9 research outputs found
Quest for Universal Standards of Judicial Integrity: Some Reflections on the Bangalore Principles
No full text
Predicting State Police Officer Performance in the Field Training Officer Program: What Can We Learn from the Cadetâs Performance in the Training Academy?
No full text
Black Bodies on the Ground: Policing Disparities in the African American CommunityâAn Analysis of Newsprint From January 1, 2015, Through December 31, 2015
No full textThe impact of Carpobrotus cfr. acinaciformis (L.) L. Bolus on soil nutrients, microbial communities structure and native plant communities in Mediterranean ecosystems
No full textRecommended from our members
The chromatin landscape of healthy and injured cell types in the human kidney
No full textThere is a need to define regions of gene activation or repression that control human kidney cells in states of health, injury, and repair to understand the molecular pathogenesis of kidney disease and design therapeutic strategies. Comprehensive integration of gene expression with epigenetic features that define regulatory elements remains a significant challenge. We measure dual single nucleus RNA expression and chromatin accessibility, DNA methylation, and H3K27ac, H3K4me1, H3K4me3, and H3K27me3 histone modifications to decipher the chromatin landscape and gene regulation of the kidney in reference and adaptive injury states. We establish a spatially-anchored epigenomic atlas to define the kidneyâs active, silent, and regulatory accessible chromatin regions across the genome. Using this atlas, we note distinct control of adaptive injury in different epithelial cell types. A proximal tubule cell transcription factor network of ELF3, KLF6, and KLF10 regulates the transition between health and injury, while in thick ascending limb cells this transition is regulated by NR2F1. Further, combined perturbation of ELF3, KLF6, and KLF10 distinguishes two adaptive proximal tubular cell subtypes, one of which manifested a repair trajectory after knockout. This atlas will serve as a foundation to facilitate targeted cell-specific therapeutics by reprogramming gene regulatory networks. © 2024, The Author(s).Open access journalThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]
