ArticleMolecular brain2020
Core transcriptional regulatory circuits in prion diseases.
Article in Molecular brain, 2020. 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, 23 citations in OpenAlex.
- Microglia-specific NF-κB signaling is a critical regulator of prion-induced glial inflammation and neuronal loss.PLoS pathogens · 2025Article
- Biological characteristics and transcriptomic profile of adipose-derived mesenchymal stem cells isolated from prion-infected murine model.Stem cell research & therapy · 2025Article
- Bioinformatics analysis of electroacupuncture treatment for ischemic stroke: exploring transcriptional regulatory mechanisms mediated by super-enhancers.Frontiers in neuroscience · 2025Article
- Expression of Toll-like receptors in the cerebellum during pathogenesis of prion disease.Frontiers in behavioral neuroscience · 2024Article
- Genomic, transcriptomic and RNA editing analysis of human MM1 and VV2 sporadic Creutzfeldt-Jakob disease.Acta neuropathologica communications · 2022Article
- Article
- Prion potentiation after life-long dormancy in mice devoid of PrP.Brain communications · 2021Article
- MicroRNA Alterations in a Tg501 Mouse Model of Prion Disease.Biomolecules · 2020Article
- RNA-seq and network analysis reveal unique glial gene expression signatures during prion infection.Molecular brain · 2020Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Complex diseases involve dynamic perturbations of pathophysiological processes during disease progression. Transcriptional programs underlying such perturbations are unknown in many diseases. Here, we present core transcriptional regulatory circuits underlying early and late perturbations in prion disease. We first identified cellular processes perturbed early and late using time-course gene expression data from three prion-infected mouse strains. We then built a transcriptional regulatory network (TRN) describing regulation of early and late processes. We found over-represented feed-forward loops (FFLs) comprising transcription factor (TF) pairs and target genes in the TRN. Using gene expression data of brain cell types, we further selected active FFLs where TF pairs and target genes were expressed in the same cell type and showed correlated temporal expression changes in the brain. We finally determined core transcriptional regulatory circuits by combining these active FFLs. These circuits provide insights into transcriptional programs for early and late pathophysiological processes in prion disease.
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