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Loss of Dnmt3a and Dnmt3b resulted in failure to silence developmental genes. We also found that fetal-enhancer regions methylated by Dnmt3a and Dnmt3b were enriched for kidney disease genetic risk loci. Methylation patterns of kidneys from patients with CKD showed defects similar to those in mice with Dnmt3a and Dnmt3b deletion. CONCLUSIONS Our results indicate a potential locus-specific convergence of genetic, epigenetic, and developmental elements in kidney disease development. Copyright © 2020 by the American Society of Nephrology.
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