The failure of B cells to induce non-canonical MYD88 splice variants correlates with lymphomagenesis via sustained NF-κB signaling
Y. Cardona Gloria, S. H. Bernhart, S. Fillinger, O.-O. Wolz, S. Dickhöfer, J. Admard, S. Ossowski, S. Nahnsen, R. Siebert, A. N. Weber
The paper shows that B cells lack a negative feedback loop that normally limits TLR signaling through MYD88 splice variants, leading to sustained NF-κB activation and lymphomagenesis.
bioRxiv · Jun 18, 2020Cancer Biology