about
Adenosine-mono-phosphate-activated protein kinase-independent effects of metformin in T cellsFunctional characterisation of the regulation of CAAT enhancer binding protein alpha by GSK-3 phosphorylation of Threonines 222/226.Glucose represses dendritic cell-induced T cell responses.Phosphatidylinositol-3-OH kinase and nutrient-sensing mTOR pathways control T lymphocyte traffickingmTORC1-dependent metabolic reprogramming is a prerequisite for NK cell effector function.Temporal differences in the dependency on phosphoinositide-dependent kinase 1 distinguish the development of invariant Valpha14 NKT cells and conventional T cellsProtein kinase B controls transcriptional programs that direct cytotoxic T cell fate but is dispensable for T cell metabolism.T cell receptor signaling controls Foxp3 expression via PI3K, Akt, and mTOR.Phosphoinositide 3-kinase and the mammalian target of rapamycin pathways control T cell migrationMetabolism, migration and memory in cytotoxic T cells.The coordination of T-cell function by serine/threonine kinases.Glucose, glycolysis and lymphocyte responses.Immunometabolism: Cellular Metabolism Turns Immune RegulatorMetabolic regulation of natural killer cells.Metabolic regulation of immune responses: therapeutic opportunities.Nutrient sensing, signal transduction and immune responses.What Fuels Natural Killers? Metabolism and NK Cell ResponsesAnalysis of hepatic gene transcription in mice expressing insulin-insensitive GSK3.TGF-β inhibits the activation and functions of NK cells by repressing the mTOR pathway.LKB1 is essential for the proliferation of T-cell progenitors and mature peripheral T cellsNotch-induced T cell development requires phosphoinositide-dependent kinase 1.Phosphoinositide (3,4,5)-triphosphate binding to phosphoinositide-dependent kinase 1 regulates a protein kinase B/Akt signaling threshold that dictates T-cell migration, not proliferation.PDK1 regulation of mTOR and hypoxia-inducible factor 1 integrate metabolism and migration of CD8+ T cells.AMPKα1: a glucose sensor that controls CD8 T-cell memory.Phosphoinositide-dependent kinase 1 controls migration and malignant transformation but not cell growth and proliferation in PTEN-null lymphocytes.IRF4 links antigen affinity to CD8+ T-cell metabolism.Sugar or Fat?-Metabolic Requirements for Immunity to Viral Infections.Srebp-controlled glucose metabolism is essential for NK cell functional responses.Metabolic Reprogramming Supports IFN-γ Production by CD56bright NK Cells.Amino acid-dependent cMyc expression is essential for NK cell metabolic and functional responses in mice.A temporal switch in the insulin-signalling pathway that regulates hepatic IGF-binding protein-1 gene expressionMetabolic reprogramming of natural killer cells in obesity limits antitumor responsesCompetition for nutrients and its role in controlling immune responsesAkt and STAT5 mediate naïve human CD4+ T-cell early metabolic response to TCR stimulationStarved human T lymphocytes keep fightingCanonical TGF-β Signaling Pathway Represses Human NK Cell MetabolismN-myristoylation of AMPK controls T cell inflammatory functionInhibitors of the NMDA-Nitric Oxide Signaling Pathway Protect Against Neuronal Atrophy and Synapse Loss Provoked by l-alpha Aminoadipic Acid-treated AstrocytesObesity Reduces mTORC1 Activity in Mucosal-Associated Invariant T Cells, Driving Defective Metabolic and Functional ResponsesImmunometabolism and natural killer cell responses
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description
hulumtues
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researcher
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հետազոտող
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name
David K. Finlay
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David K. Finlay
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David K. Finlay
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David K. Finlay
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David K. Finlay
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David K. Finlay
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David K. Finlay
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David K. Finlay
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David K. Finlay
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David K. Finlay
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David K. Finlay
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David K. Finlay
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David K. Finlay
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P31
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0000-0003-2716-6679