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Peter J. Shepard

Researcher at University of California, San Diego

Publications -  20
Citations -  1606

Peter J. Shepard is an academic researcher from University of California, San Diego. The author has contributed to research in topics: RNA splicing & Transcriptome. The author has an hindex of 13, co-authored 20 publications receiving 1369 citations. Previous affiliations of Peter J. Shepard include University of California, Irvine.

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Complex and dynamic landscape of RNA polyadenylation revealed by PAS-Seq

TL;DR: PAS-Seq analyses revealed a complex landscape of RNA polyadenylation in mammalian cells and the dynamic regulation of APA during stem cell differentiation and detected significant changes in the global APA profile that lead to lengthening of 3' untranslated regions (UTR) in many mRNAs during stem Cell differentiation.
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The SR protein family

TL;DR: Members of the family of serine/arginine (SR)-rich proteins are critical components of the machineries carrying out these essential processing events, highlighting their importance in maintaining efficient gene expression.
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Transcriptome Sequencing Reveals Potential Mechanism of Cryptic 3’ Splice Site Selection in SF3B1-mutated Cancers

TL;DR: It is proposed that cryptic 3’SS selection is a result of SF3B1 mutations causing a shift in the sterically protected region downstream of the branch point, and this model provides both a mechanistic model consistent with published experimental data and affected targets that will guide further research into the oncogenic effects of SF 3B1 mutation.
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Conserved RNA secondary structures promote alternative splicing.

TL;DR: Using structural and functional conservation, RNA structure elements within the human genome are identified that associate with alternative splice-site selection and demonstrate that RNA structure formation is an important mechanism regulating gene expression and disease.
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A trichostatin A expression signature identified by TempO-Seq targeted whole transcriptome profiling.

TL;DR: It is concluded that TSA induces a specific expression signature that is consistent across widely different cell types, that this signature contains genes not previously associated with TSA responses, and that TempO-Seq provides the sensitive differential expression detection needed to define such compound-specific, cell-independent, changes in expression.