Evidence map›Paper›PMID 41361692›Full record

ArticleEMBO reports2026

Differential contribution of TFE3 isoforms to cell motility and invasion.

Pablo S Contreras, José A Martina, Katie Rollins, Eutteum Jeong, Alberto Rissone, Rosa Puertollano

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in EMBO reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

6 authors.

Pablo S Contreras *Cell and Developmental Biology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.ORCID 0000-0002-1468-412X
José A Martina *Cell and Developmental Biology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.ORCID 0000-0001-5814-8807
Katie RollinsCell and Developmental Biology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.ORCID 0000-0002-6383-1333
Eutteum JeongCell 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.
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

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TFE3 orchestrates cellular responses to a variety of stress conditions, promoting restoration of cellular homeostasis and cell survival. Here we report the presence of two different TFE3 isoforms generated by the use of alternative transcription initiation sites. The long isoform (TFE3-L) undergoes continuous proteolytic degradation due to the presence of a phosphodegron in its N-terminal region and only accumulates under specific stress conditions. In contrast, the short isoform (TFE3-S) lacks the first 105 residues containing the phosphodegron and is constitutively expressed at high levels in most cell types. Both isoforms share the same Rags/mTORC1-dependent mechanism of regulation and display comparable capacity of inducing expression of lysosomal and autophagic genes upon activation. However, TFE3-L is considerably more efficient than TFE3-S promoting cell migration and invasion. Accordingly, specific TFE3-L depletion in a cellular model for tuberous sclerosis causes a significant reduction in cell motility and invasiveness. Our data reveal that the two TFE3 isoforms exhibit partial redundancy and that the appearance of TFE3-L following prolonged stress potentially correlates with metastatic behaviors.

Indexed as

Basic Helix-Loop-Helix Leucine Zipper Transcription FactorsCell MovementAnimalsAutophagyCell Line, TumorHumansMechanistic Target of Rapamycin Complex 1MiceMultiprotein ComplexesNeoplasm InvasivenessProtein IsoformsProteolysisTOR Serine-Threonine KinasesBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesProtein IsoformsTFE3 protein, humanTOR Serine-Threonine KinasesAutophagyIsoformsLysosomesMotilityTFE3

Identifiers

PMID41361692
PMCPMC12852735

What OpenQuestion holds

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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.