論文

査読有り 国際誌
2013年4月

FUS regulates genes coding for RNA-binding proteins in neurons by binding to their highly conserved introns.

RNA (New York, N.Y.)
  • Tadashi Nakaya
  • ,
  • Panagiotis Alexiou
  • ,
  • Manolis Maragkakis
  • ,
  • Alexandra Chang
  • ,
  • Zissimos Mourelatos

19
4
開始ページ
498
終了ページ
509
記述言語
英語
掲載種別
DOI
10.1261/rna.037804.112

Dominant mutations and mislocalization or aggregation of Fused in Sarcoma (FUS), an RNA-binding protein (RBP), cause neuronal degeneration in Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal Lobar Degeneration (FTLD), two incurable neurological diseases. However, the function of FUS in neurons is not well understood. To uncover the impact of FUS in the neuronal transcriptome, we used high-throughput sequencing of immunoprecipitated and cross-linked RNA (HITS-CLIP) of FUS in human brains and mouse neurons differentiated from embryonic stem cells, coupled with RNA-seq and FUS knockdowns. We report conserved neuronal RNA targets and networks that are regulated by FUS. We find that FUS regulates splicing of genes coding for RBPs by binding to their highly conserved introns. Our findings have important implications for understanding the impact of FUS in neurodegenerative diseases and suggest that perturbations of FUS can impact the neuronal transcriptome via perturbations of RBP transcripts.

リンク情報
DOI
https://doi.org/10.1261/rna.037804.112
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/23389473
PubMed Central
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3677260
ID情報
  • DOI : 10.1261/rna.037804.112
  • ISSN : 1355-8382
  • PubMed ID : 23389473
  • PubMed Central 記事ID : PMC3677260

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