ArticleSchizophrenia bulletin2024
Unraveling NEK4 as a Potential Drug Target in Schizophrenia and Bipolar I Disorder: A Proteomic and Genomic Approach.
Article in Schizophrenia bulletin, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- Uncovering causal associations between plasma proteins and psychiatric disorders and identifying comorbidity biomarkers: a mendelian randomization study.European archives of psychiatry and clinical neuroscience · 2026Article
- Shared genetic architecture of psychiatric disorders and ocular diseases: Evidence from genome-wide analyses.IBRO neuroscience reports · 2026Article
- MKRN1 as a prioritized drug target for postpartum depression: evidence from druggable proteome profiling and multi-layer validation.Translational psychiatry · 2026Article
- Identification of novel proteins associated with intelligence by integrating genome-wide association data and human brain proteomics.PloS one · 2025Article
- NEK4 suppresses cell proliferation in BT20 triple-negative breast cancer cells by diminishing expression of cell cycle genes, while its depletion mitigates proliferation in other cell lines.Frontiers in oncology · 2025Article
- NEK4 modulates circadian fluctuations of emotional behaviors and synaptogenesis in male mice.Nature communications · 2024Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
background and hypothesisInvestigating the shared brain protein and genetic components of schizophrenia (SCZ) and bipolar I disorder (BD-I) presents a unique opportunity to understand the underlying pathophysiological processes and pinpoint potential drug targets. STUDY
designTo identify overlapping susceptibility brain proteins in SCZ and BD-I, we carried out proteome-wide association studies (PWAS) and Mendelian Randomization (MR) by integrating human brain protein quantitative trait loci with large-scale genome-wide association studies for both disorders. We utilized transcriptome-wide association studies (TWAS) to determine the consistency of mRNA-protein dysregulation in both disorders. We applied pleiotropy-informed conditional false discovery rate (pleioFDR) analysis to identify common risk genetic loci for SCZ and BD-I. Additionally, we performed a cell-type-specific analysis in the human brain to detect risk genes notably enriched in distinct brain cell types. The impact of risk gene overexpression on dendritic arborization and axon length in neurons was also examined. STUDY
resultsOur PWAS identified 42 proteins associated with SCZ and 14 with BD-I, among which NEK4, HARS2, SUGP1, and DUS2 were common to both conditions. TWAS and MR analysis verified the significant risk gene NEK4 for both SCZ and BD-I. PleioFDR analysis further supported genetic risk loci associated with NEK4 for both conditions. The cell-type specificity analysis revealed that NEK4 is expressed on the surface of glutamatergic neurons, and its overexpression enhances dendritic arborization and axon length in cultured primary neurons.
conclusionsThese findings underscore a shared genetic origin for SCZ and BD-I, offering novel insights for potential therapeutic target identification.
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