The study reveals the structure of inactive NINJ1 and its mechanism of inhibition, demonstrating that it forms dimers that prevent premature cell membrane rupture.
Using cryogenic electron microscopy, we established that inactive NINJ1 creates face-to-face homodimers, which effectively sequester the hydrophilic face necessary for membrane rupture.
Our findings suggest that the stabilization of NINJ1 dimers is crucial for maintaining cell viability under steady-state conditions by preventing harmful membrane lysis.
Mutagenesis experiments indicate that disrupting NINJ1 dimerization could trigger membrane rupture, underscoring the importance of this dimerization in cellular homeostasis.
Collection
[
|
...
]