Evidence map›Paper›PMID 31204568›Full record

ArticleAutophagy2019

ATG9A supplies PtdIns4P to the autophagosome initiation site.

Delphine Judith, Sharon A Tooze

Abstract readComment
In one paragraph

Article in Autophagy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Emerging mechanisms of ATG8-independent non-canonical autophagy.Journal of physiology and biochemistry · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors.

Delphine Juditha Molecular Cell Biology of Autophagy, The Francis Crick Institute , London , UK.
Sharon A Toozea Molecular Cell Biology of Autophagy, The Francis Crick Institute , London , UK.ORCID 0000-0002-2182-3116

Funding

Cancer Research UK 15153Cancer Research UK FC001187Medical Research Council FC001187Wellcome Trust FC001187
6 · The paper itself

Abstract

The identity of the platform supporting the initiation and formation of the nascent autophagosome, the phagophore, is not fully understood. Nucleation and expansion of the phagophore membrane requires a coordinated flux or activation of specific proteins and membrane lipids at the initiation site. The transmembrane protein ATG9A is essential for macroautophagy/autophagy and proposed to be an initiator of the phagophore by directing or facilitating the delivery of proteins and lipids to the initiation site. Upon amino acid starvation, ATG9A-containing vesicles are formed from the Golgi complex and endosomal compartments and translocate to the initiation site. Unravelling the complement of proteins and lipids brought by ATG9A vesicles to the forming autophagosome is essential to further understand the initiation of autophagy.

Indexed as

AutophagosomesAutophagyAutophagy-Related ProteinsPhosphatidylinositol PhosphatesAutophagy-Related Proteinsphosphatidylinositol 4-phosphatePhosphatidylinositol PhosphatesARFIP2ATG13autophagosome initiation sitePI4KBPI4KIIIβ

Identifiers

PMID31204568
PMCPMC6693450

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.