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. 2017 Oct 23;37(6):756–767. doi: 10.1038/onc.2017.365

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Copyright © 2018 The Author(s)

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Model of NTSR2 function in B-CLL survival. In this schematic, NTSR2–TrkB–BDNF acts as a key regulator of B-CLL resistance to apoptosis. The NTSR2–TrkB interaction is strengthened upon BDNF stimulation, and triggers pro-survival pathways via phosphorylation of NTSR2, resulting in activation of the phosphorylation cascade of the Src and AKT kinases, as well as expression of the downstream anti-apoptotic proteins Bcl-xL and Bcl-2, leading to B-CLL cell survival and resistance to apoptosis (left panel). NTSR2 inhibition by siRNA-mediated mRNA depletion induces a drastic apoptotic cell death despite the presence of TrkB and BDNF, indicating that TrkB plays a role as a second messenger in NTSR2-mediated apoptotic resistance in B-CLL. NTSR2 deactivation by SR142948A suppresses the ability of NTSR2 to recruit the Giα1/2 subunits upon BDNF stimulation, leading to the suppression of NTSR2 phosphorylation and a decrease in the expression of anti-apoptotic proteins, thereby increasing B-CLL apoptosis (right panel). PM, plasma membrane.