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Activating Akt and the brain's resources to drive cellular survival and prevent inflammatory injury.

Activating Akt and the brain's resources to drive cellular survival and prevent inflammatory injury. Research Abstract Details 

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  • Activating Akt and the brain's resources to drive cellular survival and prevent inflammatory injury. Abstract Text:

    z z chongZ Z Chong,f liF Li,k maieseK Maiese,

    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-3 beta, beta-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.

    Activating Akt and the brain's resources to drive cellular survival and prevent inflammatory injury. Publishing Authors By Initials

    zz chongZZ Chong,f liF Li,k maieseK Maiese,

    For similar peptides: intracellular signaling peptides and proteins: apoptosis regulatory proteins: proto-oncogene proteins c-bcl-2: bcl-associated death protein research abstracts see: peptides: intracellular signaling peptides and proteins: apoptosis regulatory proteins: proto-oncogene proteins c-bcl-2: bcl-associated death protein research

    PUBMED ID PMID:

    MEDLINE DATE:

    Activating Akt and the brain's resources to drive cellular survival and prevent inflammatory injury. Journal Published:

    PUBLICATION TYPE: Review

    Journal: Histology and histopathology

    VOLUME: 20

    Page Numbers: 299-315

    Journal Abbreviation:

    ISSN: 0213-3911

    DAY: 2

    MONTH: Jan

    YEAR: 2005

    Activating Akt and the brain's resources to drive cellular survival and prevent inflammatory injury. Information

    Number of References: 145

    LANGUAGE: eng

    NlmUniqueID: 8609357

    Activating Akt and the brain's resources to drive cellular survival and prevent inflammatory injury. Keywords Mesh Terms:

    KEYWORDS: bcl-Associated Death Protein

    MESH TERMS: metabolism

    Chemical & Substance for Abstract: Activating Akt and the brain's resources to drive cellular survival and prevent inflammatory injury. Information

    Substance Name: Protein-Serine-Threonine Kinases

    Registry Number: EC 2.7.11.1

    Grant and Affiliation Information for Activating Akt and the brain's resources to drive cellular survival and prevent inflammatory injury.

    AFFILIATION: Division of Cellular and Molecular Cerebral Ischemia, Wayne State University School of Medicine, Detroit, Michigan 48201, USA.

    Country: Spain

    Spain Research PublicationSpain Research Publication

    AGENCY:

    GRANT:

    ACRONYM:

    MEDLINETA: Histol Histopathol

    REFSOURCE:

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    ACCESSION NUMBER:

    Number Hits: 0

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