Evidence map›Paper›PMID 25123787›Full record

ArticleGene2014

Alternative polyadenylation regulates CELF1/CUGBP1 target transcripts following T cell activation.

Daniel Beisang, Cavan Reilly, Paul R Bohjanen

Abstract read
In one paragraph

Article in Gene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

22 citing papers in PubMed, 29 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

3 authors at 1 institution in 1 country.

Daniel BeisangCenter for Infectious Diseases and Microbiology Translational Research, University of Minnesota, Minneapolis, MN, USA; Department of Microbiology, University of Minnesota, Minneapolis, MN, USA. Electronic address: beis0051@umn.edu.
Cavan ReillyDivision of Biostatistics, University of Minnesota, Minneapolis, MN, USA. Electronic address: cavanr@biostat.umn.edu.
Paul R BohjanenCenter for Infectious Diseases and Microbiology Translational Research, University of Minnesota, Minneapolis, MN, USA; Department of Microbiology, University of Minnesota, Minneapolis, MN, USA; Department of Medicine, University of Minnesota, Minneapolis, MN, USA. Electronic address: Bohja001@umn.edu.
University of Minnesota · US

Funding

University of Minnesota Clinical and Translational Science Institute (UMN CTSI)UL1TR000114 · NCATS · UNIVERSITY OF MINNESOTA · PI BLAZAR, BRUCE R · 2012 to 2015
$35.0M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM008244 · NIGMS · UNIVERSITY OF MINNESOTA TWIN CITIES · PI SHIMIZU, YOJI · 1988 to 2024
$13.6M
Novel Regulators of T Cell mRNA DecayR01AI072068 · NIAID · UNIVERSITY OF MINNESOTA · PI BOHJANEN, PAUL R · 2008 to 2011
$1.3M
Outcomes of Cryptococcal Meningitis in UgandaK24AI096925 · NIAID · UNIVERSITY OF MINNESOTA · PI BOHJANEN, PAUL R · 2011 to 2015
$1.0M
mRNA Decay in T Lymphocyte ActivationR56AI057484 · NIAID · UNIVERSITY OF MINNESOTA · PI BOHJANEN, PAUL R · 2006 to 2006
$324k
NCATS NIH HHS UL1 TR000114NIAID NIH HHS AI057484NIAID NIH HHS AI072068NIAID NIH HHS AI096925NIAID NIH HHS K24 AI096925NIAID NIH HHS R01 AI072068NIAID NIH HHS R56 AI057484NIGMS NIH HHS 3T32GM8244-24S2NIGMS NIH HHS T32 GM008244
6 · The paper itself

Abstract

Alternative polyadenylation (APA) is an evolutionarily conserved mechanism for regulating gene expression. Transcript 3' end shortening through changes in polyadenylation site usage occurs following T cell activation, but the consequences of APA on gene expression are poorly understood. We previously showed that GU-rich elements (GREs) found in the 3' untranslated regions of select transcripts mediate rapid mRNA decay by recruiting the protein CELF1/CUGBP1. Using a global RNA sequencing approach, we found that a network of CELF1 target transcripts involved in cell division underwent preferential 3' end shortening via APA following T cell activation, resulting in decreased inclusion of CELF1 binding sites and increased transcript expression. We present a model whereby CELF1 regulates APA site selection following T cell activation through reversible binding to nearby GRE sequences. These findings provide insight into the role of APA in controlling cellular proliferation during biological processes such as development, oncogenesis and T cell activation.

Indexed as

Transcriptional Activation3' Untranslated RegionsAlternative SplicingBinding SitesCELF1 ProteinCell DivisionCell ProliferationCells, CulturedHumansLymphocyte ActivationModels, GeneticPoly ARNA-Binding ProteinsRNA StabilitySignal TransductionT-Lymphocytes3' Untranslated RegionsCELF1 ProteinCELF1 protein, humanPoly ARNA-Binding ProteinsAlternative polyadenylationCELF1Cell divisionCUGBP1GREmRNA decayT cell stimulation

Identifiers

PMID25123787
PMCPMC4162518
OpenAlexW2128699597

What OpenQuestion holds

Textmetadata
LicenceTDM
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.