Evidence map›Paper›PMID 23904609›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013

USP47 and C terminus of Hsp70-interacting protein (CHIP) antagonistically regulate katanin-p60-mediated axonal growth.

Seung Wook Yang, Kyu Hee Oh, Esther Park, Hyun Min Chang, Jung Mi Park, Min Woo Seong, Seung Hyeun Ka, Woo Keun Song, Dong Eun Park, Peter W Baas and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

21 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. The Role of Spastin in Axon Biology.Frontiers in cell and developmental biology · 2022
    Review
  10. The Ubiquitinated Axon: Local Control of Axon Development and Function by Ubiquitin.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Review
  11. Article
  12. Role of Ubiquitin-Specific Peptidase 47 in Cancers and Other Diseases.Frontiers in cell and developmental biology · 2021
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  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

12 authors at 3 institutions in 2 countries.

Seung Wook YangSchool of Biological Sciences, College of Natural Sciences, Seoul National University, Seoul 151-742, Korea.
Kyu Hee Oh
Esther Park
Hyun Min Chang
Jung Mi Park
Min Woo Seong
Seung Hyeun Ka
Woo Keun Song
Dong Eun Park
Peter W Baas
Young Joo Jeon
Chin Ha Chung
Seoul National University · KRDrexel University · USGwangju Institute of Science and Technology · KR

Funding

MICROTUBULE DYNAMICS AND AXON GROWTHR01NS028785 · NINDS · UNIVERSITY OF WISCONSIN MADISON · PI BAAS, PETER W. · 1990 to 2021
$7.3M
NINDS NIH HHS R01 NS028785
6 · The paper itself

Abstract

Katanin is a heterodimeric enzyme that severs and disassembles microtubules. While the p60 subunit has the enzyme activity, the p80 subunit regulates the p60 activity. The microtubule-severing activity of katanin plays an essential role in axonal growth. However, the mechanisms by which neuronal cells regulate the expression of katanin-p60 remains unknown. Here we showed that USP47 and C terminus of Hsp70-interacting protein (CHIP) antagonistically regulate the stability of katanin-p60 and thereby axonal growth. USP47 was identified as a katanin-p60-specific deubiquitinating enzyme for its stabilization. We also identified CHIP as a ubiquitin E3 ligase that promotes proteasome-mediated degradation of katanin-p60. Moreover, USP47 promoted axonal growth of cultured rat hippocampal neurons, whereas CHIP inhibited it. Significantly, treatment with basic fibroblast growth factor (bFGF), an inducer of axonal growth, increased the levels of USP47 and katanin-p60, but not CHIP. Consistently, bFGF treatment resulted in a marked decrease in the level of ubiquitinated katanin-p60 and thereby in the promotion of axonal growth. On the other hand, the level of USP47, but not CHIP, decreased concurrently with that of katanin-p60 as axons reached their target cells. These results indicate that USP47 plays a crucial role in the control of axonal growth during neuronal development by antagonizing CHIP-mediated katanin-p60 degradation.

Indexed as

Adenosine TriphosphatasesAnimalsAxonsCells, CulturedEmbryo, MammalianFemaleFibroblast Growth FactorsGene Expression RegulationHippocampusHSP47 Heat-Shock ProteinsHumansImmunoprecipitationKataninMaleMiceNeuronsAdenosine TriphosphatasesFibroblast Growth FactorsHSP47 Heat-Shock ProteinsKataninKATNA1 protein, humanSTUB1 protein, humanUbiquitin-Protein Ligases

Identifiers

PMID23904609
PMCPMC4469866
OpenAlexW2078987700

What OpenQuestion holds

Textmetadata
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.