Evidence map›Paper›PMID 33112705›Full record

ArticleAutophagy2021

PTPN9-mediated dephosphorylation of VTI1B promotes ATG16L1 precursor fusion and autophagosome formation.

He-Yen Chou, Yi-Tang Lee, Yuchieh Jay Lin, Jung-Kun Wen, Wen-Hsin Peng, Pei-Lien Hsieh, Shu-Yu Lin, Chin-Chun Hung, Guang-Chao Chen

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.7field-weighted citation impact, top 14% 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

9 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Protein modification regulated autophagy inFrontiers in physiology · 2023
    Review
  7. Review
  8. Article
  9. 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.

He-Yen ChouInstitute of Biological Chemistry, Academia Sinica, Taipei, Taiwan.
Yi-Tang LeeInstitute of Biological Chemistry, Academia Sinica, Taipei, Taiwan.
Yuchieh Jay LinInstitute of Biological Chemistry, Academia Sinica, Taipei, Taiwan.
Jung-Kun WenInstitute of Biological Chemistry, Academia Sinica, Taipei, Taiwan.
Wen-Hsin PengInstitute of Biological Chemistry, Academia Sinica, Taipei, Taiwan.
Pei-Lien HsiehInstitute of Biological Chemistry, Academia Sinica, Taipei, Taiwan.
Shu-Yu LinInstitute of Biological Chemistry, Academia Sinica, Taipei, Taiwan.
Chin-Chun HungInstitute of Biological Chemistry, Academia Sinica, Taipei, Taiwan.
Guang-Chao ChenInstitute of Biological Chemistry, Academia Sinica, Taipei, Taiwan.ORCID 0000-0002-4980-4718
Institute of Biological Chemistry, Academia Sinica · TWNational Taiwan University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macroautophagy/autophagy is an evolutionarily conserved intracellular pathway for the degradation of cytoplasmic materials. Under stress conditions, autophagy is upregulated and double-membrane autophagosomes are formed by the expansion of phagophores. The ATG16L1 precursor fusion contributes to development of phagophore structures and is critical for the biogenesis of autophagosomes. Here, we discovered a novel role of the protein tyrosine phosphatase PTPN9 in the regulation of homotypic ATG16L1 vesicle fusion and early autophagosome formation. Depletion of PTPN9 and its

Indexed as

AutophagosomesAutophagy-Related ProteinsMacroautophagyProtein Tyrosine Phosphatases, Non-ReceptorQb-SNARE ProteinsAutophagyHeLa CellsHumansMembrane FusionATG16L1 protein, humanAutophagy-Related ProteinsProtein Tyrosine Phosphatases, Non-ReceptorPTPN9 protein, humanQb-SNARE ProteinsVTI1B protein, humanATG16l1AutophagosomePTPN9SNAREVTI1B

Identifiers

PMID33112705
PMCPMC8526009
OpenAlexW3094694022

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.