Evidence map›Paper›PMID 33629936›Full record

ArticleAutophagy2021

BLOC1S1/GCN5L1/BORCS1 is a critical mediator for the initiation of autolysosomal tubulation.

Kaiyuan Wu, Allen Seylani, Jing Wu, Xufeng Wu, Christopher K E Bleck, Michael N Sack

Open access · greenAbstract 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 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

28 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. BLOC1S1 regulates autolysosomal and exosomal dynamics during CD4bioRxiv : the preprint server for biology · 2026
    Article
  5. Article
  6. Article
  7. BLOC1S1 Attenuates B. Melitensis 16M LPS-Triggered Autophagy by Spatial Confinement of TDP-43.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. BLOC1S1 control of vacuolar organelle fidelity modulates TbioRxiv : the preprint server for biology · 2024
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Inhibition of Hepatitis B Virus (HBV) replication and antigen expression byFrontiers in cellular and infection microbiology · 2023
    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

6 authors at 2 institutions in 1 country.

Kaiyuan WuLaboratory of Mitochondrial Biology and Metabolism, NHLBI, National Institutes of Health, Bethesda, Maryland.
Allen SeylaniLaboratory of Mitochondrial Biology and Metabolism, NHLBI, National Institutes of Health, Bethesda, Maryland.
Jing WuLaboratory of Mitochondrial Biology and Metabolism, NHLBI, National Institutes of Health, Bethesda, Maryland.
Xufeng WuLight Microscopy Core, National Heart, Lung and Blood Institute, NIH, Bethesda, USA.
Christopher K E BleckElectron Microcopy Core, National Heart, Lung and Blood Institute, NIH, Bethesda, USA.
Michael N SackLaboratory of Mitochondrial Biology and Metabolism, NHLBI, National Institutes of Health, Bethesda, Maryland.
National Heart Lung and Blood Institute · USNational Institutes of Health · US

Funding

Mitochondrial biology in diabetesZIAHL005199 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI SACK, MICHAEL · 2009 to 2025
$17.2M
Role of intracellular organelle homeostasis in adaptation to dietary restrictive interventionsZIAHL006047 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI SACK, MICHAEL · 2010 to 2025
$15.6M
Electron Microscopy CoreZICHL005906 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI SYED, ZULFEQHAR · 2009 to 2025
$12.9M
Intramural NIH HHS ZIA HL005199
6 · The paper itself

Abstract

The mechanisms orchestrating recycling of lysosomes through autophagic lysosome reformation (ALR) is incompletely understood. Previous data show that genetic depletion of BLOC1S1/GCN5L1/BORCS1 increases autolysosome (AL) accumulation. We postulated that this phenotype may manifest due to perturbed ALR. We explored this in control and

Indexed as

Actin CytoskeletonAnimalsAutophagyHepatocytesLysosomesMiceMice, Inbred C57BLMice, KnockoutMicrotubulesMitochondrial ProteinsNerve Tissue ProteinsBLOC1S1 protein, mouseMitochondrial ProteinsNerve Tissue ProteinsAutophagic lysosome reformationautophagygcn5l1hepatocytelysosomal tubulationlysosomemtorc1

Identifiers

PMID33629936
PMCPMC8632325
OpenAlexW3130681520

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.