Evidence map›Paper›PMID 32371398›Full record

ArticleThe Journal of biological chemistry2020

The evolutionarily conserved deubiquitinase UBH1/UCH-L1 augments DAF7/TGF-β signaling, inhibits dauer larva formation, and enhances lung tumorigenesis.

Asami Nagata, Fumiko Itoh, Ayaka Sasho, Kaho Sugita, Riko Suzuki, Hiroki Hinata, Yuta Shimoda, Eri Suzuki, Yuki Maemoto, Toshihiko Inagawa and 4 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.8field-weighted citation impact, top 31% 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

8 citing papers in PubMed, 11 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

14 authors at 1 institution in 1 country.

Asami NagataLaboratory of Molecular and Chemical Biology, School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan.
Fumiko ItohLaboratory of Cardiovascular Medicine, School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan. Electronic address: mame.fumiko@gmail.com.
Ayaka SashoLaboratory of Molecular and Chemical Biology, School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan.
Kaho SugitaLaboratory of Molecular and Chemical Biology, School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan.
Riko SuzukiLaboratory of Molecular and Chemical Biology, School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan.
Hiroki HinataLaboratory of Cardiovascular Medicine, School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan.
Yuta ShimodaLaboratory of Molecular and Chemical Biology, School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan.
Eri SuzukiLaboratory of Molecular and Chemical Biology, School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan.
Yuki MaemotoLaboratory of Cell Signaling, School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan.
Toshihiko InagawaLaboratory of Cardiovascular Medicine, School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan.
Yuuta FujikawaLaboratory of Molecular and Chemical Biology, School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan.
Eri IkedaLaboratory of Molecular and Chemical Biology, School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan.
Chiaki FujiiLaboratory of Molecular and Chemical Biology, School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan.
Hideshi InoueLaboratory of Molecular and Chemical Biology, School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan. Electronic address: hinoue@toyaku.ac.jp.
Tokyo University of Pharmacy and Life Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Modification of the transforming growth factor β (TGF-β) signaling components by (de)ubiquitination is emerging as a key regulatory mechanism that controls cell signaling responses in health and disease. Here, we show that the deubiquitinating enzyme UBH-1 in

Indexed as

AnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsCarcinogenesisCell Transformation, NeoplasticDeubiquitinating EnzymesLarvaLungSignal TransductionSmad2 ProteinSmad3 ProteinTransforming Growth Factor betaUbiquitinationUbiquitin ThiolesteraseCaenorhabditis elegans ProteinsDAF-7 protein, C elegansDeubiquitinating EnzymesSmad2 ProteinSmad3 ProteinTransforming Growth Factor betaUbiquitin Thiolesterasecell signalingDAF-7deubiquitylation (deubiquitination)hypoxialung cancerlung carcinomapost-translational modification (PTM)SMAD transcription factortransforming growth factor β (TGF-β)Ubh1ubh-1/UCH-L1ubiquitin C-terminal hydrolase-L1 (UCH-L1)

Identifiers

PMID32371398
PMCPMC7335803
OpenAlexW3021851118

What OpenQuestion holds

Textmetadata
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.