Evidence map›Paper›PMID 37801430›Full record

ArticleBriefings in functional genomics2024

STAT3-dependent long non-coding RNA Lncenc1 contributes to mouse ES cells pluripotency via stabilizing Klf4 mRNA.

Emanuele Monteleone, Paola Corrieri, Paolo Provero, Daniele Viavattene, Lorenzo Pulvirenti, Laura Raggi, Elena Carbognin, Marco E Bianchi, Graziano Martello, Salvatore Oliviero and 2 more

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

Article in Briefings in functional genomics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.2field-weighted citation impact, top 40% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 2 countries.

Emanuele MonteleoneDepartment of Molecular Biotechnology and Health Science, University of Torino, Via Nizza 52, 10126 Torino, Italy.ORCID 0000-0001-7440-900X
Paola CorrieriDepartment of Molecular Biotechnology and Health Science, University of Torino, Via Nizza 52, 10126 Torino, Italy.
Paolo ProveroDepartment of Molecular Biotechnology and Health Science, University of Torino, Via Nizza 52, 10126 Torino, Italy.
Daniele ViavatteneDepartment of Molecular Biotechnology and Health Science, University of Torino, Via Nizza 52, 10126 Torino, Italy.
Lorenzo PulvirentiDepartment of Molecular Biotechnology and Health Science, University of Torino, Via Nizza 52, 10126 Torino, Italy.
Laura RaggiDepartment of Molecular Biotechnology and Health Science, University of Torino, Via Nizza 52, 10126 Torino, Italy.
Elena CarbogninDepartment of Biology, University of Padua, Italy.
Marco E BianchiUniversità Vita-Salute San Raffaele, Milan, Italy.
Graziano MartelloDepartment of Biology, University of Padua, Italy.
Salvatore OlivieroDepartment of Life Sciences and Systems Biology, University of Torino.
Pier Paolo PandolfiDepartment of Molecular Biotechnology and Health Science, University of Torino, Via Nizza 52, 10126 Torino, Italy.
Valeria PoliDepartment of Molecular Biotechnology and Health Science, University of Torino, Via Nizza 52, 10126 Torino, Italy.ORCID 0000-0002-3739-3966
University of Turin · ITUniversity of Padua · ITVita-Salute San Raffaele University · ITThe San Raffaele Telethon Institute for Gene Therapy · IT

Funding

EMBO Scientific Exchange Grant 6518Giovanni Armenise-Harvard FoundationItalian Cancer Research Association IG 27155Italian Ministry of University and Research MIUR PRIN 2017Microsoft ResearchNextGenerationEU 1.4-CN00000041Regione PiemonteTelethon Foundation GJC21157Truus and Gerrit van Riemsdijk Foundation
6 · The paper itself

Abstract

Embryonic stem cells (ESCs) preserve the unique ability to differentiate into any somatic cell lineage while maintaining their self-renewal potential, relying on a complex interplay of extracellular signals regulating the expression/activity of pluripotency transcription factors and their targets. Leukemia inhibitory factor (LIF)-activated STAT3 drives ESCs' stemness by a number of mechanisms, including the transcriptional induction of pluripotency factors such as Klf4 and the maintenance of a stem-like epigenetic landscape. However, it is unknown if STAT3 directly controls stem-cell specific non-coding RNAs, crucial to balance pluripotency and differentiation. Applying a bioinformatic pipeline, here we identify Lncenc1 in mouse ESCs as an STAT3-dependent long non-coding RNA that supports pluripotency. Lncenc1 acts in the cytoplasm as a positive feedback regulator of the LIF-STAT3 axis by competing for the binding of microRNA-128 to the 3'UTR of the Klf4 core pluripotency factor mRNA, enhancing its expression. Our results unveil a novel non-coding RNA-based mechanism for LIF-STAT3-mediated pluripotency.

Indexed as

Kruppel-Like Factor 4Kruppel-Like Transcription FactorsLeukemia Inhibitory FactorMouse Embryonic Stem CellsRNA, Long NoncodingRNA, MessengerSTAT3 Transcription FactorAnimalsCell DifferentiationMiceMicroRNAsPluripotent Stem CellsRNA StabilityKlf4 protein, mouseKruppel-Like Factor 4Kruppel-Like Transcription FactorsLeukemia Inhibitory FactorMicroRNAsRNA, Long NoncodingRNA, MessengerStat3 protein, mouseSTAT3 Transcription FactorKlf4lincRNAsmicroRNAsmiR-128naive pluripotencySTAT3

Identifiers

PMID37801430
PMCPMC11428181
OpenAlexW4387397686

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.