Evidence map›Paper›PMID 28127696›Full record

ArticleMolecular neurobiology2018

Angiogenin Prevents Progranulin A9D Mutation-Induced Neuronal-Like Cell Apoptosis Through Cleaving tRNAs into tiRNAs.

Siqi Li, Yongdui Chen, Desen Sun, Rongpai Bai, Xiangwei Gao, Yi Yang, Jinghao Sheng, Zhengping Xu

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

23 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Emerging roles of transfer RNA fragments in the CNS.Brain : a journal of neurology · 2025
    Review
  5. Review
  6. Review
  7. Review
  8. [Abnormal transfer RNA epigenetic modifications and related impact on neurodegenerative diseases].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2024
    Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Mucosal immunity and tRNA, tRF, and tiRNA.Journal of molecular medicine (Berlin, Germany) · 2021
    Review
  16. Article
  17. Action mechanisms and research methods of tRNA-derived small RNAs.Signal transduction and targeted therapy · 2020
    Review
  18. Article
  19. tRNA cleavage: a new insight.Neural regeneration research · 2020
    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

8 authors at 1 institution in 1 country.

Siqi LiInstitute of Environmental Health, School of Public Health, Zhejiang University, Hangzhou, 310058, China.
Yongdui ChenInstitute of Environmental Health, School of Public Health, Zhejiang University, Hangzhou, 310058, China.
Desen SunInstitute of Environmental Health, School of Public Health, Zhejiang University, Hangzhou, 310058, China.
Rongpai BaiInstitute of Environmental Health, School of Public Health, Zhejiang University, Hangzhou, 310058, China.
Xiangwei GaoInstitute of Environmental Health, School of Public Health, Zhejiang University, Hangzhou, 310058, China.
Yi YangSir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, 310058, China.
Jinghao ShengInstitute of Environmental Health, School of Public Health, Zhejiang University, Hangzhou, 310058, China. jhsheng@zju.edu.cn.
Zhengping XuInstitute of Environmental Health, School of Public Health, Zhejiang University, Hangzhou, 310058, China. zpxu@zju.edu.cn.
Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gene defects have been recognized as prominent factors in the etiology and pathogenesis of neurodegeneration. Among 60 neurodegeneration-related mutations in progranulin (PGRN), a mutation in PGRN gene exon 1 introduces a charged amino acid in the hydrophobic core of its signal peptide at residue 9 (named PGRN A9D) and results in incorrect cytoplasmic sorting. However, the pathogenesis of this mutation remains elusive. To address this issue, we first examined the subcellular distribution of PGRN A9D in human neuronal-like cells (SH-SY5Y). The results showed that PGRN A9D accumulated in cytosolic stress granules. Interestingly, this mis-sorting associated with a cellular redistribution of angiogenin (ANG), a stress-response factor and neurodegenerative disease-related protein, from nucleus to cytoplasmic stress granules, and there existed protein interaction between PGRN A9D and ANG. Further study revealed that the stress granule localization of PGRN A9D was dependent on ANG. Functionally, PGRN A9D abolished the nuclear ANG-mediated biological roles; on the other hand, the relocation of ANG to stress granules activated its cytoprotective stress-response program by cleaving transfer RNAs (tRNAs) to tiRNAs (tRNA-derived, stress-induced small RNAs), thus promoting PGRN A9D cell survival. Taken together, we hypothesize that PGRN A9D leads to the retention of ANG in the cytoplasm to protect cells from PGRN A9D-induced apoptosis, implying that PGRN and ANG act in concert to regulate the progress of neurodegenerative disease.

Indexed as

ApoptosisCell Line, TumorCytosolHumansMutationNeurodegenerative DiseasesNeuronsProgranulinsRibonuclease, PancreaticRNA, TransferangiogeninProgranulinsRibonuclease, PancreaticRNA, TransferAngiogeninApoptosisNeurodegenerationProgranulinTiRNA

Identifiers

PMID28127696
OpenAlexW2582898297

What OpenQuestion holds

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Read underepoch 390

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.