GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE311nnn/GSE311499/primaryOK200TranscriptomicsMus musculusExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE311499GEOGSEfalseTcf21 deletion from podocyte precursors as a model for congenital nephrotic syndromeHere, we establish a mouse model of congenital nephrotic syndrome (NS) by genetic deletion of transcription factor 21 (Tcf21), a gene required for normal podocyte development, selectively from early podocyte precursors. Single cell transcriptomics of kidneys from these mice capture glomerular and tubulointerstitial changes that occur early in the course of NS and provide additional insights into: 1) the regulation of podocyte development and function by TCF21, 2) the effects of podocyte injury on other glomerular cells, and 3) the tubulointerstitial changes that occur in response to the glomerular dysfunction and associated massive proteinuria of podocytopathies.2026/05/04GSE311499GSM9326117GSM9326114GSM9326116GSM932611521103311499Mus musculus