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Findings using a mouse model with genetic deletion of Akt3 demonstrate that the specific isoform Akt3 throughout the Akt3/GSK-3 pathway is involved during motor learning.
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The authors find in Mus musculus, each AKT isoform has a unique expression pattern in the hippocampus. AKT1, but not AKT2 or AKT3, is required for late long term potetiation (LTD) through regulating activity-induced protein synthesis. Interestingly, AKT activity inhibits mGluR-LTD, with overlapping functions for AKT1 and AKT3.
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Behavioral data on Akt3-/- and Akt1-/- mice demonstrated that Akt3 but not Akt1 is required for spatial learning. Histological analyses on synapse, dendrite, and myelin markers suggested that Akt3 but not Akt1 is important for the white matter integrity, and that Akt single isoform does not play a pivotal role on neuronal survival.
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Results show that AKT3 influences outcome of pneumococcal meningitis in human patients; validated the findings in a mouse experimental pneumococcal meningitis model.
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findings provide novel insight into the neurodevelopmental role of Akt3, identify a non-redundant role for Akt3 in the development of prefrontal cortical-mediated cognitive function and show that Akt3 is potentially the dominant regulator of AKT/mTOR signaling in brain
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these results indicate that PI3K and Akt ( Akt1-Akt3)play distinct roles, and that PI3K stimulates Akt-independent pathways that are important for GLUT4 translocation.
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miR-15b-5p is a critical regulator of human EC proliferation and migration by targeting the AKT3 pathway.
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Akt3 constitutively suppresses macropinocytosis in macrophages through a novel WNK1/SGK1/Cdc42 pathway.
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The predominant AKT isoform in the central nervous system, AKT3, induces much more robust axon regeneration than AKT1 and that activation of mTORC1 and inhibition of GSK3beta are two critical parallel pathways for AKT-induced axon regeneration.
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Downregulation of AKT3 increases migration and metastasis in triple negative breast cancer cells by upregulating S100A4.
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In viable Akt three-isoforms conditional knockout mice, total Akt levels were reduced in the adult brain. They had increased levels of phosphorylated tau, GSK3alpha and PKA substrates. No significant changes in p-tau levels were found in Akt3-/-)mice.
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untreated Akt1 and Akt2/Akt3 double knockout mice display significant hearing loss, indicating a role for these isoforms in normal hearing.
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MicroRNA-207 enhances radiation-induced apoptosis by targeting Akt3 in cochlea hair cells.
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Blocking Akt1 or Akt3 but not Akt2 expression prohibits cell proliferation and reprogramming.
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Mechanistic investigations uncovered opposing functions for different Akt isoforms in this regulation, where Akt1 promotes and Akt3 inhibits vascular tumor growth.
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MiR-29 modulates growth and promotes differentiation of skeletal muscle through the post-transcriptional downregulation of Akt3.
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AKT3 controls mitochondrial biogenesis and autophagy via regulation of the major nuclear export protein CRM-1.
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Findings demonstrate that N-cadherin suppresses Akt3 to promote cell motility and highlight the intricate regulation of Akt isoforms by N-cadherin during metastasis.
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AKT3-deficient mice have a more severe disease course than wild-type mice during experimental autoimmune encephalomyelitis (EAE), because AKT3 is necessary for proper central nervous system (CNS) cell integrity.
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Results demonstrate that integrin outside-in signaling and platelet spreading requires Src family kinase-dependent and ADP receptor-amplified activation of the PI3K-Akt-GSK-3beta pathway.
