In agreement with this notion, the reduction of K+ efflux owing to the higher expression of tau may also attenuate apoptosis and accordingly contribute to the cell growth. Furthermore, previous finding indicated that elevated levels of intracellular Ca2+ in response to opening of voltage-gated Ca2+ channels favored tumor cell growth. Thus, decreased Kv currents after tau overexpression could lead to a depolarization of membrane potential; subsequently, activation of VGCC could increase the cytoplasmic Ca2+ levels to trigger cell cycle. Collectively, the present study demonstrates for the first time that overexpression of tau inhibited the expression of Kv channels and related macroscopic currents in N2A cells and the heterologous expression system. Both the induction of tau expression and the blockage of Kv channels could improve the proliferation of N2A cells. Our evidence provides an alternative explanation for low sensitivity to anti-cancer chemicals in ER-positive cancer tissues. The myelination of peripheral nerves is achieved by wrapping of the plasma membranes of myelinating Schwann cells around the axons during postnatal development. Myelination appears to require a continuous change of SC cytoplasm, because the volumes of the axon and the number of myelin lamellae grow until the maturation of myelination is complete. When promyelinating SCs begin to myelinate axons, SCs have large cytoplasm containing numerous mitochondria, ribosome and endoplasmic reticulum. As the number of lamellae increased, cytoplasm between lamellae is excluded and confined to external mesaxon and VE-821 abaxonal cytoplasm. Abaxonal SC cytoplasm is abundant until the maximum rate of myelin addition reaches around the end of second postnatal weeks in rodents. Slow-down of the accumulation of myelin lamellae is then accompanied by the reduction of abaxonal cytoplasmic volume, resulting in little cytoplasm and few organelles in the abaxonal areas outside of the compact myelin in adult mSCs. It is still unknown whether an active cytoplasmic degradation mechanism including autophagy regulates cytoplasmic exclusion during myelin compaction and the substantial reduction of abaxonal cytoplasmic volume in the maturation period. Furthermore, the possibility of these cytoplasmic changes influencing the functional parameters of SC differentiation, such as the extent of myelination and longitudinal growth, has not been determined yet. Macroautophagy is the nonselective lysosomal degradation of cytosolic organelles and proteins. During macroautophagy, cell organelles and cytosol are sequestered into autophagosomes that are derived from the endoplasmic reticulum or other membrane sources, and lysosomal fusion with autophagosomes is the final step in this degradation process. The recent discovery of the molecular mechanisms of macroautophagy identified numerous autophagyrelated proteins. ATG complexes participate in the stepwise reactions resulting in autophagosome formation, and studies of mice with tissue-specific.