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Here is the first evidence suggesting that lithium suppressed astrogliogenesis might not through low GSK systems. We hypothesized that lithium prevents phosphorylation of STAT3, a messenger program known to stimulate astrogliogenesis. To test this hypothesis, we measured G Tyr705 CNX2006 STAT3 being an indicator of STAT3 activation. Introducing zero 5 % serum or the specific STAT3 agonist AICAR quickly increased G Tyr705 STAT3 protein and GFAP levels in NSC cultures. Lithium obstructed this P Tyr705 STAT3 and GFAP raise together with the same dose-response because it restricted astrogliogenesis. Neither SB216763 none GID5 6, a very specific molecular blocker of GSK3b obstructed stimulated R Tyr705 STAT3 or GFAP increases. Together these results provide convincing evidence that lithium inhibits astro gliogenesis in NSC cultures by avoiding STAT3 phosphoryla tion through non GSK3b components. On the other hand, GSK3b inhibition stimulates neural progenitor cells to proliferate. Both lithium and SB216763 considerably increased the fraction of Ki 67 cells amongst PSA NCAM cells Cholangiocarcinoma although not A2B5 cells. Ki 67 is actually a sign of nucleolar and nuclear protein expressed by dividing or recently separated cells. In control untreated cultures, just 14 % of PSA NCAM cells described for Ki 67 in comparison with 51 % in 1 mM lithium treated cultures and 64 % in 10 mM SB216763 treated cultures. Lithium clearly inhibits STAT3 in NSC countries. Beurel, Jope had earlier reported that STAT3 activation depends on GSK3b in astrocytes and microglia. They found that 20 mM lithium and other drugs that blocked GSK3b and suppressed STAT3 activation induced by lipopolysaccharide and interferon-gamma in mouse primary microglia and astrocytes. Like Beurel, Jope, we discovered that lithium inhibits STAT3. However, unlike Beurel and Jope, we unearthed that SB216763 did not prevent serum or AICAR activation of STAT3. We thus chose to test SCH 772984 another and more certain GSK3b blocker, i. Age. GID5 6, to find out if it would restrict serum or AICAR activation of STAT3. We speculate this discrepancy may be due to the different culture issue and the visibility of regulatory pathways among different cell types. Term of GID5 6 should restrict GSK3b, while overexpression of full-length axin will cause more inactivation of beta catenin and avoid beta catenin phosphorylation. We established that expression of GID 5 6 blocked GSK3b activity and phosphorylation of beta catenin in NSCs. Nonetheless, GID 5 6 did not influence serum or AICAR activated STAT3 activation or astrogliogenesis.