Evidence map›Paper›PMID 35869491›Full record

ArticleCell & bioscience2022

FBXL17/spastin axis as a novel therapeutic target of hereditary spastic paraplegia.

Hyun Mi Kang, Dae Hun Kim, Mijin Kim, Yoohong Min, Bohyeon Jeong, Kyung Hee Noh, Da Yong Lee, Hyun-Soo Cho, Nam-Soon Kim, Cho-Rok Jung and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 47% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. A GJA1 Variant Triggers Earlier SPG4 Onset by Destabilizing Deubiquitinase VCPIP1 to Lower SPASTIN Levels.Movement disorders : official journal of the Movement Disorder Society · 2026
    Article
  2. Article
  3. Article
  4. Unraveling Isoform Complexity: The Roles of M1- and M87-Spastin in Spastic Paraplegia 4 (SPG4).Movement disorders : official journal of the Movement Disorder Society · 2025
    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

11 authors at 4 institutions in 1 country.

Hyun Mi KangKorea Research Institute of Bioscience and Biotechnology (KRIBB), 125 Gwahak-ro, 34141, Daejeon, Republic of Korea.
Dae Hun KimKorea Research Institute of Bioscience and Biotechnology (KRIBB), 125 Gwahak-ro, 34141, Daejeon, Republic of Korea.
Mijin KimKorea Research Institute of Bioscience and Biotechnology (KRIBB), 125 Gwahak-ro, 34141, Daejeon, Republic of Korea.
Yoohong MinKorea Research Institute of Bioscience and Biotechnology (KRIBB), 125 Gwahak-ro, 34141, Daejeon, Republic of Korea.
Bohyeon JeongKorea Research Institute of Bioscience and Biotechnology (KRIBB), 125 Gwahak-ro, 34141, Daejeon, Republic of Korea.
Kyung Hee NohKorea Research Institute of Bioscience and Biotechnology (KRIBB), 125 Gwahak-ro, 34141, Daejeon, Republic of Korea.
Da Yong LeeKorea Research Institute of Bioscience and Biotechnology (KRIBB), 125 Gwahak-ro, 34141, Daejeon, Republic of Korea.
Hyun-Soo ChoKorea Research Institute of Bioscience and Biotechnology (KRIBB), 125 Gwahak-ro, 34141, Daejeon, Republic of Korea.
Nam-Soon KimKorea Research Institute of Bioscience and Biotechnology (KRIBB), 125 Gwahak-ro, 34141, Daejeon, Republic of Korea.
Cho-Rok JungKorea Research Institute of Bioscience and Biotechnology (KRIBB), 125 Gwahak-ro, 34141, Daejeon, Republic of Korea. crjung@kribb.re.kr.
Jung Hwa LimKorea Research Institute of Bioscience and Biotechnology (KRIBB), 125 Gwahak-ro, 34141, Daejeon, Republic of Korea. jhwa@kribb.re.kr.
Korea Research Institute of Bioscience and Biotechnology · KRKorea University of Science and Technology · KRChungbuk National University · KRChungnam National University · KR

Funding

Ministry of Science, ICT and Future Planning 2015M3A9D9067483Ministry of Science, ICT and Future Planning 2019R1C1C1006822Ministry of Science, ICT and Future Planning 2020R1C1C1007034Ministry of Science, ICT and Future Planning the KRIBB Research Initiative Program
6 · The paper itself

Abstract

backgroundSpastin significantly influences microtubule regulation in neurons and is implicated in the pathogenesis of hereditary spastic paraplegia (HSP). However, post-translational regulation of the spastin protein remains nebulous. The association between E3 ubiquitin ligase and spastin provides a potential therapeutic strategy.

resultsAs evidenced by protein chip analysis, FBXL17 inversely correlated with SPAST-M1 at the protein level in vitro and, also in vivo during embryonic developmental stage. SPAST-M1 protein interacted with FBXL17 specifically via the BTB domain at the N-terminus of SPAST-M1. The SCF

conclusionsWe discovered that a novel pathway, FBXL17-SPAST was involved in pathogenicity of HSP by the loss of function and the quantitative regulation. This result suggested that targeting FBXL17 could provide new insight into HSP therapeutics.

Indexed as

E3 ubiquitin ligaseFBXL17Hereditary spastic paraplegiaSCF complexSPAST

Identifiers

PMID35869491
PMCPMC9308218
OpenAlexW4286488476

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.