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- W2073654740 abstract "We have combined genetic and biochemical approaches to analyze the function of the RNA-binding protein Nova-1, the paraneoplastic opsoclonus-myoclonus ataxia (POMA) antigen. Nova-1 null mice die postnatally from a motor deficit associated with apoptotic death of spinal and brainstem neurons. Nova-1 null mice show specific splicing defects in two inhibitory receptor pre-mRNAs, glycine alpha2 exon 3A (GlyRalpha2 E3A) and GABA(A) exon gamma2L. Nova protein in brain extracts specifically bound to a previously identified GlyRalpha2 intronic (UCAUY)3 Nova target sequence, and Nova-1 acted directly on this element to increase E3A splicing in cotransfection assays. We conclude that Nova-1 binds RNA in a sequence-specific manner to regulate neuronal pre-mRNA alternative splicing; the defect in splicing in Nova-1 null mice provides a model for understanding the motor dysfunction in POMA." @default.
- W2073654740 created "2016-06-24" @default.
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- W2073654740 date "2000-02-01" @default.
- W2073654740 modified "2023-10-10" @default.
- W2073654740 title "Nova-1 Regulates Neuron-Specific Alternative Splicing and Is Essential for Neuronal Viability" @default.
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- W2073654740 doi "https://doi.org/10.1016/s0896-6273(00)80900-9" @default.
- W2073654740 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/10719891" @default.
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