Abstract
Several mutations and atypical splice variants of WISP3 (CCN6) have been linked to connective tissue disorders and different forms of malignancies. Functional studies have suggested that WISP3 contributes to tissue maintenance/homeostasis. The precise molecular mechanism of WISP3 function in different cell types, however, remains unresolved. The present study was conducted to investigate the potential impact of WISP3 on the accumulation of reactive oxygen species (ROS) and oxidative stress, which are central to cell/tissue maintenance. Our experimental results suggest that WISP3 regulates the accumulation of cellular ROS, and mutations in WISP3 or loss of expression of WISP3 compromise this function.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Base Sequence
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CCN Intercellular Signaling Proteins
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Cell Line
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Cloning, Molecular
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DNA Primers
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Humans
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Insulin-Like Growth Factor Binding Proteins / genetics
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Insulin-Like Growth Factor Binding Proteins / physiology*
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Molecular Sequence Data
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Neoplasm Proteins / genetics
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Neoplasm Proteins / physiology*
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Polymerase Chain Reaction
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RNA, Messenger / genetics
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RNA, Messenger / isolation & purification
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Reactive Oxygen Species / metabolism*
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Recombinant Proteins / metabolism
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Transfection
Substances
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CCN Intercellular Signaling Proteins
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CCN6 protein, human
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DNA Primers
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Insulin-Like Growth Factor Binding Proteins
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Neoplasm Proteins
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RNA, Messenger
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Reactive Oxygen Species
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Recombinant Proteins