ST7-AS2

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In molecular biology, ST7 antisense RNA 2 (non-protein coding), also known as ST7-AS2 is a long non-coding RNA. In humans, it is found on chromosome 7 in a locus spanning a translocation breakpoint associated with autism. It is antisense to the ST7 gene. [1]

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<span class="mw-page-title-main">ST7</span> Protein-coding gene in the species Homo sapiens

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<span class="mw-page-title-main">KCNQ1OT1</span>

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<span class="mw-page-title-main">GNAS-AS1</span> Non-coding RNA in the species Homo sapiens

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In molecular biology, RFPL3 antisense RNA 1, also known as RFPL3-AS1 is a long non-coding RNA. In humans, it is on chromosome 22. It is antisense to the RFPL3 gene encoding a RING finger domain-containing protein. It may function in the post-transcriptional regulation of this gene.

In molecular biology, ST7 antisense RNA 1, also known as ST7-AS1 is a long non-coding RNA. In humans, it is found on chromosome 7 in a locus spanning a translocation breakpoint associated with autism. It is antisense to the ST7 gene.

In molecular biology, ST7 overlapping transcript 3, also known as ST7-OT3 is a long non-coding RNA. In humans, it is found on chromosome 7 in a locus spanning a translocation breakpoint associated with autism. It overlaps the ST7 gene, spanning intron 10 to exon 14 of ST7. Some isoforms of ST7 may use exons from ST7-OT3.

In molecular biology, ST7 overlapping transcript 4, also known as ST7-OT4 is a long non-coding RNA. In humans, it is found on chromosome 7 in a locus spanning a translocation breakpoint associated with autism. It contains at least 7 exons and overlaps the ST7 gene.

<span class="mw-page-title-main">Ube3a-ATS</span> Non-coding RNA in the species Homo sapiens

UBE3A-ATS/Ube3a-ATS (human/mouse), otherwise known as ubiquitin ligase E3A-ATS, is the name for the antisense DNA strand that is transcribed as part of a larger transcript called LNCAT at the Ube3a locus. The Ube3a locus is imprinted and in the central nervous system expressed only from the maternal allele. Silencing of Ube3a on the paternal allele is thought to occur through the Ube3a-ATS part of LNCAT, since non-coding antisense transcripts are often found at imprinted loci. The deletion and/or mutation of Ube3a on the maternal chromosome causes Angelman Syndrome (AS) and Ube3a-ATS may prove to be an important aspect in finding a therapy for this disease. While in patients with AS the maternal Ube3a allele is inactive, the paternal allele is intact but epigenetically silenced. If unsilenced, the paternal allele could be a source of active Ube3a protein in AS patients. Therefore, understanding the mechanisms of how Ube3a-ATS might be involved in silencing the paternal Ube3a may lead to new therapies for AS. This possibility has been demonstrated by a recent study where the drug topotecan, administered to mice suffering from AS, activated expression of the paternal Ube3a gene by lowering the transcription of Ube3a-ATS.

ncRNA therapy

A majority of the human genome is made up of non-protein coding DNA. It infers that such sequences are not commonly employed to encode for a protein. However, even though these regions do not code for protein, they have other functions and carry necessary regulatory information.They can be classified based on the size of the ncRNA. Small noncoding RNA is usually categorized as being under 200 bp in length, whereas long noncoding RNA is greater than 200bp. In addition, they can be categorized by their function within the cell; Infrastructural and Regulatory ncRNAs. Infrastructural ncRNAs seem to have a housekeeping role in translation and splicing and include species such as rRNA, tRNA, snRNA.Regulatory ncRNAs are involved in the modification of other RNAs.

References

  1. Vincent JB, Petek E, Thevarkunnel S, Kolozsvari D, Cheung J, Patel M, et al. (2002). "The RAY1/ST7 tumor-suppressor locus on chromosome 7q31 represents a complex multi-transcript system". Genomics. 80 (3): 283–294. doi:10.1006/geno.2002.6835. PMID   12213198.