Rett Signaling Defect Addressed by Experimental Drug (IMAGE)

Cold Spring Harbor Laboratory

Rett Signaling Defect Addressed by Experimental Drug

Caption

Cartoon showing how, in healthy individuals (left side), nerve cell growth factor BDNF spurs signaling via the TRKB receptor in brain cells. The gene MECP2 keeps levels of PTP1B low, opening up the pathway. In Rett patients (right side), loss of MECP2 function enables PTP1B levels to rise substantially, in effect applying a "brake" to the pathway in which BDNF normally initiates signaling via TRKB. An experimental drug developed by CSHL's Tonks lab inhibits PTP1B in mice that model Rett syndrome, effectively releasing the brake on BDNF-TRKB signaling. Corresponding reversals in Rett-like symptoms ensued. MECP2 suppresses expression of PTP1B, which augments BDNF-induced signaling through the TRKB protein tyrosine kinase. Functional loss of MECP2 in Rett syndrome results in an increase in levels of PTP1B, which attenuates BDNF-TRKB signaling

Credit

Tonks Lab, CSHL

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