Evidence map›Paper›PMID 26116754›Full record

ArticleEMBO reports2015

PARD3 induces TAZ activation and cell growth by promoting LATS1 and PP1 interaction.

Xian-Bo Lv, Chen-Ying Liu, Zhen Wang, Yi-Ping Sun, Yue Xiong, Qun-Ying Lei, Kun-Liang Guan

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in EMBO reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.0field-weighted citation impact, top 9% 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, 58 citations in OpenAlex.

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  14. PARD3 gene variation as candidate cause of nonsyndromic cleft palate only.Journal of cellular and molecular medicine · 2022
    Article
  15. Review
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  17. Article
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  19. Dual Function of Par3 in Tumorigenesis.Frontiers in oncology · 2022
    Review
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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

7 authors at 5 institutions in 2 countries.

Xian-Bo LvKey Laboratory of Metabolism and Molecular Medicine, Ministry of Education and Department of Biochemistry and Molecular Biology Fudan University Shanghai Medical College, Shanghai, China Molecular and Cell Biology Lab, Institutes of Biomedical Sciences, Fudan University, Shanghai, China School of Life Science, Fudan University, Shanghai, China.
Chen-Ying LiuDepartment of Colorectal and Anal Surgery, Shanghai Colorectal Cancer Research Center, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
Zhen WangKey Laboratory of Metabolism and Molecular Medicine, Ministry of Education and Department of Biochemistry and Molecular Biology Fudan University Shanghai Medical College, Shanghai, China Molecular and Cell Biology Lab, Institutes of Biomedical Sciences, Fudan University, Shanghai, China School of Life Science, Fudan University, Shanghai, China.
Yi-Ping SunKey Laboratory of Metabolism and Molecular Medicine, Ministry of Education and Department of Biochemistry and Molecular Biology Fudan University Shanghai Medical College, Shanghai, China Molecular and Cell Biology Lab, Institutes of Biomedical Sciences, Fudan University, Shanghai, China School of Life Science, Fudan University, Shanghai, China.
Yue XiongKey Laboratory of Metabolism and Molecular Medicine, Ministry of Education and Department of Biochemistry and Molecular Biology Fudan University Shanghai Medical College, Shanghai, China Molecular and Cell Biology Lab, Institutes of Biomedical Sciences, Fudan University, Shanghai, China Department of Biochemistry and Biophysics, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA yxiong@mai.unc.edu qlei@fudan.edu.cn kuguan@ucsd.edu.
Qun-Ying LeiKey Laboratory of Metabolism and Molecular Medicine, Ministry of Education and Department of Biochemistry and Molecular Biology Fudan University Shanghai Medical College, Shanghai, China Molecular and Cell Biology Lab, Institutes of Biomedical Sciences, Fudan University, Shanghai, China yxiong@mai.unc.edu qlei@fudan.edu.cn kuguan@ucsd.edu.
Kun-Liang GuanKey Laboratory of Metabolism and Molecular Medicine, Ministry of Education and Department of Biochemistry and Molecular Biology Fudan University Shanghai Medical College, Shanghai, China Molecular and Cell Biology Lab, Institutes of Biomedical Sciences, Fudan University, Shanghai, China Department of Pharmacology and Moores Cancer Center, University of California San Diego, La Jolla, CA, USA yxiong@mai.unc.edu qlei@fudan.edu.cn kuguan@ucsd.edu.
Fudan University · CNShanghai Medical College of Fudan University · CNUniversity of California, San Diego · USUniversity of North Carolina at Chapel Hill · USXinHua Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Hippo pathway plays a major role in organ size control, and its dysregulation contributes to tumorigenesis. The major downstream effectors of the Hippo pathway are the YAP/TAZ transcription co-activators, which are phosphorylated and inhibited by the Hippo pathway kinase LATS1/2. Here, we report a novel mechanism of TAZ regulation by the tight junction protein PARD3. PARD3 promotes the interaction between PP1A and LATS1 to induce LATS1 dephosphorylation and inactivation, therefore leading to dephosphorylation and activation of TAZ. The cytoplasmic, but not the tight junction complex associated, PARD3 is responsible for TAZ regulation. Our study indicates a potential molecular basis for cell growth-promoting function of PARD3 by modulating the Hippo pathway signaling in response to cell contact and cell polarity signals.

Indexed as

Cell ProliferationAdaptor Proteins, Signal TransducingCell Cycle ProteinsCell Line, TumorCell PolarityGene Expression RegulationHEK293 CellsHippo Signaling PathwayHumansIntracellular Signaling Peptides and ProteinsMembrane ProteinsPhosphoprotein PhosphatasesPhosphorylationProtein Serine-Threonine KinasesSignal TransductionTight Junction ProteinsAdaptor Proteins, Signal TransducingCell Cycle ProteinsIntracellular Signaling Peptides and ProteinsLATS1 protein, humanMembrane ProteinsPARD3 protein, humanPhosphoprotein PhosphatasesProtein Serine-Threonine KinasesTight Junction ProteinsTrans-ActivatorsTranscriptional Coactivator with PDZ-Binding Motif ProteinsTranscription FactorsWWTR1 protein, humanHippo pathwayPARD3TAZtight junction

Identifiers

PMID26116754
PMCPMC4552490
OpenAlexW2137014040

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.