Genome-wide screening of circadian and non-circadian impact of Neat1 genetic deletion
Computational and Structural Biotechnology Journal, ISSN: 2001-0370, Vol: 19, Page: 2121-2132
2021
- 2Citations
- 10Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations2
- Citation Indexes2
- CrossRef2
- Captures10
- Readers10
- 10
Article Description
The functions of the long non-coding RNA, Nuclear enriched abundant transcript 1 (Neat1), are poorly understood. Neat1 is required for the formation of paraspeckles, but its respective paraspeckle-dependent or independent functions are unknown. Several studies including ours reported that Neat1 is involved in the regulation of circadian rhythms. We characterized the impact of Neat1 genetic deletion in a rat pituitary cell line. The mRNAs whose circadian expression pattern or expression level is regulated by Neat1 were identified after high-throughput RNA sequencing of the circadian transcriptome of wild-type cells compared to cells in which Neat1 was deleted by CRISPR/Cas9. The numerous RNAs affected by Neat1 deletion were found to be circadian or non-circadian, targets or non-targets of paraspeckles, and to be associated with many key biological processes showing that Neat1, in interaction with the circadian system or independently, could play crucial roles in key physiological functions through diverse mechanisms.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S2001037021001343; http://dx.doi.org/10.1016/j.csbj.2021.04.022; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85104480239&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/33995907; https://linkinghub.elsevier.com/retrieve/pii/S2001037021001343; https://dx.doi.org/10.1016/j.csbj.2021.04.022
Elsevier BV
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