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Nbd Cholesterol 22 N 7 Nitrobenz 2 Oxa 1 3 Diazol 4 Yl Amino 23 24 Bisnor 5 Cholen 3β Ol, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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nitrobenz 2 oxa 1 3 diazol 4 yl amino 2 deoxy d glucose 2 nbdg  (MedChemExpress)
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SYK deficiency impairs glycolytic flux in SCs. ( A ). ECAR profiles measured by Seahorse experiments. ( B ). Quantification of basal glycolysis, glycolytic capacity, and glycolytic reserve in ECAR. n = 4 independent biological experiments. ( C ). Glucose uptake measured <t>with</t> <t>2-NBDG</t> by flow cytometry. n = 4 independent biological experiments. ( D ). Intracellular levels of glucose-6-phosphate (G6P), pyruvate and lactate were measured by chemiluminescence. n = 4 independent biological experiments. ( E ). Protein levels of GLUT1, GLUT4, HK2, PFK-1, PFKFB3, PKM2 and LDHA in SCs were measured by western blot. n = 3 independent biological experiments. ( F ). Immunofluorescence staining and quantification of GLUT1, HK2, PFK-1, and PFKFB3 in SCs. Scale bar, 20 μm. N = 4 independent biological experiments, with n ≥ 6 fields/experiment. ( G ). Schematic depicting SYK deficiency-induced downregulation (red arrows) of glycolytic transporters, enzymes, and metabolites in SCs
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SYK deficiency impairs glycolytic flux in SCs. ( A ). ECAR profiles measured by Seahorse experiments. ( B ). Quantification of basal glycolysis, glycolytic capacity, and glycolytic reserve in ECAR. n = 4 independent biological experiments. ( C ). Glucose uptake measured <t>with</t> <t>2-NBDG</t> by flow cytometry. n = 4 independent biological experiments. ( D ). Intracellular levels of glucose-6-phosphate (G6P), pyruvate and lactate were measured by chemiluminescence. n = 4 independent biological experiments. ( E ). Protein levels of GLUT1, GLUT4, HK2, PFK-1, PFKFB3, PKM2 and LDHA in SCs were measured by western blot. n = 3 independent biological experiments. ( F ). Immunofluorescence staining and quantification of GLUT1, HK2, PFK-1, and PFKFB3 in SCs. Scale bar, 20 μm. N = 4 independent biological experiments, with n ≥ 6 fields/experiment. ( G ). Schematic depicting SYK deficiency-induced downregulation (red arrows) of glycolytic transporters, enzymes, and metabolites in SCs
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SYK deficiency impairs glycolytic flux in SCs. ( A ). ECAR profiles measured by Seahorse experiments. ( B ). Quantification of basal glycolysis, glycolytic capacity, and glycolytic reserve in ECAR. n = 4 independent biological experiments. ( C ). Glucose uptake measured <t>with</t> <t>2-NBDG</t> by flow cytometry. n = 4 independent biological experiments. ( D ). Intracellular levels of glucose-6-phosphate (G6P), pyruvate and lactate were measured by chemiluminescence. n = 4 independent biological experiments. ( E ). Protein levels of GLUT1, GLUT4, HK2, PFK-1, PFKFB3, PKM2 and LDHA in SCs were measured by western blot. n = 3 independent biological experiments. ( F ). Immunofluorescence staining and quantification of GLUT1, HK2, PFK-1, and PFKFB3 in SCs. Scale bar, 20 μm. N = 4 independent biological experiments, with n ≥ 6 fields/experiment. ( G ). Schematic depicting SYK deficiency-induced downregulation (red arrows) of glycolytic transporters, enzymes, and metabolites in SCs
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SYK deficiency impairs glycolytic flux in SCs. ( A ). ECAR profiles measured by Seahorse experiments. ( B ). Quantification of basal glycolysis, glycolytic capacity, and glycolytic reserve in ECAR. n = 4 independent biological experiments. ( C ). Glucose uptake measured <t>with</t> <t>2-NBDG</t> by flow cytometry. n = 4 independent biological experiments. ( D ). Intracellular levels of glucose-6-phosphate (G6P), pyruvate and lactate were measured by chemiluminescence. n = 4 independent biological experiments. ( E ). Protein levels of GLUT1, GLUT4, HK2, PFK-1, PFKFB3, PKM2 and LDHA in SCs were measured by western blot. n = 3 independent biological experiments. ( F ). Immunofluorescence staining and quantification of GLUT1, HK2, PFK-1, and PFKFB3 in SCs. Scale bar, 20 μm. N = 4 independent biological experiments, with n ≥ 6 fields/experiment. ( G ). Schematic depicting SYK deficiency-induced downregulation (red arrows) of glycolytic transporters, enzymes, and metabolites in SCs
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SYK deficiency impairs glycolytic flux in SCs. ( A ). ECAR profiles measured by Seahorse experiments. ( B ). Quantification of basal glycolysis, glycolytic capacity, and glycolytic reserve in ECAR. n = 4 independent biological experiments. ( C ). Glucose uptake measured <t>with</t> <t>2-NBDG</t> by flow cytometry. n = 4 independent biological experiments. ( D ). Intracellular levels of glucose-6-phosphate (G6P), pyruvate and lactate were measured by chemiluminescence. n = 4 independent biological experiments. ( E ). Protein levels of GLUT1, GLUT4, HK2, PFK-1, PFKFB3, PKM2 and LDHA in SCs were measured by western blot. n = 3 independent biological experiments. ( F ). Immunofluorescence staining and quantification of GLUT1, HK2, PFK-1, and PFKFB3 in SCs. Scale bar, 20 μm. N = 4 independent biological experiments, with n ≥ 6 fields/experiment. ( G ). Schematic depicting SYK deficiency-induced downregulation (red arrows) of glycolytic transporters, enzymes, and metabolites in SCs
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SYK deficiency impairs glycolytic flux in SCs. ( A ). ECAR profiles measured by Seahorse experiments. ( B ). Quantification of basal glycolysis, glycolytic capacity, and glycolytic reserve in ECAR. n = 4 independent biological experiments. ( C ). Glucose uptake measured <t>with</t> <t>2-NBDG</t> by flow cytometry. n = 4 independent biological experiments. ( D ). Intracellular levels of glucose-6-phosphate (G6P), pyruvate and lactate were measured by chemiluminescence. n = 4 independent biological experiments. ( E ). Protein levels of GLUT1, GLUT4, HK2, PFK-1, PFKFB3, PKM2 and LDHA in SCs were measured by western blot. n = 3 independent biological experiments. ( F ). Immunofluorescence staining and quantification of GLUT1, HK2, PFK-1, and PFKFB3 in SCs. Scale bar, 20 μm. N = 4 independent biological experiments, with n ≥ 6 fields/experiment. ( G ). Schematic depicting SYK deficiency-induced downregulation (red arrows) of glycolytic transporters, enzymes, and metabolites in SCs
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SYK deficiency impairs glycolytic flux in SCs. ( A ). ECAR profiles measured by Seahorse experiments. ( B ). Quantification of basal glycolysis, glycolytic capacity, and glycolytic reserve in ECAR. n = 4 independent biological experiments. ( C ). Glucose uptake measured <t>with</t> <t>2-NBDG</t> by flow cytometry. n = 4 independent biological experiments. ( D ). Intracellular levels of glucose-6-phosphate (G6P), pyruvate and lactate were measured by chemiluminescence. n = 4 independent biological experiments. ( E ). Protein levels of GLUT1, GLUT4, HK2, PFK-1, PFKFB3, PKM2 and LDHA in SCs were measured by western blot. n = 3 independent biological experiments. ( F ). Immunofluorescence staining and quantification of GLUT1, HK2, PFK-1, and PFKFB3 in SCs. Scale bar, 20 μm. N = 4 independent biological experiments, with n ≥ 6 fields/experiment. ( G ). Schematic depicting SYK deficiency-induced downregulation (red arrows) of glycolytic transporters, enzymes, and metabolites in SCs
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SYK deficiency impairs glycolytic flux in SCs. ( A ). ECAR profiles measured by Seahorse experiments. ( B ). Quantification of basal glycolysis, glycolytic capacity, and glycolytic reserve in ECAR. n = 4 independent biological experiments. ( C ). Glucose uptake measured with 2-NBDG by flow cytometry. n = 4 independent biological experiments. ( D ). Intracellular levels of glucose-6-phosphate (G6P), pyruvate and lactate were measured by chemiluminescence. n = 4 independent biological experiments. ( E ). Protein levels of GLUT1, GLUT4, HK2, PFK-1, PFKFB3, PKM2 and LDHA in SCs were measured by western blot. n = 3 independent biological experiments. ( F ). Immunofluorescence staining and quantification of GLUT1, HK2, PFK-1, and PFKFB3 in SCs. Scale bar, 20 μm. N = 4 independent biological experiments, with n ≥ 6 fields/experiment. ( G ). Schematic depicting SYK deficiency-induced downregulation (red arrows) of glycolytic transporters, enzymes, and metabolites in SCs

Journal: Journal of Neuroinflammation

Article Title: SYK regulates Schwann cell metabolic reprogramming to promote axonal regeneration in immune-mediated neuropathy

doi: 10.1186/s12974-025-03624-y

Figure Lengend Snippet: SYK deficiency impairs glycolytic flux in SCs. ( A ). ECAR profiles measured by Seahorse experiments. ( B ). Quantification of basal glycolysis, glycolytic capacity, and glycolytic reserve in ECAR. n = 4 independent biological experiments. ( C ). Glucose uptake measured with 2-NBDG by flow cytometry. n = 4 independent biological experiments. ( D ). Intracellular levels of glucose-6-phosphate (G6P), pyruvate and lactate were measured by chemiluminescence. n = 4 independent biological experiments. ( E ). Protein levels of GLUT1, GLUT4, HK2, PFK-1, PFKFB3, PKM2 and LDHA in SCs were measured by western blot. n = 3 independent biological experiments. ( F ). Immunofluorescence staining and quantification of GLUT1, HK2, PFK-1, and PFKFB3 in SCs. Scale bar, 20 μm. N = 4 independent biological experiments, with n ≥ 6 fields/experiment. ( G ). Schematic depicting SYK deficiency-induced downregulation (red arrows) of glycolytic transporters, enzymes, and metabolites in SCs

Article Snippet: SCs were incubated with 100 μM 2-[N-(7-nitrobenz-2-oxa-1,3- diazol-4-yl)amino]−2-deoxy-D-glucose (2-NBDG) (MCE, Cat#HY-116215) for 30 min at 37 °C in the dark.

Techniques: Flow Cytometry, Western Blot, Immunofluorescence, Staining