ArticleBiochimica et biophysica acta2013
Starvation actively inhibits splicing of glucose-6-phosphate dehydrogenase mRNA via a bifunctional ESE/ESS element bound by hnRNP K.
Article in Biochimica et biophysica acta, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Long non-coding RNA LINC01532 sustains redox homeostasis and accelerates lenvatinib resistance in hepatocellular carcinoma.Journal of advanced research · 2025Article
- Cells resist starvation through a nutrient stress splice switch.Nucleic acids research · 2025Article
- Oncogenic SRSF3 in health and diseases.International journal of biological sciences · 2023Review
- Pharmacological and physiological activation of AMPK improves the spliceopathy in DM1 mouse muscles.Human molecular genetics · 2018Article
- Intersections of post-transcriptional gene regulatory mechanisms with intermediary metabolism.Biochimica et biophysica acta. Gene regulatory mechanisms · 2017Review
- Ubiquitination of hnRNPA1 by TRAF6 links chronic innate immune signaling with myelodysplasia.Nature immunology · 2017Article
- Differential Impacts of Alternative Splicing Networks on Apoptosis.International journal of molecular sciences · 2016Review
- Impacts of Alternative Splicing Events on the Differentiation of Adipocytes.International journal of molecular sciences · 2015Review
- Role of precursor mRNA splicing in nutrient-induced alterations in gene expression and metabolism.The Journal of nutrition · 2015Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Regulated expression of glucose-6-phosphate dehydrogenase (G6PD) is due to changes in the rate of pre-mRNA splicing and not changes in its transcription. Starvation alters pre-mRNA splicing by decreasing the rate of intron removal, leading to intron retention and a decrease in the accumulation of mature mRNA. A regulatory element within exon 12 of G6PD pre-mRNA controls splicing efficiency. Starvation caused an increase in the expression of heterogeneous nuclear ribonucleoprotein (hnRNP) K protein and this increase coincided with the increase in the binding of hnRNP K to the regulatory element and a decrease in the expression of G6PD mRNA. HnRNP K bound to two C-rich motifs forming an ESS within exon 12. Overexpression of hnRNP K decreased the splicing and expression of G6PD mRNA, while siRNA-mediated depletion of hnRNP K caused an increase in the splicing and expression of G6PD mRNA. Binding of hnRNP K to the regulatory element was enhanced in vivo by starvation coinciding with a decrease in G6PD mRNA. HnRNP K binding to the C-rich motifs blocked binding of serine-arginine rich, splicing factor 3 (SRSF3), a splicing enhancer. Thus hnRNP K is a nutrient regulated splicing factor responsible for the inhibition of the splicing of G6PD during starvation.
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