Evidence map›Paper›PMID 29477615›Full record

ReviewTrends in cell biology2018

GCN5L1/BLOS1 Links Acetylation, Organelle Remodeling, and Metabolism.

Iain Scott, Lingdi Wang, Kaiyuan Wu, Dharendra Thapa, Michael N Sack

Open access · greenAbstract readReview
In one paragraph

Review in Trends in cell biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

42 citing papers in PubMed, 69 citations in OpenAlex.

  1. BLOC1S1 regulates autolysosomal and exosomal dynamics during CD4bioRxiv : the preprint server for biology · 2026
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  3. BLOC1S1 depletion via splice-switching oligonucleotides improves mitochondrial respiration and rescues ALS phenotypes.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
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  14. BLOC1S1 control of vacuolar organelle fidelity modulates TbioRxiv : the preprint server for biology · 2024
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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 2 institutions in 1 country.

Iain ScottCardiology Division, Department of Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA 15261, USA.
Lingdi WangCardiovascular Branch, National Heart, Lung, and Blood Institute, NIH, Bethesda, MD 20892, USA.
Kaiyuan WuCardiovascular Branch, National Heart, Lung, and Blood Institute, NIH, Bethesda, MD 20892, USA.
Dharendra ThapaCardiology Division, Department of Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA 15261, USA.
Michael N SackCardiovascular Branch, National Heart, Lung, and Blood Institute, NIH, Bethesda, MD 20892, USA. Electronic address: sackm@nih.gov.
National Heart Lung and Blood Institute · USUniversity of Pittsburgh Medical Center · US

Funding

Mitochondrial Biology in DiseaseZIAHL005102 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI SACK, MICHAEL · 2009 to 2025
$22.7M
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
Regulation of Fuel Utilization by Lysine Acetylation in the Failing HeartR01HL132917 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SCOTT, IAIN · 2017 to 2020
$1.9M
Mitochondrial Biology in Cardiovascular DiseaseZ01HL005102 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI SACK, MICHAEL · 2005 to 2008
$1.2M
Regulation of mitochondrial function by a novel lysine acetyltransferaseK22HL116728 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SCOTT, IAIN · 2014 to 2016
$731k
Regulation of Fuel Utilization by Lysine Acetylation in the Failing HeartR56HL132917 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SCOTT, IAIN · 2016 to 2016
$469k
Intramural NIH HHS Z01 HL005102Intramural NIH HHS ZIA HL005102Intramural NIH HHS ZIA HL006047NHLBI NIH HHS K22 HL116728NHLBI NIH HHS R01 HL132917NHLBI NIH HHS R56 HL132917
6 · The paper itself

Abstract

General control of amino acid synthesis 5 (GCN5) like-1 (GCN5L1) was identified as a novel gene with sequence homology to the histone acetyltransferase Gcn5. Subsequent protein-interaction studies identified GCN5L1 as a subunit of the multiprotein lysosome biogenesis complex, resulting in an alternative designation as biogenesis of lysosome-related organelle complex 1 subunit 1 (BLOS1 or BLOC1S1). Despite the distinct nomenclatures, GCN5L1/BLOS1 has been shown to play crucial roles in mitochondria, endosomes, lysosomes, and synaptic vesicle precursors (SVPs). GCN5L1/BLOS1 controls mitochondrial protein acetylation, modulates metabolic pathways, and orchestrates retrograde mitochondria-to-nucleus signaling. It also contributes to endosome-lysosome and vesicle trafficking and to endolysosomal function. Here we discuss the intracellular roles of GCN5L1/BLOS1 in the hope of linking mitochondria-centric effects to cytosolic vesicle biology.

Indexed as

Organelle BiogenesisAcetylationCytosolEndosomesHumansLysosomesMitochondriaNerve Tissue ProteinsProtein TransportSignal TransductionSynaptic VesiclesBLOC1S1 protein, humanNerve Tissue ProteinsBORC complexendosomal functionlysosome traffickingmitochondriaretrograde signaling

Identifiers

PMID29477615
PMCPMC5912981
OpenAlexW2789124750

What OpenQuestion holds

Textmetadata
LicenceTDM
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.