Evidence map›Paper›PMID 29282074›Full record

ArticleMolecular brain2017

The Rap activator Gef26 regulates synaptic growth and neuronal survival via inhibition of BMP signaling.

Keunjung Heo, Minyeop Nahm, Min-Jung Lee, Young-Eun Kim, Chang-Seok Ki, Seung Hyun Kim, Seungbok Lee

Open access · goldAbstract read
In one paragraph

Article in Molecular brain, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.5field-weighted citation impact, top 41% 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

13 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Rare heterozygous de novo variants in RAPGEF2 are associated with a neurodevelopmental disorder.Genetics in medicine : official journal of the American College of Medical Genetics · 2026
    Article
  3. Review
  4. Journal of biological rhythms · 2025
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  13. AExperimental neurobiology · 2018
    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

7 authors at 3 institutions in 2 countries.

Keunjung HeoDepartment of Brain and Cognitive Sciences, College of Natural Sciences, Seoul National University, Seoul, 08826, South Korea.
Minyeop NahmDepartment of Neurology, Hanyang University College of Medicine, Seoul, 04763, South Korea.
Min-Jung LeeDepartment of Brain and Cognitive Sciences, College of Natural Sciences, Seoul National University, Seoul, 08826, South Korea.
Young-Eun KimDepartment of Laboratory Medicine and Genetics, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, 06351, South Korea.
Chang-Seok KiDepartment of Laboratory Medicine and Genetics, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, 06351, South Korea.
Seung Hyun KimDepartment of Neurology, Hanyang University College of Medicine, Seoul, 04763, South Korea.
Seungbok LeeDepartment of Brain and Cognitive Sciences, College of Natural Sciences, Seoul National University, Seoul, 08826, South Korea. seunglee@snu.ac.kr.ORCID 0000-0002-6620-6269
Seoul National University · KRHanyang University · KRSamsung Medical Center · KR

Funding

National Reaserch Foundation of Korea BK21+ programNational Research Foundation of Korea 2017M3C7A1025368
6 · The paper itself

Abstract

In Drosophila, precise regulation of BMP signaling is essential for normal synaptic growth at the larval neuromuscular junction (NMJ) and neuronal survival in the adult brain. However, the molecular mechanisms underlying fine-tuning of BMP signaling in neurons remain poorly understood. We show that loss of the Drosophila PDZ guanine nucleotide exchange factor Gef26 significantly increases synaptic growth at the NMJ and enhances BMP signaling in motor neurons. We further show that Gef26 functions upstream of Rap1 in motor neurons to restrain synaptic growth. Synaptic overgrowth in gef26 or rap1 mutants requires BMP signaling, indicating that Gef26 and Rap1 regulate synaptic growth via inhibition of BMP signaling. We also show that Gef26 is involved in the endocytic downregulation of surface expression of the BMP receptors thickveins (Tkv) and wishful thinking (Wit). Finally, we demonstrate that loss of Gef26 also induces progressive brain neurodegeneration through Rap1- and BMP signaling-dependent mechanisms. Taken together, these results suggest that the Gef26-Rap1 signaling pathway regulates both synaptic growth and neuronal survival by controlling BMP signaling.

Indexed as

Signal TransductionAnimalsBrainCell LineCell SurvivalDrosophila melanogasterDrosophila ProteinsEndocytosisEpistasis, GeneticFragile X Messenger Ribonucleoprotein 1MicrotubulesModels, BiologicalNerve DegenerationNeuromuscular JunctionNeuronsProtein Serine-Threonine KinasesDrosophila ProteinsFMR1 protein, DrosophilaFragile X Messenger Ribonucleoprotein 1Protein Serine-Threonine Kinasesrap1 GTP-Binding ProteinsReceptors, Cell Surfacetkv protein, Drosophilawit protein, DrosophilaDrosophilaEndocytic regulation of BMP signalingGef26NeurodegenerationSynaptic growth

Identifiers

PMID29282074
PMCPMC5745669
OpenAlexW2780173448

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.