Matches in DBpedia 2016-04 for { ?s ?p "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. 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."@en }
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- BACE1-AS abstract "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. 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.".
- Q4834493 abstract "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. 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.".