Abstract
The transcriptional silencing of one of the female X-chromosomes is a finely regulated process that requires accumulation in cis of the long non-coding RNA X-inactive-specific transcript (Xist) followed by a series of epigenetic modifications. Little is known about the molecular machinery regulating initiation and maintenance of chromosomal silencing. Here, we introduce a new version of our algorithm catRAPID to investigate Xist associations with a number of proteins involved in epigenetic regulation, nuclear scaffolding, transcription and splicing processes. Our method correctly identifies binding regions and affinities of protein interactions, providing a powerful theoretical framework for the study of X-chromosome inactivation and other events mediated by ribonucleoprotein associations.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Algorithms*
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Animals
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Binding Sites
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Enhancer of Zeste Homolog 2 Protein
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Female
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Heterogeneous-Nuclear Ribonucleoprotein U / metabolism
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Matrix Attachment Region Binding Proteins / metabolism
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Mice
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Nuclear Proteins / metabolism
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Polycomb Repressive Complex 2 / metabolism
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RNA, Long Noncoding / chemistry
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RNA, Long Noncoding / metabolism*
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RNA-Binding Proteins / metabolism*
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Repetitive Sequences, Nucleic Acid
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Serine-Arginine Splicing Factors
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X Chromosome Inactivation*
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YY1 Transcription Factor / metabolism
Substances
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Heterogeneous-Nuclear Ribonucleoprotein U
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Matrix Attachment Region Binding Proteins
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Nuclear Proteins
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RNA, Long Noncoding
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RNA-Binding Proteins
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SAF-A protein, mouse
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Satb1 protein, mouse
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Suz12 protein, mouse
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XIST non-coding RNA
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YY1 Transcription Factor
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Serine-Arginine Splicing Factors
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Enhancer of Zeste Homolog 2 Protein
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Ezh2 protein, mouse
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Polycomb Repressive Complex 2