Abstract
GNAQ and GNA11 are frequently mutated in uveal melanoma, but they remain difficult therapeutic targets. In this issue of Cancer Cell, Feng and colleagues and Yu and colleagues demonstrate that the oncogenic activity of mutant GNAQ/11 is mediated at least in part through YAP, potentially uncovering a new therapeutic strategy.
Copyright © 2014 Elsevier Inc. All rights reserved.
MeSH terms
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Adaptor Proteins, Signal Transducing / genetics*
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Animals
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Cell Cycle Proteins
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Female
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GTP Phosphohydrolases / metabolism*
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GTP-Binding Protein alpha Subunits / genetics*
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GTP-Binding Protein alpha Subunits, Gq-G11 / genetics*
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Hippo Signaling Pathway
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Humans
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Male
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Melanoma / genetics*
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Mutation*
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Nuclear Proteins / genetics*
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Phosphoproteins / genetics*
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Protein Serine-Threonine Kinases / metabolism*
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Transcription Factors / genetics*
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Uveal Melanoma
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Uveal Neoplasms / genetics*
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YAP-Signaling Proteins
Substances
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Adaptor Proteins, Signal Transducing
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Cell Cycle Proteins
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GNAQ protein, human
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GTP-Binding Protein alpha Subunits
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Nuclear Proteins
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Phosphoproteins
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Transcription Factors
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YAP-Signaling Proteins
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YY1AP1 protein, human
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Yap1 protein, mouse
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Protein Serine-Threonine Kinases
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GTP Phosphohydrolases
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GTP-Binding Protein alpha Subunits, Gq-G11