National Institute of Health American Cancer Society National Science Foundation career award. T1 - Natural antisense RNA promotes 3′ end processing and maturation of MALAT1 lncRNA Together, our data demonstrate a novel feed-forward positive regulatory loop that is established to maintain the high cellular levels of MALAT1, and also unravel the existence of sense-antisense mediated regulatory mechanism for cellular lncRNAs that display RNase P-mediated 3′ end processing.",
Interestingly, TALAM1 is also positively regulated by MALAT1 at the level of both transcription and RNA stability. Conversely, overexpression of TALAM1 facilitates the cleavage reaction in trans. Depletion of TALAM1 leads to defects in the 3′ end cleavage reaction and compromises cellular accumulation of MALAT1. TALAM1 RNA preferentially localizes at the site of transcription, and also interacts with MALAT1 RNA. Here we characterize a broadly expressed natural antisense transcript at the MALAT1 locus, designated as TALAM1, that positively regulates MALAT1 levels by promoting the 3′ end cleavage and maturation of MALAT1 RNA. The regulation of this cleavage event is largely undetermined. Together, our data demonstrate a novel feed-forward positive regulatory loop that is established to maintain the high cellular levels of MALAT1, and also unravel the existence of sense-antisense mediated regulatory mechanism for cellular lncRNAs that display RNase P-mediated 3′ end processing.Ībstract = "The RNase P-mediated endonucleolytic cleavage plays a crucial role in the 3′ end processing and cellular accumulation of MALAT1, a nuclear-retained long noncoding RNA that promotes malignancy.
The RNase P-mediated endonucleolytic cleavage plays a crucial role in the 3′ end processing and cellular accumulation of MALAT1, a nuclear-retained long noncoding RNA that promotes malignancy.
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