Evidence map›Paper›PMID 25908851›Full record

ArticleJournal of cell science2015

The transcriptional activator Gli2 modulates T-cell receptor signalling through attenuation of AP-1 and NFκB activity.

Anna L Furmanski, Alessandro Barbarulo, Anisha Solanki, Ching-In Lau, Hemant Sahni, Jose Ignacio Saldana, Fulvio D'Acquisto, Tessa Crompton

Open access · hybridAbstract read
In one paragraph

Article in Journal of cell science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

33 citing papers in PubMed, 49 citations in OpenAlex.

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  9. Emerging Roles of Hedgehog Signaling in Cancer Immunity.International journal of molecular sciences · 2023
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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.

Anna L FurmanskiImmunobiology Section, Institute of Child Health, University College London, London WC1N 1EH, UK anna.furmanski@beds.ac.uk.
Alessandro BarbaruloImmunobiology Section, Institute of Child Health, University College London, London WC1N 1EH, UK.
Anisha SolankiImmunobiology Section, Institute of Child Health, University College London, London WC1N 1EH, UK.
Ching-In LauImmunobiology Section, Institute of Child Health, University College London, London WC1N 1EH, UK.
Hemant SahniImmunobiology Section, Institute of Child Health, University College London, London WC1N 1EH, UK.
Jose Ignacio SaldanaImmunobiology Section, Institute of Child Health, University College London, London WC1N 1EH, UK.
Fulvio D'AcquistoCentre for Biochemical Pharmacology, William Harvey Research Institute, QMUL, London EC1M 6BQ, UK.
Tessa CromptonImmunobiology Section, Institute of Child Health, University College London, London WC1N 1EH, UK.
University College London · GBWilliam Harvey Research Institute · GB

Funding

Biotechnology and Biological Sciences Research Council BB/I026324/1Medical Research Council G0900161Wellcome TrustWellcome Trust 094255MF
6 · The paper itself

Abstract

Different tissues contain diverse and dynamic cellular niches, providing distinct signals to tissue-resident or migratory infiltrating immune cells. Hedgehog (Hh) proteins are secreted inter-cellular signalling molecules, which are essential during development and are important in cancer, post-natal tissue homeostasis and repair. Hh signalling mediated by the Hh-responsive transcription factor Gli2 also has multiple roles in T-lymphocyte development and differentiation. Here, we investigate the function of Gli2 in T-cell signalling and activation. Gene transcription driven by the Gli2 transcriptional activator isoform (Gli2A) attenuated T-cell activation and proliferation following T-cell receptor (TCR) stimulation. Expression of Gli2A in T-cells altered gene expression profiles, impaired the TCR-induced Ca(2+) flux and nuclear expression of NFAT2, suppressed upregulation of molecules essential for activation, and attenuated signalling pathways upstream of the AP-1 and NFκB complexes, leading to reduced activation of these important transcription factors. Inhibition of physiological Hh-dependent transcription increased NFκB activity upon TCR ligation. These data are important for understanding the molecular mechanisms of immunomodulation, particularly in tissues where Hh proteins or other Gli-activating ligands such as TGFβ are upregulated, including during inflammation, tissue damage and repair, and in tumour microenvironments.

Indexed as

AnimalsCell DifferentiationCell ProliferationGene Expression RegulationHedgehog ProteinsKruppel-Like Transcription FactorsLymphocyte ActivationMiceMice, Inbred C57BLNFATC Transcription FactorsNF-kappa BReceptors, Antigen, T-CellSignal TransductionT-LymphocytesTranscriptional ActivationTranscription Factor AP-1Gli2 protein, mouseHedgehog ProteinsKruppel-Like Transcription FactorsNfatc1 protein, mouseNFATC Transcription FactorsNF-kappa BReceptors, Antigen, T-CellTranscription Factor AP-1Transforming Growth Factor betaZinc Finger Protein Gli2AP-1Gli2HedgehogIL-2NFκBT-cellTCR

Identifiers

PMID25908851
PMCPMC4450292
OpenAlexW2161663577

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.