Evidence map›Paper›PMID 26924931›Full record

ArticleExperimental neurobiology2016

Drosophila Homolog of Human KIF22 at the Autism-Linked 16p11.2 Loci Influences Synaptic Connectivity at Larval Neuromuscular Junctions.

Sang Mee Park, J Troy Littleton, Hae Ryoun Park, Ji Hye Lee

Open access · bronzeAbstract read
In one paragraph

Article in Experimental neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.8field-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

18 citing papers in PubMed, 27 citations in OpenAlex.

  1. Research progress of kinesin family in neurological diseases.Frontiers in cellular neuroscience · 2025
    Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Autism Spectrum Disorder-Related Syndromes: Modeling withInternational journal of molecular sciences · 2019
    Review
  11. Article
  12. Article
  13. High Expression of KIF22/Kinesin-Like DNA Binding Protein (Kid) as a Poor Prognostic Factor in Prostate Cancer Patients.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. 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

4 authors at 3 institutions in 2 countries.

Sang Mee ParkDepartment of Oral Pathology, School of Dentistry, Pusan National University, Yangsan 50612, Korea.
J Troy LittletonThe Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.; Department of Biology & Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Hae Ryoun ParkDepartment of Oral Pathology, School of Dentistry, Pusan National University, Yangsan 50612, Korea.; Institute of Translational Dental Sciences, Pusan National University, Yangsan 50612, Korea.
Ji Hye LeeDepartment of Oral Pathology, School of Dentistry, Pusan National University, Yangsan 50612, Korea.; Institute of Translational Dental Sciences, Pusan National University, Yangsan 50612, Korea.; The Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Institute for Learning and Development · USPusan National University · KRPusan National University Dental Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Copy number variations at multiple chromosomal loci, including 16p11.2, have recently been implicated in the pathogenesis of autism spectrum disorder (ASD), a neurodevelopmental disease that affects 1~3% of children worldwide. The aim of this study was to investigate the roles of human genes at the 16p11.2 loci in synaptic development using Drosophila larval neuromuscular junctions (NMJ), a well-established model synapse with stereotypic innervation patterns. We conducted a preliminary genetic screen based on RNA interference in combination with the GAL4-UAS system, followed by mutational analyses. Our result indicated that disruption of klp68D, a gene closely related to human KIF22, caused ectopic innervations of axon branches forming type III boutons in muscle 13, along with less frequent re-routing of other axon branches. In addition, mutations in klp64D, of which gene product forms Kinesin-2 complex with KLP68D, led to similar targeting errors of type III axons. Mutant phenotypes were at least partially reproduced by knockdown of each gene via RNA interference. Taken together, our data suggest the roles of Kinesin-2 proteins, including KLP68D and KLP64D, in ensuring proper synaptic wiring.

Indexed as

16p11.2AutismCopy number variationsDrosophilaKinesin-2

Identifiers

PMID26924931
PMCPMC4766112
OpenAlexW2282157314

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.