Abstract
The recent publication of two detailed studies of mouse spermatogenesis, either after chemical inhibition of the BET bromodomains, or in the context of genetic alterations of one specific BET member, Brdt, provides the unique opportunity to assess the functional impact of BET bromodomain inhibitors.
Keywords:
Brd2; Brd3; Brd4; Brdt; acetylation; cancer; chromatin; histone; infertility; pTEFb; spermatogenesis.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Azepines / pharmacology
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Chromosomal Proteins, Non-Histone
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Gene Expression Regulation / drug effects
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Male
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Mice
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Nerve Tissue Proteins / antagonists & inhibitors
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Nerve Tissue Proteins / metabolism*
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Nuclear Proteins / antagonists & inhibitors*
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Nuclear Proteins / genetics
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Nuclear Proteins / metabolism
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Protein Serine-Threonine Kinases / antagonists & inhibitors*
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Protein Serine-Threonine Kinases / metabolism
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Receptors, Cell Surface / antagonists & inhibitors
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Receptors, Cell Surface / metabolism*
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Spermatogenesis / drug effects
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Transcription Factors / antagonists & inhibitors*
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Transcription Factors / metabolism
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Triazoles / pharmacology
Substances
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(+)-JQ1 compound
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Azepines
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BRDT protein, mouse
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Brd2 protein, mouse
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Brd3 protein, mouse
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Brd4 protein, mouse
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Chromosomal Proteins, Non-Histone
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Dner protein, mouse
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Nerve Tissue Proteins
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Nuclear Proteins
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Receptors, Cell Surface
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Transcription Factors
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Triazoles
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Protein Serine-Threonine Kinases