Evidence map›Paper›PMID 30126838›Full record

ArticleThe Journal of cell biology2018

KIF1Bβ mutations detected in hereditary neuropathy impair IGF1R transport and axon growth.

Fang Xu, Hironori Takahashi, Yosuke Tanaka, Sotaro Ichinose, Shinsuke Niwa, Matthew P Wicklund, Nobutaka Hirokawa

Abstract read
In one paragraph

Article in The Journal of cell biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

24 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. KIF1B Regulates NLRP3-Mediated Pyroptosis in Asthma Progression.Journal of cellular and molecular medicine · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Research progress of kinesin family in neurological diseases.Frontiers in cellular neuroscience · 2025
    Review
  10. Article
  11. Involvement of kinesins in skeletal dysplasia: a review.American journal of physiology. Cell physiology · 2024
    Review
  12. Review
  13. Article
  14. Biallelic Loss-of-Function Variants inInternational journal of molecular sciences · 2023
    Article
  15. Article
  16. RNA processing in neurological tissue: development, aging and disease.Seminars in cell & developmental biology · 2021
    Review
  17. Article
  18. Review
  19. Review
  20. 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

7 authors at 3 institutions in 3 countries.

Fang XuDepartment of Cell Biology and Anatomy, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Hironori TakahashiDepartment of Cell Biology and Anatomy, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Yosuke TanakaDepartment of Cell Biology and Anatomy, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID 0000-0001-5376-5726
Sotaro IchinoseDepartment of Cell Biology and Anatomy, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Shinsuke NiwaDepartment of Cell Biology and Anatomy, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Matthew P WicklundDepartment of Neurology, Penn State Hershey Medical Center, Hershey, PA.
Nobutaka HirokawaDepartment of Cell Biology and Anatomy, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan hirokawa@m.u-tokyo.ac.jp.ORCID 0000-0002-0081-5264
The University of Tokyo · JPKing Abdulaziz University · SAPenn State Milton S. Hershey Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

KIF1Bβ is a kinesin-3 family anterograde motor protein essential for neuronal development, viability, and function. KIF1Bβ mutations have previously been reported in a limited number of pedigrees of Charcot-Marie-Tooth disease type 2A (CMT2A) neuropathy. However, the gene responsible for CMT2A is still controversial, and the mechanism of pathogenesis remains elusive. In this study, we show that the receptor tyrosine kinase IGF1R is a new direct binding partner of KIF1Bβ, and its binding and transport is specifically impaired by the Y1087C mutation of KIF1Bβ, which we detected in hereditary neuropathic patients. The axonal outgrowth and IGF-I signaling of

Indexed as

Gene Expression Regulation, DevelopmentalMutation, MissenseNeuronal OutgrowthSignal TransductionAnimalsCharcot-Marie-Tooth DiseaseKinesinsMiceMice, Inbred ICRMice, KnockoutProtein TransportReceptor, IGF Type 1Igf1r protein, mouseKif1b protein, mouseKinesinsReceptor, IGF Type 1

Identifiers

PMID30126838
PMCPMC6168269
OpenAlexW2888188523

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.