ArticleNeurobiology of aging2018
An alternative transcript of the Alzheimer's disease risk gene SORL1 encodes a truncated receptor.
Article in Neurobiology of aging, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Finding memo: versatile interactions of the VPS10p-Domain receptors in Alzheimer's disease.Molecular neurodegeneration · 2022Pooled it
- A genetically modified minipig model for Alzheimer's disease with SORL1 haploinsufficiency.Cell reports. Medicine · 2022Article
- Expression of an alternatively spliced variant of SORL1 in neuronal dendrites is decreased in patients with Alzheimer's disease.Acta neuropathologica communications · 2021Article
- Modulation of Small RNA Signatures in Schwann-Cell-Derived Extracellular Vesicles by the p75 Neurotrophin Receptor and Sortilin.Biomedicines · 2020Article
- Sorting Out the Role of theJournal of Alzheimer's disease reports · 2020Review
- Sequence and Evolutionary Features for the Alternatively Spliced Exons of Eukaryotic Genes.International journal of molecular sciences · 2019Review
- Cerebral amyloid angiopathy-related inflammation: a case report presenting with a rare variant in SORL1 gene.BMC neurology · 2019Article
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12 authors.
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Abstract
SORL1 encodes a 250-kDa protein named sorLA, a functional sorting receptor for the amyloid precursor protein (APP). Several single nucleotide polymorphisms of the gene SORL1, encoding sorLA, are genetically associated with Alzheimer's disease (AD). In the existing literature, SORL1 is insufficiently described at the transcriptional level, and there is very limited amount of functional data defining different transcripts. We have characterized a SORL1 transcript containing a novel exon 30B. The transcript is expressed in most brain regions with highest expression in the temporal lobe and hippocampus. Exon 30B is spliced to exon 31, leading to a mature transcript that encodes an 829 amino acid sorLA receptor. This receptor variant lacks the binding site for APP and is unlikely to function in APP sorting. This transcript is expressed in equal amounts in the cerebellum from AD and non-AD individuals. Our data describe a transcript that encodes a truncated sorLA receptor, suggesting novel neuronal functions for sorLA and that alternative transcription provides a mechanism for SORL1 activity regulation.
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