Evidence map›Paper›PMID 38150153›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2024

Asymmetric post-translational modifications regulate the nuclear translocation of STAT3 homodimers in response to leukemia inhibitory factor.

Mickael Diallo, Constança Pimenta, Fernanda Murtinheira, Daniela Martins-Alves, Francisco R Pinto, André Abrantes da Costa, Ricardo Letra-Vilela, Vanesa Martin, Carmen Rodriguez, Mário S Rodrigues and 1 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 25% 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

4 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. Article
  3. Cellular signaling meets bacterial infection: the integrative role of STAT3.Frontiers in cellular and infection microbiology · 2026
    Review
  4. AhR and STAT3: A Dangerous Duo in Chemical Carcinogenesis.International journal of molecular sciences · 2025
    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

11 authors at 3 institutions in 2 countries.

Mickael DialloBioISI - Instituto de Biosistemas e Ciências Integrativas, Faculdade de Ciências da Universidade de Lisboa, Lisbon, 1749-016, Portugal.
Constança PimentaBioISI - Instituto de Biosistemas e Ciências Integrativas, Faculdade de Ciências da Universidade de Lisboa, Lisbon, 1749-016, Portugal.
Fernanda MurtinheiraBioISI - Instituto de Biosistemas e Ciências Integrativas, Faculdade de Ciências da Universidade de Lisboa, Lisbon, 1749-016, Portugal.
Daniela Martins-AlvesBioISI - Instituto de Biosistemas e Ciências Integrativas, Faculdade de Ciências da Universidade de Lisboa, Lisbon, 1749-016, Portugal.
Francisco R PintoBioISI - Instituto de Biosistemas e Ciências Integrativas, Faculdade de Ciências da Universidade de Lisboa, Lisbon, 1749-016, Portugal.
André Abrantes da CostaBioISI - Instituto de Biosistemas e Ciências Integrativas, Faculdade de Ciências da Universidade de Lisboa, Lisbon, 1749-016, Portugal.
Ricardo Letra-VilelaBioISI - Instituto de Biosistemas e Ciências Integrativas, Faculdade de Ciências da Universidade de Lisboa, Lisbon, 1749-016, Portugal.
Vanesa MartinDepartamento de Morfología y Biología Celular, Facultad de Medicina, University of Oviedo, c/Julian Claveria, Oviedo, 33006, Spain.
Carmen RodriguezDepartamento de Morfología y Biología Celular, Facultad de Medicina, University of Oviedo, c/Julian Claveria, Oviedo, 33006, Spain.
Mário S RodriguesBioISI - Instituto de Biosistemas e Ciências Integrativas, Faculdade de Ciências da Universidade de Lisboa, Lisbon, 1749-016, Portugal.
Federico HerreraBioISI - Instituto de Biosistemas e Ciências Integrativas, Faculdade de Ciências da Universidade de Lisboa, Lisbon, 1749-016, Portugal. fherrera@fc.ul.pt.
Universidade Nova de Lisboa · PTInstituto de Investigación Sanitaria del Principado de Asturias · ESUniversidad de Oviedo · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

STAT3 is a pleiotropic transcription factor overactivated in 70% of solid tumours. We have recently reported that inactivating mutations on residues susceptible to post-translational modifications (PTMs) in only one of the monomers (i.e. asymmetric) caused changes in the cellular distribution of STAT3 homodimers. Here, we used more controlled experimental conditions, i.e. without the interference of endogenous STAT3 (STAT3-/- HeLa cells) and in the presence of a defined cytokine stimulus (Leukemia Inhibitory Factor, LIF), to provide further evidence that asymmetric PTMs affect the nuclear translocation of STAT3 homodimers. Time-lapse microscopy for 20 min after LIF stimulation showed that S727 dephosphorylation (S727A) and K685 inactivation (K685R) slightly enhanced the nuclear translocation of STAT3 homodimers, while K49 inactivation (K49R) delayed STAT3 nuclear translocation. Our findings suggest that asymmetrically modified STAT3 homodimers could be a new level of STAT3 regulation and, therefore, a potential target for cancer therapy.

Indexed as

Cell NucleusLeukemia Inhibitory FactorProtein MultimerizationProtein Processing, Post-TranslationalSTAT3 Transcription FactorActive Transport, Cell NucleusHeLa CellsHumansPhosphorylationProtein TransportLeukemia Inhibitory FactorLIF protein, humanSTAT3 protein, humanSTAT3 Transcription FactorHomodimerizationLeukemia inhibitory factorPost-translational modificationsSTAT3

Identifiers

PMID38150153
PMCPMC11219437
OpenAlexW4390274354

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.