Akt exists in three isoforms that display strong homology but are coded by different genes. Akt can phosphorylate GSK3B at the serine 9 position and GSK3 at the serine 21 position and thus restrict their action. Traditionally, GSK3 was connected with glycogen synthesis in response to insulin. It also exists in two closely connected isoforms coded on different Bicalutamide Calutide genes. GSK3 is definitely an strange serine/threonine kinase that is constitutively active and is mainly controlled by inhibition. Furthermore, GSK3 preferentially phosphorylates pre primed substrates and has over 40 substrates including metabolic and signaling proteins to transcription factors and structural proteins. Other kinases may hence affect GSK3 signaling straight of indirectly, by pre phosphorylating its substrates. GSK3 is therefore a point of convergence and velocity for multiple signaling pathways. The GSK3 isoforms have overlapping but not identical substrates as illustrated by the apparent nature of GSK3a activation in promoting amyloid beta protein creation while Chromoblastomycosis GSK3B activation promotes tau protein phosphorylation. For all substrates however, the quantity of overlap in activity between GSK3 and B isoforms hasn’t been completely elucidated. In addition to its other functions in inflammation, power generation, and apoptosis, GSK3B has been proved to be a powerful negative regulator of myelination and oligodendrocyte differentiation that may over-ride the effects of other pathways including Wnt signaling by handling multiple specialists. Effective GSK3B retards the repopulation of demyelinated axons while its inhibition encourages myelination. At amounts reached in vivo, lithium along with several other endogenous and exogenous compounds prevents GSK3B and promotes oligodendrocyte CX-4945 solubility differentiation and myelination without apparent affect neurons, axons, or astrocytes. Because Akt initial inhibits GSK3, activators of Akt also provide while Akt deficiency can impair prefrontal cortex function and expression of myelin genes promyelinating outcomes. The effects of the Akt/GSK3 signaling pathway on mind may be significant. When Akt is driven to be constitutively energetic, hypermyelination without growing oligodendrocyte numbers is particularly observed in CNS however not in PNS. However, over expression of GSK3B lowers myelination, head size, and cortical thickness with no drop in neuron number and thus leads to increased neuronal density. That neuronal density increase is comparable to increases observed in SZ which have been proposed to be due, at least in part, to inferior intracortical myelination. Additional supporting evidence for the role of GSK3 in myelination arises from up regulating insulin growth factor 1, which also eventually checks GSK3 and encourages myelination.