Evidence map›Paper›PMID 41188647›Full record

ArticleThe EMBO journal2025

Annexin A7 enhances TIA1 axonal trafficking to counteract pathological aggregation in neurons.

Yu Feng, Tongshu Luan, Zhenda Zhang, Wei Wang, Yuanyuan Chu, Sijia Wan, Xiaorong Pan, Jie Li, Yifan Liu, Yaqian Xu and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The EMBO journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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.

Yu Feng *School of Life Science and Technology, ShanghaiTech University, Shanghai, 201210, China.ORCID http://orcid.org/0000-0003-4579-4214
Tongshu Luan *School of Life Science and Technology, ShanghaiTech University, Shanghai, 201210, China.
Zhenda ZhangSchool of Life Science and Technology, ShanghaiTech University, Shanghai, 201210, China.
Wei WangSchool of Life Science and Technology, ShanghaiTech University, Shanghai, 201210, China.
Yuanyuan ChuSchool of Life Science and Technology, ShanghaiTech University, Shanghai, 201210, China.
Sijia WanSchool of Life Science and Technology, ShanghaiTech University, Shanghai, 201210, China.
Xiaorong PanSchool of Life Science and Technology, ShanghaiTech University, Shanghai, 201210, China.ORCID http://orcid.org/0000-0002-7921-7354
Jie LiDivision of Chemistry and Physical Biology, School of Physical Science and Technology, ShanghaiTech University, Shanghai, 201210, China.
Yifan LiuDivision of Chemistry and Physical Biology, School of Physical Science and Technology, ShanghaiTech University, Shanghai, 201210, China.
Yaqian XuSchool of Life Science and Technology, ShanghaiTech University, Shanghai, 201210, China.
Kun DouSchool of Life Science and Technology, ShanghaiTech University, Shanghai, 201210, China.
Tong WangSchool of Life Science and Technology, ShanghaiTech University, Shanghai, 201210, China. wangtong@shanghaitech.edu.cn.ORCID http://orcid.org/0000-0002-3680-8189

Funding

MOST | National Natural Science Foundation of China (NSFC) 32100777MOST | National Natural Science Foundation of China (NSFC) 32271001National Natural Science Foundation of China 32370604Science and Technology Commission of Shanghai Municipality 24490713800ShanghaiTech University (ShanghaiTech) SYLDX0302022ShanghaiTech University (ShanghaiTech) SYLPOC0022022
6 · The paper itself

Abstract

Directed axonal trafficking of mRNA via ribonucleoprotein (RNP) complexes is essential for neuronal function and survival. However, mechanisms governing retrograde RNP transport remain poorly understood. Here, we reveal that Annexin A7 (ANXA7) promotes the recruitment of aggregation-prone T-cell intracellular antigen 1 (TIA1)-containing RNPs to cytoplasmic dynein, enabling their retrograde trafficking to the soma for degradation. Both persistent and transient Ca²⁺ elevation disrupted this function of ANXA7, leading to the detachment of TIA1 granules from dynein, impairing their transport, and subsequently triggering pathological TIA1 aggregation within axons. Similarly, ANXA7 knockdown decouples TIA1 granules from dynein, preventing their transport and inducing pathological aggregation of TIA1, which culminates in axonopathy and neurodegeneration both in vitro and in vivo. Conversely, ANXA7 overexpression reinforces trafficking and counteracts aberrant aggregation of TIA1-containing RNPs in axons. We describe here a Ca

Indexed as

Annexin A7Axonal TransportAxonsNeuronsPoly(A)-Binding ProteinsAnimalsCalciumCytoplasmic DyneinsHumansMiceProtein TransportT-Cell Intracellular Antigen-1Annexin A7CalciumCytoplasmic DyneinsPoly(A)-Binding ProteinsT-Cell Intracellular Antigen-1TIA1 protein, humanTia1 protein, mouseAxon TraffickingCalcium SignalingDyneinPhase SeparationProtein Aggregates

Identifiers

PMID41188647
PMCPMC12706091

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.