Evidence map›Paper›PMID 38168055›Full record

ArticleNature communications2024

TMEM55B links autophagy flux, lysosomal repair, and TFE3 activation in response to oxidative stress.

Eutteum Jeong, Rose Willett, Alberto Rissone, Martina La Spina, Rosa Puertollano

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
8.9field-weighted citation impact, top 2% 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

16 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Review
  3. Co-option of Lysosomal Machinery for Sponge Biosilicification.bioRxiv : the preprint server for biology · 2026
    Article
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  6. Review
  7. Article
  8. Article
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  11. Article
  12. Article
  13. Article
  14. Lysosomal Repair in Health and Disease.Journal of cellular physiology · 2025
    Review
  15. Article
  16. 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

5 authors at 1 institution in 1 country.

Eutteum JeongCell and Developmental Biology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Rose WillettCell and Developmental Biology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Alberto RissoneCell and Developmental Biology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Martina La SpinaCell and Developmental Biology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Rosa PuertollanoCell and Developmental Biology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA. puertolr@mail.nih.gov.ORCID 0000-0002-1106-5489
National Institutes of Health · US

Funding

Role of endolysosomal channels in calcium homeostasis and traffickingZIAHL006075 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI PUERTOLLANO, ROSA · 2010 to 2025
$8.7M
Intramural NIH HHS ZIA HL006075
6 · The paper itself

Abstract

Lysosomes have emerged as critical regulators of cellular homeostasis. Here we show that the lysosomal protein TMEM55B contributes to restore cellular homeostasis in response to oxidative stress by three different mechanisms: (1) TMEM55B mediates NEDD4-dependent PLEKHM1 ubiquitination, causing PLEKHM1 proteasomal degradation and halting autophagosome/lysosome fusion; (2) TMEM55B promotes recruitment of components of the ESCRT machinery to lysosomal membranes to stimulate lysosomal repair; and (3) TMEM55B sequesters the FLCN/FNIP complex to facilitate translocation of the transcription factor TFE3 to the nucleus, allowing expression of transcriptional programs that enable cellular adaptation to stress. Knockout of tmem55 genes in zebrafish embryos increases their susceptibility to oxidative stress, causing early death of tmem55-KO animals in response to arsenite toxicity. Altogether, our work identifies a role for TMEM55B as a molecular sensor that coordinates autophagosome degradation, lysosomal repair, and activation of stress responses.

Indexed as

AutophagyZebrafishAnimalsBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsLysosomesOxidative StressBasic Helix-Loop-Helix Leucine Zipper Transcription Factors

Identifiers

PMID38168055
PMCPMC10761734
OpenAlexW4390499631

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.