Yongfang Zhang

TL;DR: It is demonstrated that chronic antidepressant treatment induces CRE-mediated gene expression in a neuroanatomically differentiated pattern and further elucidate the molecular mechanisms underlying the actions of these widely used therapeutic agents.

TL;DR: A novel mechanism by which differential NMDAR stimulation regulates STEP61 to promote either ERK1/2 or p38 activation is suggested and calpain cleavage of STEP61 is identified as a valid target for the development of neuroprotective therapy.

TL;DR: It is shown that STEP61 levels are progressively increased in the cortex of Tg2576 mice over the first year, as well as in prefrontal cortex of human AD brains, revealing a novel mechanism by which Aβ-mediated accumulation of STEP61 results in increased internalization of NR1/NR2B receptor that may contribute to the cognitive deficits in AD.

TL;DR: A role for STEP is suggested in the regulation of AMPAR trafficking after it was found that (RS)-3,5-dihydroxyphenylglycine (DHPG) stimulation triggered a dose-dependent increase in STEP translation in hippocampal slices and synaptoneurosomes.

TL;DR: Genetic manipulations are used to reduce STEP activity in a triple transgenic AD mouse model and show that a decrease in STEP levels reverses cognitive and cellular deficits observed in these mice, suggesting that STEP inhibitors may prove therapeutic for this devastating disorder.