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BACE1 antisense RNA
~2 kb; two splice variants were identified for human and mouse BACE1-AS. Transcribed from an intron of the beta-secretase-1 (BACE1) gene in antisense direction it also completely overlapps exon 6 of BACE-1 (Faghihi (2008)).
BACE1AS expression is elevated in Alzheimers disease (Faghihi (2008)). It was shown to regulate BACE1 mRNA and protein expression in vitro and in vivo ie: over-expression, shRNA and siRNA knockdown of BACE1AS affected BACE1 expression, influencing amyloid-beta 1-42 levels (Faghihi (2008)). It was proposed that BACE1-AS and BACE1 form an RNA duplex and this increases the stability of BACE1 (Faghihi (2008)). More recently, it was suggested that BACE1AS may prevent translational repression of BACE1 mRNA by miR-485-5p via masking the binding site for the microRNA. Supporting this hypothesis, BACE1AS over-expression prevented miRNA-induced suppression (Faghihi (2010)). Expression of BACE1-AS as well as miR-485-5p are dysregulated in RNA samples from Alzheimer's disease subjects compared to control individuals (Faghihi (2010)). BACE1-AS may also be involved in sporadic inclusion-body myositis (s-IBM), whose muscle-fiber phenotype shares molecular similarities with Alzheimer-disease brain (including increased BACE1 protein). BACE1-AS and BACE1 transcripts are significantly increased in s-IBM, and experimental induction of endoplasmic reticulum (ER) stress increased both BACE1-AS and BACE1 transcripts. These results suggest that ER stress and increased BACE1-AS expression may be involved in s-IBM (Nogalska (2010)).
BACE1 and BACE1AS are co-expressed in a wide range of tissues and cell lines in mice and humans. BACE1 mRNA expression levels are higher than BACE1-AS levels across all tissues examined, except in Alzheimer's disease (AD) where, in contrast, BACE1-AS is expressed at a higher level in brain. Bace1 and Bace1-AS transcripts are also observed in various regions of the mouse brain (Faghihi (2008), Faghihi (2010)). Several cell stressors, such as high temperature, serum starvation, amyloid-beta 1-42, H2O2 and high glucose, specifically increase BACE1-AS RNA and BACE1 protein levels (Faghihi (2008)). Showed increased expression in sporadic inclusion-body myositis (s-IBM) muscle fibers (possibly caused by endoplasmic reticulum stress). Nevertheless, unlike in AD and AD-transgenic mouse brain samples in which BACE1-AS transcript was increased more than the sense BACE1 transcript , in s-IBM muscle biopsies the reversed was found (Nogalska (2010)). Mouse RNA stability was very close to median for lncRNAs, with a half-life 3.6 hr in N2A (neuroblastoma) cells (Clark (2012)).
BACE1-AS transcript has been identified in mouse and humans, with a conserved association with BACE1 across species (Faghihi (2008)).
Mouse AK078885 and human CB960709 full-length clones are unspliced and are ~1.2kb- and 798b-long, but two spliced variants were extended by RACE by Faghini et al., 2008.
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Allelic Information and Variation
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Labs working on this lncRNA
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