Evidence map›Paper›PMID 35664701›Full record

ArticleMolecular therapy. Nucleic acids2022

U1A is a positive regulator of the expression of heterologous and cellular genes involved in cell proliferation and migration.

Eric Rovira, Beatriz Moreno, Nerea Razquin, Roland Hjerpe, Monika Gonzalez-Lopez, Rosa Barrio, Igor Ruiz de Los Mozos, Jernej Ule, Fernando Pastor, Lorea Blazquez and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular therapy. Nucleic acids, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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.

Eric RoviraDepartment of Gene Therapy and Regulation of Gene Expression, Center for Applied Medical Research (CIMA), University of Navarra (UNAV), 31008 Pamplona, Spain.
Beatriz MorenoDepartment of Molecular Therapy, Aptamer Unit, Center for Applied Medical Research (CIMA), University of Navarra (UNAV), 31008 Pamplona, Spain.
Nerea RazquinDepartment of Gene Therapy and Regulation of Gene Expression, Center for Applied Medical Research (CIMA), University of Navarra (UNAV), 31008 Pamplona, Spain.
Roland HjerpeDepartment of Functional Genomics, Center for Cooperative Research in Biosciences (CIC bioGUNE), Basque Research and Technology Alliance (BRTA), Bizkaia Technology Park, Building 801A, 48160 Derio, Spain.
Monika Gonzalez-LopezDepartment of Functional Genomics, Center for Cooperative Research in Biosciences (CIC bioGUNE), Basque Research and Technology Alliance (BRTA), Bizkaia Technology Park, Building 801A, 48160 Derio, Spain.
Rosa BarrioDepartment of Functional Genomics, Center for Cooperative Research in Biosciences (CIC bioGUNE), Basque Research and Technology Alliance (BRTA), Bizkaia Technology Park, Building 801A, 48160 Derio, Spain.
Igor Ruiz de Los MozosDepartment of Neuromuscular Diseases, Institute of Neurology, UCL, WC1B5EH London, UK.
Jernej UleDepartment of Neuromuscular Diseases, Institute of Neurology, UCL, WC1B5EH London, UK.
Fernando PastorDepartment of Molecular Therapy, Aptamer Unit, Center for Applied Medical Research (CIMA), University of Navarra (UNAV), 31008 Pamplona, Spain.
Lorea BlazquezDepartment of Neuromuscular Diseases, Institute of Neurology, UCL, WC1B5EH London, UK.
Puri FortesDepartment of Gene Therapy and Regulation of Gene Expression, Center for Applied Medical Research (CIMA), University of Navarra (UNAV), 31008 Pamplona, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Here, we show that direct recruitment of U1A to target transcripts can increase gene expression. This is a new regulatory role, in addition to previous knowledge showing that U1A decreases the levels of U1A mRNA and other specific targets. In fact, genome-wide, U1A more often increases rather than represses gene expression and many U1A-upregulated transcripts are directly bound by U1A according to individual nucleotide resolution crosslinking and immunoprecipitation (iCLIP) studies. Interestingly, U1A-mediated positive regulation can be transferred to a heterologous system for biotechnological purposes. Finally, U1A-bound genes are enriched for those involved in cell cycle and adhesion. In agreement with this, higher U1A mRNA expression associates with lower disease-free survival and overall survival in many cancer types, and U1A mRNA levels positively correlate with those of some oncogenes involved in cell proliferation. Accordingly, U1A depletion leads to decreased expression of these genes and the migration-related gene

Indexed as

cell migrationCTGFexpression regulationiCLIPMT: RNA/DNA EditingproliferationRNA therapytelescriptingU1AU1iU1 snRNP

Identifiers

PMID35664701
PMCPMC9136276

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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.