A KDM6A–KLF10 reinforcing feedback mechanism aggravates diabetic podocyte dysfunction - Lin, Chun‐Liang; Hsu, Yung‐Chien; Huang, Yu‐Ting; Shih, Ya‐Hsueh; Wang, Ching‐Jen; Chiang, Wen‐Chih; Chang, Pey‐Jium (EMBO molecular medicine, 2019)
Keywords: Animals; Base Sequence; Cell Line, Transformed; Deoxyribonucleic acid; Diabetes; Diabetes mellitus; Diabetic Nephropathies - metabolism; Diabetic Nephropathies - pathology; Diabetic Nephropathies - physiopathology; Diabetic Nephropathies - urine; Diabetic nephropathy; DNA; DNA methylation; DNMT1 protein; Down-Regulation; Early Growth Response Transcription Factors - genetics; Early Growth Response Transcription Factors - metabolism; EMBO21; EMBO45; Enzymes; Epigenesis, Genetic; Epigenetics; Epithelial cells; Exosomes; Exosomes - metabolism; Experiments; Feedback; Feedback, Physiological; Gene expression; Histone Demethylases - genetics; Histone Demethylases - metabolism; Hospitals; Humans; KDM6A; Kidney - metabolism; Kidney - pathology; Kidney - physiopathology; Kidneys; KLF10; Kruppel-Like Transcription Factors - genetics; Kruppel-Like Transcription Factors - metabolism; Laboratory animals; Lysine; Male; Medical research; Membrane Proteins - metabolism; Methyltransferase; Mice, Inbred C57BL; Mice, Knockout; Nephropathy; Phenotype; podocyte dysfunction; Podocytes - metabolism; Podocytes - pathology; Promoter Regions, Genetic - genetics; Protein Binding; Proteins; Proteinuria; Renal function; Research Article; Signal transduction; Taiwan; KLF10; podocyte dysfunction; diabetic nephropathy; epigenetics; KDM6A