Evidence map›Paper›PMID 11358867›Full record

ArticleGenes & development2001

TEAD/TEF transcription factors utilize the activation domain of YAP65, a Src/Yes-associated protein localized in the cytoplasm.

A Vassilev, K J Kaneko, H Shu, Y Zhao, M L DePamphilis

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Article in Genes & development, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 404 papers.

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0cells of the map it votes in
404citing papers in PubMed
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1 · What the graph read from it

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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

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3 · Its place in the literature

Who cites it

404 citing papers in PubMed, 712 citations in OpenAlex.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors at 3 institutions in 2 countries.

A VassilevNational Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892-2753, USA.
K J Kaneko
H Shu
Y Zhao
M L DePamphilis
Eunice Kennedy Shriver National Institute of Child Health and Human Development · USNational Institute of Child Health · PKNational Institutes of Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mammals express four highly conserved TEAD/TEF transcription factors that bind the same DNA sequence, but serve different functions during development. TEAD-2/TEF-4 protein purified from mouse cells was associated predominantly with a novel TEAD-binding domain at the amino terminus of YAP65, a powerful transcriptional coactivator. YAP65 interacted specifically with the carboxyl terminus of all four TEAD proteins. Both this interaction and sequence-specific DNA binding by TEAD were required for transcriptional activation in mouse cells. Expression of YAP in lymphocytic cells that normally do not support TEAD-dependent transcription (e.g., MPC11) resulted in up to 300-fold induction of TEAD activity. Conversely, TEAD overexpression squelched YAP activity. Therefore, the carboxy-terminal acidic activation domain in YAP is the transcriptional activation domain for TEAD transcription factors. However, whereas TEAD was concentrated in the nucleus, excess YAP65 accumulated in the cytoplasm as a complex with the cytoplasmic localization protein, 14-3-3. Because TEAD-dependent transcription was limited by YAP65, and YAP65 also binds Src/Yes protein tyrosine kinases, we propose that YAP65 regulates TEAD-dependent transcription in response to mitogenic signals.

Indexed as

Adaptor Proteins, Signal Transducing3T3 CellsAnimalsCarrier ProteinsCell Cycle ProteinsCytoplasmDimerizationDNA-Binding ProteinsElectrophoresis, Polyacrylamide GelFluorescent Antibody TechniqueMass SpectrometryMicePhosphoproteinsProtein BindingProtein Structure, Tertiarysrc-Family KinasesAdaptor Proteins, Signal TransducingCarrier ProteinsCell Cycle ProteinsDNA-Binding ProteinsPhosphoproteinssrc-Family KinasesTead2 protein, mouseTEA Domain Transcription FactorsTranscription FactorsYap1 protein, mouseYAP-Signaling Proteins

Identifiers

PMID11358867
PMCPMC313800
OpenAlexW2159196011

What OpenQuestion holds

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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.