ArticleNucleic acids research2012
Control of alternative splicing by forskolin through hnRNP K during neuronal differentiation.
Article in Nucleic acids research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 62 citations in OpenAlex.
- Prion propagation is controlled by a hierarchical network involving the nuclear Tfap2c and hnRNP K factors and the cytosolic mTORC1 complex.PLoS pathogens · 2026Article
- TDP43 and hnRNP K Regulate Alternative Splicing of DNAJC5.Cell biology international · 2026Article
- KATMAP infers splicing factor activity and regulatory targets from knockdown data.Nature biotechnology · 2025Article
- pyPAGE: A framework for Addressing biases in gene-set enrichment analysis-A case study on Alzheimer's disease.PLoS computational biology · 2024Article
- hnRNPs: roles in neurodevelopment and implication for brain disorders.Frontiers in molecular neuroscience · 2024Review
- Review
- Development of a mammalian neurosensory full-thickness skin equivalent and its application to screen sensitizing stimuli.Bioengineering & translational medicine · 2023Article
- Regulation of Pre-mRNA Splicing: Indispensable Role of Post-Translational Modifications of Splicing Factors.Life (Basel, Switzerland) · 2023Review
- Heterogeneous nuclear ribonucleoprotein K is overexpressed in acute myeloid leukemia and causes myeloproliferation in mice via alteredNAR cancer · 2022Article
- Kinetics of mRNA nuclear export regulate innate immune response gene expression.Nature communications · 2022Article
- HnRNPK maintains single strand RNA through controlling double-strand RNA in mammalian cells.Nature communications · 2022Article
- Review
- Oncogenic dysregulation of pre-mRNA processing by protein kinases: challenges and therapeutic opportunities.The FEBS journal · 2021Review
- Nuclear speckle specific hnRNP D-like prevents age- and AD-related cognitive decline by modulating RNA splicing.Molecular neurodegeneration · 2021Article
- A Novel Long Noncoding RNA lincRNA00892 Activates CD4Frontiers in pharmacology · 2021Article
- Article
- Diagnostic utility of integrated analysis of exome and transcriptome: Successful diagnosis of Au-Kline syndrome in a patient with submucous cleft palate, scaphocephaly, and intellectual disabilities.Molecular genetics & genomic medicine · 2020Article
- RNA-binding motifs of hnRNP K are critical for induction of antibody diversification by activation-induced cytidine deaminase.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- RNA-Binding Proteins in Acute Leukemias.International journal of molecular sciences · 2020Review
- Molecular mechanism of nur77 gene expression and downstream target genes in the early stage of forskolin-induced differentiation in PC12 cells.Scientific reports · 2020Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The molecular basis of cell signal-regulated alternative splicing at the 3' splice site remains largely unknown. We isolated a protein kinase A-responsive ribonucleic acid (RNA) element from a 3' splice site of the synaptosomal-associated protein 25 (Snap25) gene for forskolin-inhibited splicing during neuronal differentiation of rat pheochromocytoma PC12 cells. The element binds specifically to heterogeneous nuclear ribonucleo protein (hnRNP) K in a phosphatase-sensitive way, which directly competes with the U2 auxiliary factor U2AF65, an essential component of early spliceosomes. Transcripts with similarly localized hnRNP K target motifs upstream of alternative exons are enriched in genes often associated with neurological diseases. We show that such motifs upstream of the Runx1 exon 6 also bind hnRNP K, and importantly, hnRNP K is required for forskolin-induced repression of the exon. Interestingly, this exon encodes the peptide domain that determines the switch of the transcriptional repressor/activator activity of Runx1, a change known to be critical in specifying neuron lineages. Consistent with an important role of the target genes in neurons, knocking down hnRNP K severely disrupts forskolin-induced neurite growth. Thus, through hnRNP K, the neuronal differentiation stimulus forskolin targets a critical 3' splice site component of the splicing machinery to control alternative splicing of crucial genes. This also provides a regulated direct competitor of U2AF65 for cell signal control of 3' splice site usage.
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