Evidence map›Paper›PMID 26167908›Full record

ArticlePloS one2015

Drosophila Cbp53E Regulates Axon Growth at the Neuromuscular Junction.

Kimberly R Hagel, Jane Beriont, Charles R Tessier

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.6field-weighted citation impact, top 37% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Loss of calcium-binding proteinbioRxiv : the preprint server for biology · 2026
    Article
  2. Article
  3. Article
  4. Molecular Logic of Synaptic Diversity BetweenbioRxiv : the preprint server for biology · 2023
    Article
  5. Article
  6. Structural and mechanistic insights into secretagogin-mediated exocytosis.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  7. Article
  8. 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 at 2 institutions in 1 country.

Kimberly R HagelDepartment of Biological Sciences, University of Notre Dame, Notre Dame, Indiana, United States of America.
Jane BeriontDepartment of Biological Sciences, University of Notre Dame, Notre Dame, Indiana, United States of America.
Charles R TessierDepartment of Medical and Molecular Genetics, Indiana University School of Medicine-South Bend, South Bend, Indiana, United States of America.
University of Notre Dame · USIndiana University School of Medicine

Funding

Resource Component: Acquisition, maintenance and distribution of Drosophila stocksP40OD018537 · OD · TRUSTEES OF INDIANA UNIVERSITY · PI Annette L. Parks · 2014 to 2026
$13.5M
NIH HHS P40 OD018537NIH HHS P40OD018537
6 · The paper itself

Abstract

Calcium is a primary second messenger in all cells that functions in processes ranging from cellular proliferation to synaptic transmission. Proper regulation of calcium is achieved through numerous mechanisms involving channels, sensors, and buffers notably containing one or more EF-hand calcium binding domains. The Drosophila genome encodes only a single 6 EF-hand domain containing protein, Cbp53E, which is likely the prototypic member of a small family of related mammalian proteins that act as calcium buffers and calcium sensors. Like the mammalian homologs, Cbp53E is broadly though discretely expressed throughout the nervous system. Despite the importance of calcium in neuronal function and growth, nothing is known about Cbp53E's function in neuronal development. To address this deficiency, we generated novel null alleles of Drosophila Cbp53E and examined neuronal development at the well-characterized larval neuromuscular junction. Loss of Cbp53E resulted in increases in axonal branching at both peptidergic and glutamatergic neuronal terminals. This overgrowth could be completely rescued by expression of exogenous Cbp53E. Overexpression of Cbp53E, however, only affected the growth of peptidergic neuronal processes. These findings indicate that Cbp53E plays a significant role in neuronal growth and suggest that it may function in both local synaptic and global cellular mechanisms.

Indexed as

AxonsAnimalsCalbindinsDrosophilaDrosophila ProteinsNeuromuscular JunctionCalbindinsCbp53E protein, DrosophilaDrosophila Proteins

Identifiers

PMID26167908
PMCPMC4500412
OpenAlexW2209771297

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.