| BACE1-AS | |||||||||||||||||||||||||||||||||||||||||||||||||||
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| Identifiers | |||||||||||||||||||||||||||||||||||||||||||||||||||
| Aliases | BACE1-AS, BACE1 antisense RNA, BACE1-AS1, FJ573250, NCRNA00177 | ||||||||||||||||||||||||||||||||||||||||||||||||||
| External IDs | OMIM: 614263 GeneCards: BACE1-AS | ||||||||||||||||||||||||||||||||||||||||||||||||||
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| Wikidata | |||||||||||||||||||||||||||||||||||||||||||||||||||
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BACE1-AS, also known as BACE1 antisense RNA (non-protein coding), is a human gene at 11q23.3 encoding a long noncoding RNA molecule. It is transcribed from the opposite strand to BACE1 and is upregulated in patients with Alzheimer's disease.[2] BACE1-AS regulates the expression of BACE1 by increasing BACE1 mRNA stability and generating additional BACE1 through a post-transcriptional feed-forward mechanism. By the same mechanism it also raises concentrations of beta amyloid, the main constituent of senile plaques. BACE1-AS concentrations are elevated in subjects with Alzheimer's disease and in amyloid precursor protein transgenic mice.
Knocking down BACE1-AS reduces amyloid production and plaque deposition.[3]
References
- ↑ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
- ↑ Faghihi MA, Modarresi F, Khalil AM, Wood DE, Sahagan BG, Morgan TE, Finch CE, St Laurent G, Kenny PJ, Wahlestedt C (2008). "Expression of a noncoding RNA is elevated in Alzheimer's disease and drives rapid feed-forward regulation of beta-secretase". Nat Med. 14 (7): 723–730. doi:10.1038/nm1784. PMC 2826895. PMID 18587408.
- ↑ Modarresi F, Faghihi MA, Patel NS, Sahagan BG, Wahlestedt C, Lopez-Toledano MA (2011). "Knockdown of BACE1-AS Nonprotein-Coding Transcript Modulates Beta-Amyloid-Related Hippocampal Neurogenesis". Int. J. Alzheimer's Dis. 2011: 929042. doi:10.4061/2011/929042. PMC 3139208. PMID 21785702.
External links
- Human BACE1-AS genome location and BACE1-AS gene details page in the UCSC Genome Browser.
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