Publication: Activating Akt and the brain’s resources to drive
cellular survival and prevent inflammatory injury
Authors
Chong, Z.Z. ; Li, F. ; Maiese, K.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Protein kinase B, also known as Akt, is a
serine/threonine kinase and plays a critical role in the
modulation of cell development, growth, and survival.
Interestingly, Akt is ubiquitously expressed throughout
the body, but its expression in the nervous system is
substantially up-regulated during cellular stress,
suggesting a more expansive role for Akt in the nervous
system that may involve cellular protection. In this
regard, a body of recent work has identified a robust
capacity for Akt and its downstream substrates to foster
both neuronal and vascular survival during apoptotic
injury. Cell survival by Akt is driven by the modulation
of both intrinsic cellular pathways that oversee genomic
DNA integrity and extrinsic mechanisms that control
inflammatory microglial activation. A series of distinct
pathways are regulated by Akt that include the Forkhead
family of transcription factors, GSK-3ß, ß-catenin, c-
Jun, CREB, Bad, IKK, and p53. Culminating below
these substrates of Akt are the control of caspase
mediated pathways that promote genomic integrity as
well as prevent inflammatory cell demise. With further
levels of progress in defining the cellular role of Akt, the
attractiveness of Akt as a vital and broad cytoprotectant
for both neuronal and vascular cell populations should
continue to escalate.
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