Evidence map›Paper›PMID 33461576›Full record

ArticleMolecular brain2021

Schizophrenia-associated dysbindin modulates axonal mitochondrial movement in cooperation with p150

Bo Kyoung Suh, Seol-Ae Lee, Cana Park, Yeongjun Suh, Soo Jeong Kim, Youngsik Woo, Truong Thi My Nhung, Su Been Lee, Dong Jin Mun, Bon Seong Goo and 3 more

Open access · goldAbstract read
In one paragraph

Article in Molecular brain, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Ratiometric measurement of MAM CaNature communications · 2023
    Article
  6. Article
  7. Article
  8. Article
  9. Axonal transport deficits in neuropsychiatric disorders.Molecular and cellular neurosciences · 2022
    Article
  10. Article
  11. Review
  12. Review
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

13 authors at 1 institution in 2 countries.

Bo Kyoung SuhDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Republic of Korea.
Seol-Ae LeeDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Republic of Korea.
Cana ParkDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Republic of Korea.
Yeongjun SuhDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Republic of Korea.
Soo Jeong KimDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Republic of Korea.
Youngsik WooDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Republic of Korea.
Truong Thi My NhungDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Republic of Korea.
Su Been LeeDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Republic of Korea.
Dong Jin MunDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Republic of Korea.
Bon Seong GooDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Republic of Korea.
Hyun Sun ChoiDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Republic of Korea.
So Jung KimDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Republic of Korea.
Sang Ki ParkDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Republic of Korea. skpark@postech.ac.kr.
Pohang University of Science and Technology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial movement in neurons is finely regulated to meet the local demand for energy and calcium buffering. Elaborate transport machinery including motor complexes is required to deliver and localize mitochondria to appropriate positions. Defects in mitochondrial transport are associated with various neurological disorders without a detailed mechanistic information. In this study, we present evidence that dystrobrevin-binding protein 1 (dysbindin), a schizophrenia-associated factor, plays a critical role in axonal mitochondrial movement. We observed that mitochondrial movement was impaired in dysbindin knockout mouse neurons. Reduced mitochondrial motility caused by dysbindin deficiency decreased the density of mitochondria in the distal part of axons. Moreover, the transport and distribution of mitochondria were regulated by the association between dysbindin and p150

Indexed as

AnimalsAxonsCalciumDynactin ComplexDysbindinHEK293 CellsHomeostasisHumansMiceMice, Inbred C57BLMicrotubulesMitochondriaModels, BiologicalPresynaptic TerminalsProtein BindingSchizophreniaCalciumDynactin ComplexDysbindinCalcium homeostasisDynactin complexDysbindinMitochondrial movementp150glued

Identifiers

PMID33461576
PMCPMC7814725
OpenAlexW3124760023

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.