Evidence map›Paper›PMID 39807990›Full record

ArticleASN neuro2025

New Atg9 Phosphorylation Sites Regulate Autophagic Trafficking in Glia.

Linfang Wang, Shuanglong Yi, Shiping Zhang, Yu-Ting Tsai, Yi-Hsuan Cheng, Yu-Tung Lin, Chia-Ching Lin, Yi-Hua Lee, Honglei Wang, Margaret S Ho

Abstract read
In one paragraph

Article in ASN neuro, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. Autophagy · 2025
    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

10 authors.

Linfang WangSchool of Life Science and Technology, ShanghaiTech University, Shanghai, China.
Shuanglong YiSchool of Life Science and Technology, ShanghaiTech University, Shanghai, China.
Shiping ZhangSchool of Life Science and Technology, ShanghaiTech University, Shanghai, China.
Yu-Ting TsaiInstitute of Neuroscience, National Yang Ming Chiao Tung University, Taipei, Taiwan.
Yi-Hsuan ChengInstitute of Neuroscience, National Yang Ming Chiao Tung University, Taipei, Taiwan.
Yu-Tung LinInstitute of Neuroscience, National Yang Ming Chiao Tung University, Taipei, Taiwan.
Chia-Ching LinInstitute of Neuroscience, National Yang Ming Chiao Tung University, Taipei, Taiwan.
Yi-Hua LeeInstitute of Neuroscience, National Yang Ming Chiao Tung University, Taipei, Taiwan.
Honglei WangSchool of Life Science and Technology, ShanghaiTech University, Shanghai, China.
Margaret S HoSchool of Life Science and Technology, ShanghaiTech University, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We previously identified a role for dAuxilin (dAux), the fly homolog of Cyclin G-associated kinase, in glial autophagy contributing to Parkinson's disease (PD). To further dissect the mechanism, we present evidence here that lack of glial dAux enhanced the phosphorylation of the autophagy-related protein Atg9 at two newly identified threonine residues, T62 and T69. The enhanced Atg9 phosphorylation in the absence of dAux promotes autophagosome formation and Atg9 trafficking to the autophagosomes in glia. Whereas the expression of the non-phosphorylatable Atg9 variants suppresses the lack of dAux-induced increase in both autophagosome formation and Atg9 trafficking to autophagosome, the expression of the phosphomimetic Atg9 variants restores the lack of Atg1-induced decrease in both events. In relation to pathophysiology, Atg9 phosphorylation at T62 and T69 contributes to dopaminergic neurodegeneration and locomotor dysfunction in a

Indexed as

AutophagyAutophagy-Related ProteinsDrosophila ProteinsNeurogliaAnimalsAnimals, Genetically ModifiedDrosophilaHumansPhosphorylationProtein TransportAutophagy-Related ProteinsDrosophila ProteinsAtg1Atg9dAuxilingliaParkinson’s disease

Identifiers

PMID39807990
PMCPMC11877618

What OpenQuestion holds

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Registered trials

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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.