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- W4378172813 abstract "Steroid hormone signaling pathways are critical for organismal development and act through binding to nuclear receptors (NRs) driving transcriptional regulation. In this review, we summarize evidence for another-underrated-mechanism of action for steroid hormones: their ability to modulate the alternative splicing of pre-messenger RNA. Thirty years ago, pioneering studies used in vitro transfection of plasmids expressing alternative exons under the control of hormone-responsive promoters in cell lines. These studies demonstrated that steroid hormones binding to their NRs affected both gene transcription and alternative splicing outcomes. The advent of exon arrays and next-generation sequencing has allowed researchers to observe the effect of steroid hormones at the whole-transcriptome level. These studies demonstrate that steroid hormones regulate alternative splicing in a time-, gene-, and tissue-specific manner. We provide examples of the mechanisms by which steroid hormones regulate alternative splicing including 1) recruitment of dual-function proteins that behave as coregulators and splicing factors, 2) transcriptional regulation of splicing factor levels, 3) the alternative splicing of splicing factors or transcription factors that feed-forward regulate steroid hormone signaling, and 4) regulation of elongation rate. Experiments performed in vivo and in cancer cell lines highlight that steroid hormone-mediated alternative splicing occurs both in physiological and pathophysiologic states. Studying the effect of steroid hormones on alternative splicing is a fruitful avenue for research that should be exploited to discover new targets for therapeutic intervention." @default.
- W4378172813 created "2023-05-26" @default.
- W4378172813 creator A5031897495 @default.
- W4378172813 creator A5047677606 @default.
- W4378172813 creator A5092014635 @default.
- W4378172813 date "2023-05-24" @default.
- W4378172813 modified "2023-10-18" @default.
- W4378172813 title "Regulation of Alternative Splicing by Steroid Hormones" @default.
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- W4378172813 doi "https://doi.org/10.1210/endocr/bqad081" @default.
- W4378172813 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37226268" @default.
- W4378172813 hasPublicationYear "2023" @default.