The abstract is read at the publisher; the summary is JClub's.
TNIP1 functions as an aggrephagy receptor by accumulating at polyubiquitinated protein aggregates under proteotoxic stress and assembling clearance machinery.
- Why it matters: Defects in selective autophagy receptors are linked to neurodegeneration, metabolic disorders, and cancer, but TNIP1’s role in aggregate removal was unclear.
- What they did: In proteotoxic stress models, TNIP1 depletion reduced protein aggregate clearance and increased axonal degeneration; TNIP1 promoted recruitment of SQSTM1/p62 and TAX1BP1 to aggregates.
- The result: TNIP1 expression is reduced in ALS patients with TDP-43 inclusion pathology, and an ALS-associated TNIP1 mutant impaired binding to TDP-43 aggregates and failed to rescue autophagy-mediated degradation.
The findingWhy it mattersWhat they didThe result
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