Evidence map›Paper›PMID 29746542›Full record

ArticlePloS one2018

Depletion of mRNA export regulator DBP5/DDX19, GLE1 or IPPK that is a key enzyme for the production of IP6, resulting in differentially altered cytoplasmic mRNA expression and specific cell defect.

Masumi Okamura, Yasutaka Yamanaka, Maki Shigemoto, Yuya Kitadani, Yuhko Kobayashi, Taiho Kambe, Masaya Nagao, Issei Kobayashi, Katsuzumi Okumura, Seiji Masuda

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

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  8. CHERP Regulates the Alternative Splicing of pre-mRNAs in the Nucleus.International journal of molecular sciences · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Masumi OkamuraDivision of Integrated Life Sciences, Graduate School of Biostudies, Kyoto University, Kyoto, Kyoto, Japan.
Yasutaka YamanakaDivision of Integrated Life Sciences, Graduate School of Biostudies, Kyoto University, Kyoto, Kyoto, Japan.
Maki ShigemotoDivision of Integrated Life Sciences, Graduate School of Biostudies, Kyoto University, Kyoto, Kyoto, Japan.
Yuya KitadaniDivision of Integrated Life Sciences, Graduate School of Biostudies, Kyoto University, Kyoto, Kyoto, Japan.
Yuhko KobayashiCenter for Molecular Biology and Genetics, Mie University, Tsu, Mie, Japan.
Taiho KambeDivision of Integrated Life Sciences, Graduate School of Biostudies, Kyoto University, Kyoto, Kyoto, Japan.
Masaya NagaoDivision of Integrated Life Sciences, Graduate School of Biostudies, Kyoto University, Kyoto, Kyoto, Japan.
Issei KobayashiCenter for Molecular Biology and Genetics, Mie University, Tsu, Mie, Japan.
Katsuzumi OkumuraDepartment of Life Sciences, Graduate School of Bioresources, Mie University, Tsu, Mie, Japan.
Seiji MasudaDivision of Integrated Life Sciences, Graduate School of Biostudies, Kyoto University, Kyoto, Kyoto, Japan.ORCID 0000-0003-0295-6789
Kyoto University · JPMie University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DBP5, also known as DDX19, GLE1 and inositol hexakisphosphate (IP6) function in messenger RNA (mRNA) export at the cytoplasmic surface of the nuclear pore complex in eukaryotic cells. DBP5 is a DEAD-box RNA helicase, and its activity is stimulated by interactions with GLE1 and IP6. In addition, these three factors also have unique role(s). To investigate how these factors influenced the cytoplasmic mRNA expression and cell phenotype change, we performed RNA microarray analysis to detect the effect and function of DBP5, GLE1 and IP6 on the cytoplasmic mRNA expression. The expression of some cytoplasmic mRNA subsets (e.g. cell cycle, DNA replication) was commonly suppressed by the knock-down of DBP5, GLE1 and IPPK (IP6 synthetic enzyme). The GLE1 knock-down selectively reduced the cytoplasmic mRNA expression required for mitotic progression, results in an abnormal spindle phenotype and caused the delay of mitotic process. Meanwhile, G1/S cell cycle arrest was observed in DBP5 and IPPK knock-down cells. Several factors that function in immune response were also down-regulated in DBP5 or IPPK knock-down cells. Thereby, IFNβ-1 mRNA transcription evoked by poly(I:C) treatment was suppressed. These results imply that DBP5, GLE1 and IP6 have a conserved and individual function in the cytoplasmic mRNA expression. Variations in phenotype are due to the difference in each function of DBP5, GLE1 and IPPK in intracellular mRNA metabolism.

Indexed as

G1 PhaseS PhaseBiological Transport, ActiveCytoplasmDEAD-box RNA HelicasesHeLa CellsHumansInterferon-betaNucleocytoplasmic Transport ProteinsPhosphotransferases (Alcohol Group Acceptor)Phytic AcidRNA, MessengerDDX19B protein, humanDEAD-box RNA HelicasesGle1 protein, humaninositol pentakisphosphate kinaseInterferon-betaNucleocytoplasmic Transport ProteinsPhosphotransferases (Alcohol Group Acceptor)Phytic AcidRNA, Messenger

Identifiers

PMID29746542
PMCPMC5945018
OpenAlexW2800688743

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.