Evidence map›Paper›PMID 30679431›Full record

ArticleNature communications2019

TAZ couples Hippo/Wnt signalling and insulin sensitivity through Irs1 expression.

Jun-Ha Hwang, A Rum Kim, Kyung Min Kim, Jung Il Park, Ho Taek Oh, Sung A Moon, Mi Ran Byun, Hana Jeong, Hyo Kyung Kim, Michael B Yaffe and 2 more

Open access · goldFull text read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

30 citing papers in PubMed, 50 citations in OpenAlex.

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  16. Hippo pathway in intestinal diseases: focusing on ferroptosis.Frontiers in cell and developmental biology · 2023
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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

12 authors at 3 institutions in 2 countries.

Jun-Ha HwangDepartment of Life Sciences, School of Life Sciences and Biotechnology, Korea University, Seoul, 02841, South Korea.
A Rum KimDepartment of Life Sciences, School of Life Sciences and Biotechnology, Korea University, Seoul, 02841, South Korea.
Kyung Min KimDepartment of Life Sciences, School of Life Sciences and Biotechnology, Korea University, Seoul, 02841, South Korea.
Jung Il ParkDepartment of Life Sciences, School of Life Sciences and Biotechnology, Korea University, Seoul, 02841, South Korea.
Ho Taek OhDepartment of Life Sciences, School of Life Sciences and Biotechnology, Korea University, Seoul, 02841, South Korea.
Sung A MoonDepartment of Life Sciences, School of Life Sciences and Biotechnology, Korea University, Seoul, 02841, South Korea.
Mi Ran ByunDepartment of Life Sciences, School of Life Sciences and Biotechnology, Korea University, Seoul, 02841, South Korea.
Hana JeongCollege of Pharmacy, Ewha Womans University, Seoul, 03760, South Korea.
Hyo Kyung KimCollege of Pharmacy, Ewha Womans University, Seoul, 03760, South Korea.
Michael B YaffeDavid H. Koch Institute for Integrative Cancer Research, Department of Biology, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Eun Sook HwangCollege of Pharmacy, Ewha Womans University, Seoul, 03760, South Korea. eshwang@ewha.ac.kr.
Jeong-Ho HongDepartment of Life Sciences, School of Life Sciences and Biotechnology, Korea University, Seoul, 02841, South Korea. jh_hong@korea.ac.kr.
Korea University · KREwha Womans University · KRMassachusetts Institute of Technology · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulin regulates blood glucose levels by binding its receptor and stimulating downstream proteins through the insulin receptor substrate (IRS). Impaired insulin signalling leads to metabolic syndrome, but the regulation of this process is not well understood. Here, we describe a novel insulin signalling regulatory pathway involving TAZ. TAZ upregulates IRS1 and stimulates Akt- and Glut4-mediated glucose uptake in muscle cells. Muscle-specific TAZ-knockout mice shows significantly decreased Irs1 expression and insulin sensitivity. Furthermore, TAZ is required for Wnt signalling-induced Irs1 expression, as observed by decreased Irs1 expression and insulin sensitivity in muscle-specific APC- and TAZ-double-knockout mice. TAZ physically interacts with c-Jun and Tead4 to induce Irs1 transcription. Finally, statin administration decreases TAZ, IRS1 level and insulin sensitivity. However, in myoblasts, the statin-mediated decrease in insulin sensitivity is counteracted by the expression of a constitutively active TAZ mutant. These results suggest that TAZ is a novel insulin signalling activator that increases insulin sensitivity and couples Hippo/Wnt signalling and insulin sensitivity.

Indexed as

Signal TransductionAcyltransferasesAnimalsBlood GlucoseCell LineGene Expression ProfilingGene Expression RegulationGlucoseGlucose Transporter Type 4HEK293 CellsHippo Signaling PathwayHumansInsulinInsulin Receptor Substrate ProteinsInsulin ResistanceMiceAcyltransferasesBlood GlucoseGlucoseGlucose Transporter Type 4InsulinInsulin Receptor Substrate ProteinsIrs1 protein, mousePharmaceutical VehiclesProtein Serine-Threonine KinasesSimvastatintafazzin protein, mouseTranscription Factors

Identifiers

PMID30679431
PMCPMC6345998
OpenAlexW2911334612

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Textfull text, public
LicenceCC BY
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Registered trials

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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.