Evidence map›Paper›PMID 24452013›Full record

ArticleNature communications2014

The splicing activator DAZAP1 integrates splicing control into MEK/Erk-regulated cell proliferation and migration.

Rajarshi Choudhury, Sreerupa Ghose Roy, Yihsuan S Tsai, Ashutosh Tripathy, Lee M Graves, Zefeng Wang

Open access · bronzeAbstract read
In one paragraph

Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Alternative splicing and cancer: a systematic review.Signal transduction and targeted therapy · 2021
    Pooled it
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  9. Multi-omics-based investigation ofFrontiers in microbiology · 2024
    Article
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  11. Review
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  14. DAZAP1 overexpression promotes growth of HCC cell lines: a primary study using CEUS.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Article
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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

6 authors at 2 institutions in 1 country.

Rajarshi ChoudhuryDepartment of Pharmacology, University of North Carolina, Chapel Hill, North Carolina 27599, USA.
Sreerupa Ghose RoyDepartment of Pharmacology, University of North Carolina, Chapel Hill, North Carolina 27599, USA.
Yihsuan S Tsai1] Department of Pharmacology, University of North Carolina, Chapel Hill, North Carolina 27599, USA [2] Curriculum in Bioinformatics and Computational Biology, University of North Carolina, Chapel Hill, North Carolina 27599, USA.
Ashutosh TripathyDepartment of Biochemistry and Biophysics, University of North Carolina, Chapel Hill, North Carolina 27599, USA.
Lee M Graves1] Department of Pharmacology, University of North Carolina, Chapel Hill, North Carolina 27599, USA [2] Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, North Carolina 27599, USA.
Zefeng Wang1] Department of Pharmacology, University of North Carolina, Chapel Hill, North Carolina 27599, USA [2] Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, North Carolina 27599, USA.
University of North Carolina at Chapel Hill · USUNC Lineberger Comprehensive Cancer Center

Funding

Virology Research Program (Program 4)P30CA016086 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Deborah F. Tate · 1985 to 2026
$201.5M
Modulation of VEGF-A alternative splicing as new anti-angiogenic therapeuticsR01CA158283 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI WANG, ZEFENG · 2011 to 2015
$1.4M
NCI NIH HHS P30 CA016086NCI NIH HHS R01 CA158283NCI NIH HHS R01-CA158283
6 · The paper itself

Abstract

Alternative splicing of pre-messenger RNA (mRNA) is a critical stage of gene regulation in response to environmental stimuli. Here we show that DAZAP1, an RNA-binding protein involved in mammalian development and spermatogenesis, promotes inclusion of weak exons through specific recognition of diverse cis-elements. The carboxy-terminal proline-rich domain of DAZAP1 interacts with and neutralizes general splicing inhibitors, and is sufficient to activate splicing when recruited to pre-mRNA. This domain is phosphorylated by the MEK/Erk (extracellular signal-regulated protein kinase) pathway and this modification is essential for the splicing regulatory activity and the nuclear/cytoplasmic translocation of DAZAP1. Using mRNA-seq, we identify endogenous splicing events regulated by DAZAP1, many of which are involved in maintaining cell growth. Knockdown or over-expression of DAZAP1 causes a cell proliferation defect. Taken together, these studies reveal a molecular mechanism that integrates splicing control into MEK/Erk-regulated cell proliferation.

Indexed as

Alternative SplicingCell MovementCell ProliferationCells, CulturedExonsExtracellular Signal-Regulated MAP KinasesHEK293 CellsHeterogeneous-Nuclear RibonucleoproteinsHomeostasisHumansKidneyMAP Kinase Kinase KinasesPhosphorylationRNA-Binding ProteinsSignal TransductionDAZAP1 protein, humanExtracellular Signal-Regulated MAP KinasesHeterogeneous-Nuclear RibonucleoproteinsMAP Kinase Kinase KinasesRNA-Binding Proteins

Identifiers

PMID24452013
PMCPMC4146490
OpenAlexW2092616354

What OpenQuestion holds

Textmetadata
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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.