ArticleThe Journal of biological chemistry2016
The Coronary Artery Disease-associated Coding Variant in Zinc Finger C3HC-type Containing 1 (ZC3HC1) Affects Cell Cycle Regulation.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Prioritization of causal genes for coronary artery disease based on cumulative evidence from experimental and in silico studies.Scientific reports · 2020Pooled it
- Dissecting shared genetic architecture between pan-cancer and aging-related traits: a genome-wide cross-trait analysis.Biogerontology · 2026Article
- Causal relationships between four types of lipids and breast cancer risk with potential mediators: evidence from Mendelian randomization study and bioinformatics analysis.Discover oncology · 2025Article
- Advances in the understanding of nuclear pore complexes in human diseases.Journal of cancer research and clinical oncology · 2024Review
- An evolutionarily conserved bimodular domain anchors ZC3HC1 and its yeast homologue Pml39p to the nuclear basket.Molecular biology of the cell · 2023Article
- Article
- Genetic colocalization atlas points to common regulatory sites and genes for hematopoietic traits and hematopoietic contributions to disease phenotypes.BMC medical genomics · 2020Article
- CAUSALdb: a database for disease/trait causal variants identified using summary statistics of genome-wide association studies.Nucleic acids research · 2020Article
- From Genotype to Phenotype: A Primer on the Functional Follow-up of Genome-Wide Association Studies in Cardiovascular Disease.Circulation. Genomic and precision medicine · 2018Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genome-wide association studies have to date identified multiple coronary artery disease (CAD)-associated loci; however, for most of these loci the mechanism by which they affect CAD risk is unclear. The CAD-associated locus 7q32.2 is unusual in that the lead variant, rs11556924, is not in strong linkage disequilibrium with any other variant and introduces a coding change in ZC3HC1, which encodes NIPA. In this study, we show that rs11556924 polymorphism is associated with lower regulatory phosphorylation of NIPA in the risk variant, resulting in NIPA with higher activity. Using a genome-editing approach we show that this causes an effective decrease in cyclin-B1 stability in the nucleus, thereby slowing its nuclear accumulation. By perturbing the rate of nuclear cyclin-B1 accumulation, rs11556924 alters the regulation of mitotic progression resulting in an extended mitosis. This study shows that the CAD-associated coding polymorphism in ZC3HC1 alters the dynamics of cell-cycle regulation by NIPA.
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