ArticleBioinformatics (Oxford, England)2018
ZCCHC17 is a master regulator of synaptic gene expression in Alzheimer's disease.
Article in Bioinformatics (Oxford, England), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- ZCCHC17: a target for synaptic dysfunction and neuronal excitability in Alzheimer's disease.Frontiers in aging neuroscience · 2026Review
- An analysis of RNA quality metrics in human brain tissue.Journal of neuropathology and experimental neurology · 2025Article
- ZCCHC17 knockdown phenocopies Alzheimer's disease-related loss of synaptic proteins and hyperexcitability.Journal of neuropathology and experimental neurology · 2024Article
- ZCCHC17 Modulates Neuronal RNA Splicing and Supports Cognitive Resilience in Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Skeletal muscle transcriptomics identifies common pathways in nerve crush injury and ageing.Skeletal muscle · 2022Article
- Article
- The distinct roles of zinc finger CCHC-type (ZCCHC) superfamily proteins in the regulation of RNA metabolism.RNA biology · 2021Review
- Age-dependent shift in the de novo proteome accompanies pathogenesis in an Alzheimer's disease mouse model.Communications biology · 2021Article
- ZCCHC17 Served as a Predictive Biomarker for Prognosis and Immunotherapy in Hepatocellular Carcinoma.Frontiers in oncology · 2021Article
- Identification of RNA-Binding Proteins as Targetable Putative Oncogenes in Neuroblastoma.International journal of molecular sciences · 2020Article
- Article
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Authors and funding
5 authors.
Funding
Abstract
Motivation: In an effort to better understand the molecular drivers of synaptic and neurophysiologic dysfunction in Alzheimer's disease (AD), we analyzed neuronal gene expression data from human AD brain tissue to identify master regulators of synaptic gene expression. Results: Master regulator analysis identifies ZCCHC17 as normally supporting the expression of a network of synaptic genes, and predicts that ZCCHC17 dysfunction in AD leads to lower expression of these genes. We demonstrate that ZCCHC17 is normally expressed in neurons and is reduced early in the course of AD pathology. We show that ZCCHC17 loss in rat neurons leads to lower expression of the majority of the predicted synaptic targets and that ZCCHC17 drives the expression of a similar gene network in humans and rats. These findings support a conserved function for ZCCHC17 between species and identify ZCCHC17 loss as an important early driver of lower synaptic gene expression in AD. Availability and implementation: Matlab and R scripts used in this paper are available at https://github.com/afteich/AD_ZCC. Contact: aft25@cumc.columbia.edu. Supplementary information: Supplementary data are available at Bioinformatics online.
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