A. Ashkenazi

This study modifies myeloid cells to elicit tumor-specific cytotoxicity using chimeric receptors that signal through IgM and bind tumor antigens.

The paper shows polyalanine disease mutations disrupt UBA6-USE1 interactions, impairing ubiquitination and affecting synaptic protein levels in neurons.

This study reveals that IRE1α activation involves reversible dimer-to-oligomer assembly in response to ER stress, with phosphorylation occurring after oligomerization.

The paper shows antigen-derived peptides activate IRE1α in dendritic cells, reducing MHC-I expression and cross-presentation, and demonstrates that IRE1 inhibition enhances anti-tumor immunity.

The paper identifies a noncanonical mRNA decay process, RIDDLE, mediated by IRE1α oligomers in cancer cells, which promotes survival by degrading mRNAs without XBP1-like endomotifs.

This study determines the in-situ structure of IRE1 oligomers in ER tubes using cryo-CLEM, revealing helical filaments formed by IRE1 lumenal domain dimers and suggesting positive feedback in IRE1 signaling.

The paper identifies Pumilio's role in protecting Xbp1spliced mRNA from RIDD by Ire1-mediated phosphorylation in Drosophila.

The paper identifies a neuronal circuit regulated by ER stress that suppresses germline differentiation in C. elegans via serotonin signaling and FLP-6 neuropeptide decay.

This study identifies phospholipid flipping as essential for annexin translocation from the inner to outer leaflet of the plasma membrane, with TMEM16F playing a key role.