Evidence map›Paper›PMID 25995450›Full record

ArticleThe Journal of biological chemistry2015

Hippo Component TAZ Functions as a Co-repressor and Negatively Regulates ΔNp63 Transcription through TEA Domain (TEAD) Transcription Factor.

Ivette Valencia-Sama, Yulei Zhao, Dulcie Lai, Helena J Janse van Rensburg, Yawei Hao, Xiaolong Yang

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.4field-weighted citation impact, top 13% 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

26 citing papers in PubMed, 45 citations in OpenAlex.

  1. Vasopressin-Sensitive Aqp2 Regulation Mediated by the TAZ-NR4A1 Axis in Renal Collecting Duct Cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  2. Hippo signaling in mammalian reproduction.Reproduction (Cambridge, England) · 2025
    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

6 authors at 1 institution in 1 country.

Ivette Valencia-SamaFrom the Department of Pathology and Molecular Medicine, Queen's University, Kingston, Ontario K7L 3N6, Canada.
Yulei ZhaoFrom the Department of Pathology and Molecular Medicine, Queen's University, Kingston, Ontario K7L 3N6, Canada.
Dulcie LaiFrom the Department of Pathology and Molecular Medicine, Queen's University, Kingston, Ontario K7L 3N6, Canada.
Helena J Janse van RensburgFrom the Department of Pathology and Molecular Medicine, Queen's University, Kingston, Ontario K7L 3N6, Canada.
Yawei HaoFrom the Department of Pathology and Molecular Medicine, Queen's University, Kingston, Ontario K7L 3N6, Canada.
Xiaolong YangFrom the Department of Pathology and Molecular Medicine, Queen's University, Kingston, Ontario K7L 3N6, Canada yang@path.queensu.ca.
Queen's University · CA

Funding

Canadian Institutes of Health Research 119325
6 · The paper itself

Abstract

Transcriptional co-activator with a PDZ binding domain (TAZ) is a WW domain-containing transcriptional co-activator and a core component of an emerging Hippo signaling pathway that regulates organ size, tumorigenesis, metastasis, and drug resistance. TAZ regulates these biological functions by up-regulating downstream cellular genes through transactivation of transcription factors such as TEAD and TTF1. To understand the molecular mechanisms underlying TAZ-induced tumorigenesis, we have recently performed a gene expression profile analysis by overexpressing TAZ in mammary cells. In addition to the TAZ-up-regulated genes that were confirmed in our previous studies, we identified a large number of cellular genes that were down-regulated by TAZ. In this study, we have confirmed these down-regulated genes (including cytokines, chemokines, and p53 gene family members) as bona fide downstream transcriptional targets of TAZ. By using human breast and lung epithelial cells, we have further characterized ΔNp63, a p53 gene family member, and shown that TAZ suppresses ΔNp63 mRNA, protein expression, and promoter activity through interaction with the transcription factor TEAD. We also show that TEAD can inhibit ΔNp63 promoter activity and that TAZ can directly interact with ΔNp63 promoter-containing TEAD binding sites. Finally, we provide functional evidence that down-regulation of ΔNp63 by TAZ may play a role in regulating cell migration. Altogether, this study provides novel evidence that the Hippo component TAZ can function as a co-repressor and regulate biological functions by negatively regulating downstream cellular genes.

Indexed as

Down-RegulationCell Line, TumorCo-Repressor ProteinsDNA-Binding ProteinsHippo Signaling PathwayHumansIntracellular Signaling Peptides and ProteinsMuscle ProteinsNeoplasmsNuclear ProteinsPromoter Regions, GeneticProtein BindingProtein Serine-Threonine KinasesProtein Structure, TertiaryTEA Domain Transcription FactorsTrans-ActivatorsCo-Repressor ProteinsDNA-Binding ProteinsIntracellular Signaling Peptides and ProteinsMuscle ProteinsNuclear ProteinsProtein Serine-Threonine KinasesTEAD1 protein, humanTEAD2 protein, humanTEAD3 protein, humanTEAD4 protein, humanTEA Domain Transcription FactorsTP63 protein, humanTrans-ActivatorsTranscriptional Coactivator with PDZ-Binding Motif ProteinsTranscription FactorsTumor Suppressor ProteinsWWTR1 protein, humancell migrationHippo pathwayoncogenetranscription coactivatortranscription corepressor

Identifiers

PMID25995450
PMCPMC4505436
OpenAlexW1523013484

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.