ArticleMolecular and cellular biology2010
HMGA1a trapping of U1 snRNP at an authentic 5' splice site induces aberrant exon skipping in sporadic Alzheimer's disease.
Article in Molecular and cellular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Meta-Analysis of Gene Expression Changes in the Blood of Patients with Mild Cognitive Impairment and Alzheimer's Disease Dementia.International journal of molecular sciences · 2019Pooled it
- HMGA proteins in the nervous system: role in brain tumorigenesis and neurodegeneration.Cell death discovery · 2026Review
- The plasma peptides of Alzheimer's disease.Clinical proteomics · 2021Article
- Phylogenetic comparison and splice site conservation of eukaryotic U1 snRNP-specific U1-70K gene family.Scientific reports · 2021Article
- High-mobility group A1 proteins may be involved in estrogen receptor status of breast cancer.Translational cancer research · 2020Article
- Innate Immunity: A Common Denominator between Neurodegenerative and Neuropsychiatric Diseases.International journal of molecular sciences · 2020Review
- HMGA1a Induces Alternative Splicing of theFrontiers in molecular biosciences · 2018Article
- Saturation mutagenesis reveals manifold determinants of exon definition.Genome research · 2018Article
- U1 snRNP Alteration and Neuronal Cell Cycle Reentry in Alzheimer Disease.Frontiers in aging neuroscience · 2018Review
- A mechanism underlying position-specific regulation of alternative splicing.Nucleic acids research · 2017Article
- RBM24 promotes U1 snRNP recognition of the mutated 5' splice site in theRNA (New York, N.Y.) · 2017Article
- The High Mobility Group A1 (HMGA1) Transcriptome in Cancer and Development.Current molecular medicine · 2016Review
- HnRNP L and hnRNP LL antagonistically modulate PTB-mediated splicing suppression of CHRNA1 pre-mRNA.Scientific reports · 2013Article
- Pick one, but be quick: 5' splice sites and the problems of too many choices.Genes & development · 2013Review
- Tailoring of membrane proteins by alternative splicing of pre-mRNA.Biochemistry · 2012Review
- Genomics of Dementia: APOE- and CYP2D6-Related Pharmacogenetics.International journal of Alzheimer's disease · 2012Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Overexpression of high-mobility group A protein 1a (HMGA1a) causes aberrant exon 5 skipping of the Presenilin-2 (PS2) pre-mRNA, which is almost exclusively detected in patients with sporadic Alzheimer's disease. An electrophoretic mobility shift assay confirmed aberrant U1 small nuclear ribonucleoprotein particle (snRNP)-HMGA1a complex formation (via the U1-70K component), with RNA containing a specific HMGA1a-binding site and an adjacent 5' splice site. Psoralen cross-linking analysis demonstrated that the binding of HMGA1a adjacent to the 5' splice site induces unusually extended association of U1 snRNP to the 5' splice site. As a result, spliceosome assembly across either the intron or the exon is arrested at an early ATP-independent stage. We conclude that the HMGA1a-induced aberrant exon skipping is caused by impaired dissociation of U1 snRNP from the 5' splice site, leading to a defect in exon definition. The proposed molecular mechanism has profound implications for other known posttranscriptional modulation strategies in various organisms, all of which are triggered by aberrant U1 snRNP binding.
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