Evidence map›Paper›PMID 29215607›Full record

ArticleCell death & disease2017

Proteomic and functional analysis identifies galectin-1 as a novel regulatory component of the cytotoxic granule machinery.

Tiago Clemente, Narcisio J Vieira, Juan P Cerliani, Colin Adrain, Alexander Luthi, Mariana R Dominguez, Monica Yon, Fernanda C Barrence, Thalita B Riul, Richard D Cummings and 7 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

16 citing papers in PubMed, 30 citations in OpenAlex.

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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

17 authors at 9 institutions in 6 countries.

Tiago ClementeInstituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil.
Narcisio J VieiraInstituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil.
Juan P CerlianiLaboratorio de Inmunopatología, Instituto de Biología y Medicina Experimental (IBYME), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), C1428 Buenos Aires, Argentina.
Colin AdrainInstituto Gulbenkian de Ciência, Oeiras, Portugal.
Alexander LuthiDepartment of Genetics, Smurfit Institute, Trinity College, Dublin, Ireland.
Mariana R DominguezCentro de Terapia Celular e Molecular (CTCMol) and Departamento de Microbiologia, Imunologia e Parasitologia, Universidade Federal de São Paulo-Escola Paulista de Medicina, São Paulo, São Paulo, Brazil.
Monica YonInstituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil.
Fernanda C BarrenceDepartamento de Biologia Celular e do Desenvolvimento, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil.
Thalita B RiulDepartamento de Análises Clínicas, Toxicológicas e Bromatológicas, Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, Brazil.
Richard D CummingsDepartment of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Telma M ZornDepartamento de Biologia Celular e do Desenvolvimento, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil.
Sebastian AmigorenaInstitut Curie, PSL Research University, INSERM U932, Paris Cedex 05, France.
Marcelo Dias-BaruffiDepartamento de Análises Clínicas, Toxicológicas e Bromatológicas, Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, Brazil.
Maurício M RodriguesCentro de Terapia Celular e Molecular (CTCMol) and Departamento de Microbiologia, Imunologia e Parasitologia, Universidade Federal de São Paulo-Escola Paulista de Medicina, São Paulo, São Paulo, Brazil.
Seamus J MartinDepartment of Genetics, Smurfit Institute, Trinity College, Dublin, Ireland.
Gabriel A RabinovichLaboratorio de Inmunopatología, Instituto de Biología y Medicina Experimental (IBYME), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), C1428 Buenos Aires, Argentina.
Gustavo P Amarante-MendesInstituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil.
Universidade de São Paulo · BRTrinity College Dublin · IEInstituto Nacional de Ciência e Tecnologia em Entomologia Molecular · BRUniversidade Federal de São Paulo · BRExperimental Medicine and Biology Institute · ARFundación Ciencias Exactas y Naturales · ARHarvard University · USInstituto Gulbenkian de Ciência · PTUniversité Paris Sciences et Lettres · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Secretory granules released by cytotoxic T lymphocytes (CTLs) are powerful weapons against intracellular microbes and tumor cells. Despite significant progress, there is still limited information on the molecular mechanisms implicated in target-driven degranulation, effector cell survival and composition and structure of the lytic granules. Here, using a proteomic approach we identified a panel of putative cytotoxic granule proteins, including some already known granule constituents and novel proteins that contribute to regulate the CTL lytic machinery. Particularly, we identified galectin-1 (Gal1), an endogenous immune regulatory lectin, as an integral component of the secretory granule machinery and unveil the unexpected function of this lectin in regulating CTL killing activity. Mechanistic studies revealed the ability of Gal1 to control the non-secretory lytic pathway by influencing Fas-Fas ligand interactions. This study offers new insights on the composition of the cytotoxic granule machinery, highlighting the dynamic cross talk between secretory and non-secretory pathways in controlling CTL lytic function.

Indexed as

Cytotoxicity, ImmunologicAnimalsCell DegranulationCell ProliferationFas Ligand Proteinfas ReceptorGalectin 1Gene Expression ProfilingGene Expression RegulationLymphocyte ActivationMaleMiceMice, Inbred C57BLMice, KnockoutProteomicsSecretory VesiclesFas Ligand ProteinFasl protein, mouseFas protein, mousefas ReceptorGalectin 1

Identifiers

PMID29215607
PMCPMC5827204
OpenAlexW2775268769

What OpenQuestion holds

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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.