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Background
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RAC-alpha serine/threonine-protein kinase (AKT1) is also known as PKB, Protein kinase B alpha, PKB alpha, Proto-oncogene c-Akt and RAC-PK-alpha, which belongs to the protein kinase superfamily, AGC Ser/Thr protein kinase family and RAC subfamily and is expressed in prostate cancer and levels increase from the normal to the malignant state (at protein level). AKT1 is one of three closely related serine/threonine-protein kinases (AKT1, AKT2 and AKT3) called the AKT kinase, and which regulate many processes including metabolism, proliferation, cell survival, growth and angiogenesis. AKT is responsible of the regulation of glucose uptake by mediating insulin-induced translocation of the SLC2A4/GLUT4 glucose transporter to the cell surface. AKT regulates also the storage of glucose in the form of glycogen by phosphorylating GSK3A at 'Ser-21' and GSK3B at 'Ser-9', resulting in inhibition of its kinase activity. Phosphorylation of GSK3 isoforms by AKT is also thought to be one mechanism by which cell proliferation is driven. AKT regulates also cell survival via the phosphorylation of MAP3K5 (apoptosis signal-related kinase).
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Pathways
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PI3K-Akt Signaling, RTK Signaling, TCR Signaling, AMPK Signaling, Interferon-gamma Pathway, TLR Signaling, Fc-epsilon Receptor Signaling Pathway, Neurotrophin Signaling Pathway, Response to Water Deprivation, Regulation of Actin Filament Polymerization, Carbohydrate Homeostasis, Glycosaminoglycan Metabolic Process, Cellular Glucan Metabolic Process, Regulation of Muscle Cell Differentiation, Regulation of Cell Size, Skeletal Muscle Fiber Development, Regulation of Carbohydrate Metabolic Process, Hepatitis C, Protein targeting to Nucleus, CXCR4-mediated Signaling Events, Signaling Events mediated by VEGFR1 and VEGFR2, Negative Regulation of intrinsic apoptotic Signaling, Thromboxane A2 Receptor Signaling, Positive Regulation of fat Cell Differentiation, VEGFR1 Specific Signals
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