Evidence map›Paper›PMID 28820282›Full record

ArticleAutophagy2017

Mir505-3p regulates axonal development via inhibiting the autophagy pathway by targeting Atg12.

Kan Yang, Bin Yu, Cheng Cheng, Tianlin Cheng, Bo Yuan, Kai Li, Junhua Xiao, Zilong Qiu, Yuxun Zhou

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Autophagy in axonal and presynaptic development.Current opinion in neurobiology · 2021
    Review
  7. Article
  8. Circulating RNAs as Potential Biomarkers in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2020
    Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. 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

9 authors at 2 institutions in 1 country.

Kan Yanga Department of Biological Engineering, College of Chemistry, Chemical Engineering & Biotechnology , Donghua University , Shanghai , China.
Bin Yuc Institute of Neuroscience, CAS Center for Excellence in Brain Science and Intelligence Technology, Shanghai Institutes for Biological Sciences , Chinese Academy of Sciences , Shanghai , China.
Cheng Chengc Institute of Neuroscience, CAS Center for Excellence in Brain Science and Intelligence Technology, Shanghai Institutes for Biological Sciences , Chinese Academy of Sciences , Shanghai , China.
Tianlin Chengc Institute of Neuroscience, CAS Center for Excellence in Brain Science and Intelligence Technology, Shanghai Institutes for Biological Sciences , Chinese Academy of Sciences , Shanghai , China.
Bo Yuanc Institute of Neuroscience, CAS Center for Excellence in Brain Science and Intelligence Technology, Shanghai Institutes for Biological Sciences , Chinese Academy of Sciences , Shanghai , China.
Kai Lia Department of Biological Engineering, College of Chemistry, Chemical Engineering & Biotechnology , Donghua University , Shanghai , China.
Junhua Xiaoa Department of Biological Engineering, College of Chemistry, Chemical Engineering & Biotechnology , Donghua University , Shanghai , China.
Zilong Qiuc Institute of Neuroscience, CAS Center for Excellence in Brain Science and Intelligence Technology, Shanghai Institutes for Biological Sciences , Chinese Academy of Sciences , Shanghai , China.ORCID http://orcid.org/0000-0003-4286-3288
Yuxun Zhoua Department of Biological Engineering, College of Chemistry, Chemical Engineering & Biotechnology , Donghua University , Shanghai , China.
Chinese Academy of Sciences · CNDonghua University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In addition to the canonical role in protein homeostasis, autophagy has recently been found to be involved in axonal dystrophy and neurodegeneration. Whether autophagy may also be involved in neural development remains largely unclear. Here we report that Mir505-3p is a crucial regulator for axonal elongation and branching in vitro and in vivo, through modulating autophagy in neurons. We identify that the key target gene of Mir505-3p in neurons is Atg12, encoding ATG12 (autophagy-related 12) which is an essential component of the autophagy machinery during the initiation and expansion steps of autophagosome formation. Importantly, axonal development is compromised in brains of mir505 knockout mice, in which autophagy signaling and formation of autophagosomes are consistently enhanced. These results define Mir505-3p-ATG12 as a vital signaling cascade for axonal development via the autophagy pathway, further suggesting the critical role of autophagy in neural development.

Indexed as

AnimalsAutophagyAutophagy-Related Protein 12AxonsCells, CulturedDown-RegulationEmbryo, MammalianGene Expression Regulation, DevelopmentalHEK293 CellsHumansMiceMice, Inbred C57BLMice, KnockoutMicroRNAsNeurogenesisSignal TransductionAtg12 protein, mouseAutophagy-Related Protein 12MicroRNAsMIRN505 microRNA, mouseATG12autophagyaxonal developmentmicroRNAMir505–3p

Identifiers

PMID28820282
PMCPMC5640177
OpenAlexW2747270959

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.