Evidence map›Paper›PMID 25027988›Full record

ReviewEMBO reports2014

Getting ready for building: signaling and autophagosome biogenesis.

Adi Abada, Zvulun Elazar

Open access · bronzeAbstract readReview
In one paragraph

Review in EMBO reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.

0numbers the graph read from it
0cells of the map it votes in
103citing papers in PubMed
13.1field-weighted citation impact, top 1% 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

103 citing papers in PubMed, 170 citations in OpenAlex.

  1. Article
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  17. Review
  18. Autophagy in acute myeloid leukemia: a paradoxical role in chemoresistance.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Review
  19. Repurposing autophagy regulators in brain tumors.International journal of cancer · 2022
    Review
  20. Review

43 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Adi AbadaDepartment of Biological Chemistry, The Weizmann Institute of Science, Rehovot, Israel.
Zvulun ElazarDepartment of Biological Chemistry, The Weizmann Institute of Science, Rehovot, Israel zvulun.elazar@weizmann.ac.il.
Weizmann Institute of Science · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is the main cellular catabolic process responsible for degrading organelles and large protein aggregates. It is initiated by the formation of a unique membrane structure, the phagophore, which engulfs part of the cytoplasm and forms a double-membrane vesicle termed the autophagosome. Fusion of the outer autophagosomal membrane with the lysosome and degradation of the inner membrane contents complete the process. The extent of autophagy must be tightly regulated to avoid destruction of proteins and organelles essential for cell survival. Autophagic activity is thus regulated by external and internal cues, which initiate the formation of well-defined autophagy-related protein complexes that mediate autophagosome formation and selective cargo recruitment into these organelles. Autophagosome formation and the signaling pathways that regulate it have recently attracted substantial attention. In this review, we analyze the different signaling pathways that regulate autophagy and discuss recent progress in our understanding of autophagosome biogenesis.

Indexed as

AutophagySignal TransductionAnimalsEnergy MetabolismHumansMicrotubule-Associated ProteinsOxidation-ReductionPhagosomesVesicular Transport ProteinsMicrotubule-Associated ProteinsVesicular Transport ProteinsAtgsautophagosome biogenesisautophagymTORsignaling

Identifiers

PMID25027988
PMCPMC4197041
OpenAlexW2056478340

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.