A long nuclear‐retained non‐coding RNA regulates synaptogenesis by modulating gene expression

By Delphine Bernard, K. Prasanth, Vidisha Tripathi, Sabrina Colasse, Tetsuya Nakamura, Zhenyu Xuan, Michael Q. Zhang, F. Sedel, Laurent Jourdren, F. Coulpier and 3 more. EMBO Journal, 2010

727 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/15fa006a9cf728e169aa22b7b7dc2db225dfcca9

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Citations in the corpus

TANRIC: An interactive open platform to explore the function of lncRNAs in cancer (2015, unknown): “Emerging evidence has indicated that lncRNAs contribute to tumor initiation and progression through diverse mechanisms ranging from epigenetic regulation of key cancer genes (5, 6) and enhancer-associated activity (7) to posttranscriptional processing of mRNAs (8, 9).”
Long Non-coding RNAs in the Cytoplasm (2016, background): “For example, nuclear lncRNAs control the epigenetic state of particular genes [11], participate in transcriptional regulation [12], get involved in alternative splicing and constitute subnuclear compartments [13,14].”
Nuclear speckles. (2011, background): “Recent studies have implicated MALAT1 in the recruitment of SR splicing factors from nuclear speckles to sites of transcription (Bernard et al. 2010) and in the regulation of alternative splicing by modulating SF2/ ASF phosphorylation (Tripathi et al. 2010).”
Biogenesis and Function of Nuclear Bodies (2011, background): “Knockdown of Malat1 results in a reduction in the recruitment of SR family splicing factors to the transcription site of a transgene array, suggesting that Malat1 plays an important role in splicing factor dynamics [72].”
Long Noncoding RNAs: Past, Present, and Future (2013, background): “Its neighbor, NEAT2 or MALAT1, has been shown to localize serine/arginine (SR) splicing factors to a compartment called nuclear speckles where they can be stored and modified by phosphorylation (Bernard et al. 2010).”
Long Noncoding RNA MALAT1 Controls Cell Cycle Progression by Regulating the Expression of Oncogenic Transcription Factor B-MYB (2013, background): “In this context it is known that in mouse, MALAT1 shows a tissue-specific and developmental statespecific expression [43,58].”