We need angiogenesis and neurogenesis and Akt to help cell migration. Have Akt lasso those newborn neurons and drag them to the correct spot.
http://w3serv.nagoya-u.ac.jp/coemed/en/meetings/meetings/international/dr-masahide-takahashi-1/
The
serine/threonine kinase Akt is involved in a variety of cellular processes
including cell proliferation, survival and gene expression. Akt has also been
shown to be required for cell migration in different organisms. However, the
mechanism by which Akt functions to promote cell migration is not fully
understood. We identified a new Akt substrate, Girdin (girders of actin
filament) which is an actin-binding protein, and found that Girdin is essential
for the integrity of the actin cytoskeleton and cell migration. Girdin is
expressed in immature endothelial cells, neuronal cells and some types of
cancer cells, such as breast cancer and glioblastoma. Akt phosphorylates serine
at position 1416 in Girdin, and phosphorylated Girdin accumulates at the
leading edge of migrating cells. Cells expressing mutant Girdin, in which
serine 1416 was replaced with alanine, exhibited limited migration and
lamellipodia formation. Girdin-deficient mice exhibited neuronal migration
defect which results in hypoplasia of the olfactory bulb and granule cell dispersion
in the dentate gyrus. In addition, we obtained evidence that Akt-mediated
phosphorylation of Girdin promotes VEGF-dependent migration and capillary
formation of endothelial cells. Depletion of Girdin also resulted in severe
impairment of cancer cell migration and invasion. A significant observation is that Girdin is dispensable for cell
migratory events during embryonic development. Our findings suggest that Girdin
and its interacting proteins are potential pharmaceutical targets for cancer
therapies and pathological angiogenesis, including tumor angiogenesis.
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