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Linking genetic variants to kidney disease via the epigenome
The largest GWAS for kidney function so far provided the starting point for integrated multi-stage annotation of genetic loci. Whole kidney and single-cell epigenomic information is crucial for translating GWAS information to the identification of causal genes and pathogenetic (and potentially targetable) cellular and molecular mechanisms of kidney disease.
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Genetic variants associated with subjective well-being, depressive symptoms, and neuroticism identified through genome-wide analyses
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Allelic imbalance of chromatin accessibility in cancer identifies candidate causal risk variants and their mechanisms
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Single-cell analyses define a continuum of cell state and composition changes in the malignant transformation of polyps to colorectal cancer
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A novel gene encoding an integral membrane protein is mutated in nephropathic cystinosis
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