Secretion is a second fate for p62 and is coupled to KEAP1/NRF2 signaling
Cells degrade the autophagy receptor p62/sequestosome 1 (SQSTM1) in lysosomes. By knocking the HiBiT peptide into the endogenous SQSTM1 locus, we show that export is a second, quantitatively comparable fate. Specifically, p62 leaves cells continuously inside membrane-enclosed carriers at a rate similar to that of LC3B. Blocking lysosomal degradation amplifies release through an ATG5- and…
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