The RNA-binding protein BICC1 can act as a genetic disease modifier for kidney cyst formation, potentially explaining the high variability of disease onset and severity in autosomal-dominant polycystic kidney disease patients.
Three newly developed biosensors demonstrate that the C-terminal tail of α-tubulin does not freely extend from the microtubule surface as widely thought, but rather is inaccessible along most microtubules in cells.
Small-molecule mitochondrial transcription factor A modulators stabilize mtDNA, preventing cytosolic escape and suppressing cGAS-STING interferon signaling, while improving bioenergetics and fibrosis markers in disease models.
