Evidence map›Paper›PMID 15663199›Full record

ArticleMolecular and cellular biochemistry2004

Regulated expression of galectin-1 during T-cell activation involves Lck and Fyn kinases and signaling through MEK1/ERK, p38 MAP kinase and p70S6 kinase.

Mercedes B Fuertes, Luciana L Molinero, Marta A Toscano, Juan M Ilarregui, Natalia Rubinstein, Leonardo Fainboim, Norberto W Zwirner, Gabriel A Rabinovich

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Molecular and cellular biochemistry, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

30 citing papers in PubMed, 81 citations in OpenAlex.

  1. Circulating galectin-1 delineates response to bevacizumab in melanoma patients and reprograms endothelial cell biology.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Trial
  2. Article
  3. Unraveling the GMACS bio & med chem Au · 2025
    Article
  4. Galectins and Liver Diseases.International journal of molecular sciences · 2025
    Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Galectins in Early Pregnancy and Pregnancy-Associated Pathologies.International journal of molecular sciences · 2021
    Review
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  13. Article
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  15. Review
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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

8 authors at 2 institutions in 1 country.

Mercedes B FuertesDivision of Immunogenetics, Hospital de Clínicas José de San Martín, Department of Microbiology, Faculty of Medicine, University of Buenos Aires, Buenos Aires, Argentina.
Luciana L Molinero
Marta A Toscano
Juan M Ilarregui
Natalia Rubinstein
Leonardo Fainboim
Norberto W Zwirner
Gabriel A Rabinovich
University of Buenos Aires · ARHospital de Clínicas "José de San Martín" · AR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent evidence has implicated galectins and their carbohydrate ligands as novel regulators of T-cell homeostasis. Galectin-1 (Gal-1), a member of this family, inhibits clonal expansion, induces apoptosis of antigen-primed T lymphocytes and suppresses the development of T-cell-mediated autoimmune diseases in vivo. Because the beta-galactoside-binding protein is expressed in activated but not resting T cells, it has been hypothesized that Gal-1-induced apoptosis may constitute an autocrine suicide mechanism to eliminate activated T cells contributing to the termination of an effector immune response. We undertook this study to investigate the signals and intracellular pathways leading to Gal-1 expression during T-cell activation. When T cells were stimulated either with anti-CD3 or anti-CD28 monoclonal antibody plus PMA in the presence of accessory cells, a sustained up-regulation of Gal-1 was observed, reaching a plateau between days 3 and 5 following CD3 engagement or costimulation through CD28. Investigation of the signal transduction events involved in this process revealed a role for Lck and Fyn kinases, since the Src kinase inhibitor PP1 inhibited the up-regulated expression of Gal-1 following T-cell activation. Downstream signaling routes involve mitogen-activated protein kinase (MAPK) kinase (MEK)1/extracellular signal-regulated kinase (ERK) and p38 MAPK, as Gal-1 expression was prevented by U0126 and SB202190. In addition, expression of Gal-1 involves interleukin (IL)-2-dependent signaling routes triggered by p70S6 kinase, as it could be inhibited by rapamycin. This is the first demonstration of the intracellular pathways that control activation-induced expression of Gal-1, which may reveal potential targets for immune intervention to modulate expression of this beta-galactoside-binding protein in pathological disorders.

Indexed as

Antibodies, MonoclonalBlotting, WesternButadienesCell ProliferationElectrophoresis, Polyacrylamide GelEnzyme InhibitorsGalectin 1Gene Expression RegulationHumansImidazolesInterleukin-2Leukocytes, MononuclearLymphocyte ActivationLymphocyte Specific Protein Tyrosine Kinase p56(lck)MAP Kinase Kinase 1Models, Biological4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazoleAntibodies, MonoclonalButadienesEnzyme InhibitorsFYN protein, humanGalectin 1ImidazolesInterleukin-2Lymphocyte Specific Protein Tyrosine Kinase p56(lck)MAP Kinase Kinase 1Nitrilesp38 Mitogen-Activated Protein KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-fynPyridinesRibosomal Protein S6 Kinases, 70-kDaSirolimussrc-Family KinasesTetradecanoylphorbol AcetateU 0126

Identifiers

PMID15663199
OpenAlexW1973253582

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.