Evidence map›Paper›PMID 29146937›Full record

ArticleNature communications2017

TFEB regulates lysosomal positioning by modulating TMEM55B expression and JIP4 recruitment to lysosomes.

Rose Willett, José A Martina, James P Zewe, Rachel Wills, Gerald R V Hammond, Rosa Puertollano

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers.

0numbers the graph read from it
0cells of the map it votes in
128citing papers in PubMed
9.7field-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

128 citing papers in PubMed, 216 citations in OpenAlex.

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  9. Subcellular Cartography of the Phosphoinositide Multiverse.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2026
    Review
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68 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

6 authors at 2 institutions in 1 country.

Rose WillettCell Biology and Physiology Center, National Heart, Lung and Blood Institute, National Institutes of Health, 50 South Drive, Building 50, Room 3537, Bethesda, MD, 20892, USA.
José A MartinaCell Biology and Physiology Center, National Heart, Lung and Blood Institute, National Institutes of Health, 50 South Drive, Building 50, Room 3537, Bethesda, MD, 20892, USA.ORCID http://orcid.org/0000-0001-5814-8807
James P ZeweDepartment of Cell Biology, University of Pittsburgh School of Medicine, 200 Lothrop Street, Room S332 Biomedical Sciences Tower, Pittsburgh, PA, 15213, USA.
Rachel WillsDepartment of Cell Biology, University of Pittsburgh School of Medicine, 200 Lothrop Street, Room S332 Biomedical Sciences Tower, Pittsburgh, PA, 15213, USA.
Gerald R V HammondDepartment of Cell Biology, University of Pittsburgh School of Medicine, 200 Lothrop Street, Room S332 Biomedical Sciences Tower, Pittsburgh, PA, 15213, USA.
Rosa PuertollanoCell Biology and Physiology Center, National Heart, Lung and Blood Institute, National Institutes of Health, 50 South Drive, Building 50, Room 3537, Bethesda, MD, 20892, USA. puertolr@mail.nih.gov.
National Institutes of Health · USUniversity of Pittsburgh · 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
Directing Membrane Function with Inositol Lipids in Health and DiseaseR35GM119412 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Gerald R Hammond · 2016 to 2026
$4.3M
NIGMS NIH HHS R35 GM119412
6 · The paper itself

Abstract

Lysosomal distribution is linked to the role of lysosomes in many cellular functions, including autophagosome degradation, cholesterol homeostasis, antigen presentation, and cell invasion. Alterations in lysosomal positioning contribute to different human pathologies, such as cancer, neurodegeneration, and lysosomal storage diseases. Here we report the identification of a novel mechanism of lysosomal trafficking regulation. We found that the lysosomal transmembrane protein TMEM55B recruits JIP4 to the lysosomal surface, inducing dynein-dependent transport of lysosomes toward the microtubules minus-end. TMEM55B overexpression causes lysosomes to collapse into the cell center, whereas depletion of either TMEM55B or JIP4 results in dispersion toward the cell periphery. TMEM55B levels are transcriptionally upregulated following TFEB and TFE3 activation by starvation or cholesterol-induced lysosomal stress. TMEM55B or JIP4 depletion abolishes starvation-induced retrograde lysosomal transport and prevents autophagosome-lysosome fusion. Overall our data suggest that the TFEB/TMEM55B/JIP4 pathway coordinates lysosome movement in response to a variety of stress conditions.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCell Line, TumorChlorocebus aethiopsCOS CellsGene Expression RegulationHeLa CellsHumansLysosomal Membrane ProteinsLysosomesMicrotubulesPhosphoinositide PhosphatasesProtein TransportRNA InterferenceRNA, Small InterferingAdaptor Proteins, Signal TransducingBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsLysosomal Membrane ProteinsPhosphoinositide PhosphatasesPIP4P1 protein, humanRNA, Small InterferingSPAG9 protein, humanTFE3 protein, humanTFEB protein, humanVesicular Transport Proteins

Identifiers

PMID29146937
PMCPMC5691037
OpenAlexW2770609313

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.