GEO series
RNA-seq analysis of thick ascending limb (TAL) epithelium isolated from uromodulin (UMOD) deletion mutation and wild type (WT) kidney organoids with or without mesencephalic astrocyte-derived neurotrophic factor (MANF) overexpression
GSE329325
Homo sapiens
Expression profiling by high throughput sequencing
12 samples
2026/07/11
GPL34284
Summary
Autosomal dominant tubulointerstitial kidney disease due to uromodulin mutations (ADTKD-UMOD) is one of the leading hereditary kidney diseases. Currently there is no targeted treatment. To illuminate human relevance of mesencephalic astrocyte-derived neurotrophic factor (MANF)-based therapy, we have established patient induced pluripotent stem cell (iPSC)-derived kidney organoid model carrying UMOD p.H177-R185del, the leading mutation causing ADTKD. We have discovered that MANF can directly bind and repress ER calcium release channel IP3R1, thus enhancing AMPK-induced autophagy in a TRIB3-dependent manner. The therapeutic implication of this finding may well be extended to other protein misfolding diseases.
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