u-0126 and Fragile-X-Syndrome

u-0126 has been researched along with Fragile-X-Syndrome* in 1 studies

Other Studies

1 other study(ies) available for u-0126 and Fragile-X-Syndrome

ArticleYear
Lovastatin corrects ERK pathway hyperactivation in fragile X syndrome: potential of platelet's signaling cascades as new outcome measures in clinical trials.
    Biomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals, 2016, Volume: 21, Issue:6

    To establish whether platelets from fragile X syndrome (FXS) individuals recapitulate FXS mouse neurons' defects in ERK and Akt pathways, and to evaluate the effect of lovastatin on these pathways.. ERK and Akt phosphorylation (pERK, pAkt) statuses were assessed with quantitative Western blotting before and after a 12-week lovastatin trial.. Levels of pERK and pAkt were increased in FXS platelets, and lovastatin specifically normalized ERK activity. Changes in ERK phosphorylation were correlated with clinical response to lovastatin.. Platelets' signaling pathways provide biomarkers that can be used as treatment outcome measures in FXS clinical trials.

    Topics: Anticholesteremic Agents; Blood Platelets; Butadienes; Cell Line; Clinical Trials as Topic; Extracellular Signal-Regulated MAP Kinases; Female; Fragile X Syndrome; Humans; Lovastatin; Male; MAP Kinase Signaling System; Megakaryocytes; Nitriles; Phosphorylation; Protein Processing, Post-Translational; Proto-Oncogene Proteins c-akt; Treatment Outcome

2016