title: The PI3K pathway in B cell metabolism.
abstract: B cell growth and proliferation is tightly regulated by signaling through the B cell receptor and by other membrane bound receptors responding to different cytokines. The PI3K signaling pathway has been shown to play a crucial role in B cell activation, differentiation and survival. Activated B cells undergo metabolic reprograming in response to changing energetic and biosynthetic demands. B cells also need to be able to coordinate metabolic activity and proliferation with nutrient availability. The PI3K signaling network has been implicated in regulating nutrient acquisition, utilization and biosynthesis, thus integrating receptor-mediated signaling with cell metabolism. In this review, we discuss the current knowledge about metabolic changes induced in activated B cells, strategies to adapt to metabolic stress and the role of PI3K signaling in these processes.
authors: a BIOSS Centre for Biological Signalling Studies, Albert-Ludwigs-University Freiburg , Freiburg , Germany.|b Max Planck Institute of Immunobiology and Epigenetics , Freiburg , Germany.
authors: Julia
authors: J
authors: Jellusova
authors: c Sanford Burnham Prebys Medical Discovery Institute , La Jolla , CA , USA.
authors: Robert C
authors: RC
authors: Rickert
mesh_terms: D000818:Animals; D001343:Autophagy; D001402:B-Lymphocytes / Q000166:cytology / Q000378:metabolism*; D002454:Cell Differentiation; D049109:Cell Proliferation; D006801:Humans; D053858:Metabolic Networks and Pathways; D008928:Mitochondria / Q000378:metabolism; D009369:Neoplasms / Q000378:metabolism; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism
chemical_list: D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt; D017382:Reactive Oxygen Species; D058570:TOR Serine-Threonine Kinases
keywords: Akt; glycolysis; lymphocyte; mTOR; mitochondria