ-related diseases beyond the congenital myasthenic syndromes.Frontiers in cell and developmental biology · 2023
    Review
  2. Article
  3. Review
  4. A Role of Lamin A/C in Preventing Neuromuscular Junction Decline in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  5. Review
  6. Catalytic deficiency of O-GlcNAc transferase leads to X-linked intellectual disability.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  7. Article
  8. Article
  9. Article
  10. Proteomic analysis of HIV-infected macrophages.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2011
    Review
  11. Article
  12. Article
  13. Critical requirement of GABPalpha for normal T cell development.The Journal of biological chemistry · 2010
    Article
  14. 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

3 authors.

Alexander JaworskiThe Helen L. and Martin S. Kimmel Center for Biology and Medicine, Skirball Institute of Biomoledular Medicine, NYU School of Medicine, New York, NY 10016, USA.
Cynthia L Smith
Steven J Burden

Funding

REGULATION OF ACHR GENE EXPRESSION--ELECTRICAL ACTIVITYR01NS027963 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI BURDEN, STEVEN · 1990 to 2004
$2.1M
NINDS NIH HHS NS27963NINDS NIH HHS NS31963NINDS NIH HHS R01 NS027963
6 · The paper itself

Abstract

The mRNAs encoding postsynaptic components at the neuromuscular junction are concentrated in the synaptic region of muscle fibers. Accumulation of these RNAs in the synaptic region is mediated, at least in part, by selective transcription of the corresponding genes in synaptic myofiber nuclei. The transcriptional mechanisms that are responsible for synapse-specific gene expression are largely unknown, but an Ets site in the promoter regions of acetylcholine receptor (AChR) subunit genes and other "synaptic" genes is required for synapse-specific transcription. The Ets domain transcription factor GA-binding protein (GABP) has been implicated to mediate synapse-specific gene expression. Inactivation of GABPalpha, the DNA-binding subunit of GABP, leads to early embryonic lethality, preventing analysis of synapse formation in gabpalpha mutant mice. To study the role of GABP at neuromuscular synapses, we conditionally inactivated gabpalpha in skeletal muscle and studied synaptic differentiation and muscle gene expression. Although expression of rb, a target of GABP, is elevated in muscle tissue deficient in GABPalpha, clustering of synaptic AChRs at synapses and synapse-specific gene expression are normal in these mice. These data indicate that GABP is dispensable for synapse-specific transcription and maintenance of normal AChR expression at synapses.

Indexed as

Gene Expression RegulationAllelesAnimalsAnimals, NewbornEmbryonic DevelopmentGA-Binding Protein Transcription FactorGene TargetingMiceMuscle, SkeletalMutant ProteinsNeuromuscular JunctionReceptors, CholinergicRetinoblastoma ProteinRNA, MessengerGA-Binding Protein Transcription FactorGabpa protein, mouseMutant ProteinsReceptors, CholinergicRetinoblastoma ProteinRNA, Messenger

Identifiers

PMID17485447
PMCPMC1951497
OpenAlexW2114508686

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.