Tohoku University · Biochemistry, Genetics and Molecular Biology
Professor Yoshiteru Kagawa's research lab focuses on the role of intracellular lipid-binding proteins, particularly Fatty Acid Binding Protein 7 (FABP7), in brain development, glioma biology, and neuroinflammation. The lab investigates how FABP7 regulates lipid metabolism, membrane microdomain dynamics (e.g., lipid rafts), and signal transduction in astrocytes and glial cells, with implications for brain tumor progression and neurodegenerative processes. A central theme is the interplay between FABP7 and metabolic pathways such as acetyl-CoA production via ATP-citrate lyase, as well as its role in modulating responses to bioactive lipids and cannabinoids. The lab also explores FABP4 in microglial immunometabolism, highlighting its contribution to neuroinflammatory diseases.
Figures are computed from collected data and may differ slightly.
Fatty acid-binding proteins (FABPs) bind and solubilize long-chain fatty acids, controlling intracellular lipid dynamics. FABP7 is expressed by astrocytes in the developing brain, and suggested to be involved in the control of astrocyte lipid homeostasis. In this study, we sought to examine the role of FABP7 in astrocytes, focusing on plasma membrane lipid raft function, which is important for receptor-mediated signal transduction in response to extracellular stimuli. In FABP7-knockout (KO) astr
Fatty acid binding protein 7 (FABP7) is an intracellular fatty acid chaperon that is highly expressed in astrocytes, oligodendrocyte-precursor cells, and malignant glioma. Previously, we reported that FABP7 regulates the response to extracellular stimuli by controlling the expression of caveolin-1, an important component of lipid raft. Here, we explored the detailed mechanisms underlying FABP7 regulation of caveolin-1 expression using primary cultured FABP7-KO astrocytes as a model of loss of fu
Fatty acid-binding protein 7 (FABP7), one of the fatty acid (FA) chaperones involved in the modulation of intracellular FA metabolism, is highly expressed in glioblastoma, and its expression is associated with decreased patients' prognosis. Previously, we demonstrated that FABP7 requires its binding partner to exert its function and that a mutation in the FA-binding site of FABP7 affects tumour biology. Here, we explored the role of FA ligand binding for FABP7 function in tumour proliferation an
Prolonged activation of microglia leads to excessive release of proinflammatory mediators, which are detrimental to brain health. Therefore, there are significant efforts to identify pathways mediating microglial activation. Recent studies have demonstrated that fatty acid-binding protein 4 (FABP4), a lipid binding protein, is a critical player in macrophage-mediated inflammation. Given that we have previously identified FABP4 in microglia, the aim of this study was to assess whether FABP4 activ
Isocitrate dehydrogenase 1 (IDH1) is a key enzyme in cellular metabolism. IDH1 mutation (IDH1mut) is the most important genetic alteration in lower grade glioma, whereas glioblastoma (GB), the most common malignant brain tumor, often has wild-type IDH1 (IDH1wt). Although there is no effective treatment yet for neither IDH1wt nor IDHmut GB, it is important to note that the survival span of IDH1wt GB patients is significantly shorter than those with IDH1mut GB. Thus, understanding IDH1wt GB biolog
Fatty acid binding protein 7 (FABP7) is present in the brain, but its interaction with the endocannabinoid system and phytocannabinoids is still not well understood. FABP7 has been proposed as a shuttle protein for trafficking endogenous cannabinoids, as well as an intracellular carrier of THC. In a mouse model of FABP7 global deletion, we used ultra-high performance liquid chromatography- tandem mass spectrometry (UPLC-MS/MS) to measure brain levels of Δ9 tetrahydrocannabinol (THC) as well as i
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