Evidence map›Paper›PMID 27702999›Full record

ArticleThe Journal of biological chemistry2016

Ohgata, the Single Drosophila Ortholog of Human Cereblon, Regulates Insulin Signaling-dependent Organismic Growth.

Satoru Wakabayashi, Naoya Sawamura, André Voelzmann, Meike Broemer, Toru Asahi, Michael Hoch

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.3field-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

5 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
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  4. Zoological research · 2018
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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 4 institutions in 3 countries.

Satoru WakabayashiFrom the Faculty of Science and Engineering, Waseda University, TWIns, 2-2 Wakamatsu, Shinjuku, Tokyo 162-8480, Japan.
Naoya SawamuraFrom the Faculty of Science and Engineering, Waseda University, TWIns, 2-2 Wakamatsu, Shinjuku, Tokyo 162-8480, Japan, naoya.sawamura@gmail.com.
André Voelzmannthe Faculty of Biology, Medicine and Health, The University of Manchester, Michael Smith Building, Oxford Road, Manchester M13 9PT, United Kingdom.ORCID http://orcid.org/0000-0002-7682-5637
Meike Broemerthe German Center for Neurodegenerative Diseases (DZNE), c/o Life and Medical Sciences (LIMES) Institute, Carl-Troll-Strasse 31, 53115 Bonn, Germany, and.
Toru AsahiFrom the Faculty of Science and Engineering, Waseda University, TWIns, 2-2 Wakamatsu, Shinjuku, Tokyo 162-8480, Japan, tasahi@waseda.jp.
Michael HochProgram Unit Development, Genetics and Molecular Physiology, Laboratory for Molecular Developmental Biology, LIMES Institute, University of Bonn, Carl-Troll-Strasse 31, 53115 Bonn, Germany m.hoch@uni-bonn.de.
Waseda University · JPGerman Center for Neurodegenerative Diseases · DEUniversity of Bonn · DEUniversity of Manchester · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cereblon (CRBN) is a substrate receptor of the E3 ubiquitin ligase complex that is highly conserved in animals and plants. CRBN proteins have been implicated in various biological processes such as development, metabolism, learning, and memory formation, and their impairment has been linked to autosomal recessive non-syndromic intellectual disability and cancer. Furthermore, human CRBN was identified as the primary target of thalidomide teratogenicity. Data on functional analysis of CRBN family members in vivo, however, are still scarce. Here we identify Ohgata (OHGT), the Drosophila ortholog of CRBN, as a regulator of insulin signaling-mediated growth. Using ohgt mutants that we generated by targeted mutagenesis, we show that its loss results in increased body weight and organ size without changes of the body proportions. We demonstrate that ohgt knockdown in the fat body, an organ analogous to mammalian liver and adipose tissue, phenocopies the growth phenotypes. We further show that overgrowth is due to an elevation of insulin signaling in ohgt mutants and to the down-regulation of inhibitory cofactors of circulating Drosophila insulin-like peptides (DILPs), named acid-labile subunit and imaginal morphogenesis protein-late 2. The two inhibitory proteins were previously shown to be components of a heterotrimeric complex with growth-promoting DILP2 and DILP5. Our study reveals OHGT as a novel regulator of insulin-dependent organismic growth in Drosophila.

Indexed as

Drosophila ProteinsInsulinsAdaptor Proteins, Signal TransducingAnimalsCell LineDrosophila melanogasterGene Knockdown TechniquesHumansPeptide HydrolasesSignal TransductionUbiquitin-Protein LigasesAdaptor Proteins, Signal TransducingCRBN protein, humanDrosophila ProteinsIlp5 protein, DrosophilaInsulinsPeptide HydrolasesUbiquitin-Protein LigasesCereblonCRISPR/CasdevelopmentDrosophila geneticsE3 ubiquitin ligaseinsulin

Identifiers

PMID27702999
PMCPMC5122779
OpenAlexW2527755472

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.