c11 bodipy lipid peroxidation sensor Search Results


bodipy 581/591 c11 (lipid peroxidation sensor)  (Fisher Scientific)
90
Fisher Scientific bodipy 581/591 c11 (lipid peroxidation sensor)

Bodipy 581/591 C11 (Lipid Peroxidation Sensor), supplied by Fisher Scientific, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/bodipy 581/591 c11 (lipid peroxidation sensor)/product/Fisher Scientific
Average 90 stars, based on 1 article reviews
bodipy 581/591 c11 (lipid peroxidation sensor) - by Bioz Stars, 2026-02
90/100 stars
  Buy from Supplier
bodipy 581/591 c11 lipid peroxidation sensor  (Becton Dickinson)
90
Becton Dickinson bodipy 581/591 c11 lipid peroxidation sensor
Control ( UBC-CreER/Arf1 f/+ , WT), Nlrp3 -deficient ( Nlrp3 -/- ), Arf1-ablated ( UBC-CreER/Arf1 f/f , Arf1 -/- ), and Arf1-ablated in an Nlrp3 -deficient background (UBC-CreER/Arf1 f/f /Nlrp3 -/- , Arf1 -/- Nlrp3 -/- ) mice were assayed on the following indicated phenotypes. (a) Immunofluorescence staining for BODIPY 581/591 <t>C11</t> <t>(BD-C11),</t> IBA1, and Hoechst in the brain sections and spinal cords from mice with the indicated genotypes. Scale bar: 100 μm (upper panel), 10 μm (bottom panel). (b) Quantification of BD-C11 level in the different brain regions and spinal cords of control and Arf1-ablated mice. (c) Quantification of ATP amount in the spinal cord lysates of mice with the indicated genotypes (n = 5 mice per group). (d) Increased chemokine levels in the spinal cord lysates of mice with the indicated genotypes. (e) BODIPY 493/503 (BD493) staining of lipid droplets in N2A cells treated with DMSO or Arf1 inhibitor GCA. Scale bar: 10 μm. (f) Malondialdehyde (MDA, a lipid peroxidation marker) in N2A cells treated with DMSO or GCA (n = 4). (g) ATP levels in culture medium of N2A cells treated with DMSO, GCA, or BFA for 24 hours (n = 5). (h) Immunoblot with anti-ApoE antibody to demonstrate that ApoE shRNA effectively knocked down ApoE protein expression in N2A cells. (i) Neuronal N2A cells were transfected with the indicated shRNAs, cocultured with microglial EOC 20 cells for 48 hours, and assayed for IL-1β by ELISA (n = 5 per group). (j) Western blot using antibodies of caspase-1 (Cas-1), IL-1β, and Arf1 to show that Arf1 ablation in N2A neuronal cells increased IL-1β expression and Cas-1 activation (p20) in cocultured microglial EOC 20 cells. (k–m) Nlrp3 deficiency almost completely suppressed the neurodegenerative phenotypes of Arf1-ablated mice, including neurological score (k), induction of IL-1β (l), and induction of IFNγ, (m) (n = 5 per group). Data are represented as mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001 using two-tailed t-test.
Bodipy 581/591 C11 Lipid Peroxidation Sensor, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/bodipy 581/591 c11 lipid peroxidation sensor/product/Becton Dickinson
Average 90 stars, based on 1 article reviews
bodipy 581/591 c11 lipid peroxidation sensor - by Bioz Stars, 2026-02
90/100 stars
  Buy from Supplier

Image Search Results


Journal: Cell

Article Title: SYK coordinates neuroprotective microglial responses in neurodegenerative disease

doi: 10.1016/j.cell.2022.09.030

Figure Lengend Snippet:

Article Snippet: BODIPY 581/591 C11 (Lipid Peroxidation Sensor) , Fisher Scientific , Cat# D3861.

Techniques: Purification, Marker, Virus, Recombinant, Adjuvant, Protease Inhibitor, Staining, Protein Extraction, Saline, Suspension, Blocking Assay, Lysis, Phospho-proteomics, In Situ, Enzyme-linked Immunosorbent Assay, Flow Cytometry, cDNA Synthesis, Gene Expression, Software, Microscopy, Spectrophotometry, Real-time Polymerase Chain Reaction, Next-Generation Sequencing, Imaging

Control ( UBC-CreER/Arf1 f/+ , WT), Nlrp3 -deficient ( Nlrp3 -/- ), Arf1-ablated ( UBC-CreER/Arf1 f/f , Arf1 -/- ), and Arf1-ablated in an Nlrp3 -deficient background (UBC-CreER/Arf1 f/f /Nlrp3 -/- , Arf1 -/- Nlrp3 -/- ) mice were assayed on the following indicated phenotypes. (a) Immunofluorescence staining for BODIPY 581/591 C11 (BD-C11), IBA1, and Hoechst in the brain sections and spinal cords from mice with the indicated genotypes. Scale bar: 100 μm (upper panel), 10 μm (bottom panel). (b) Quantification of BD-C11 level in the different brain regions and spinal cords of control and Arf1-ablated mice. (c) Quantification of ATP amount in the spinal cord lysates of mice with the indicated genotypes (n = 5 mice per group). (d) Increased chemokine levels in the spinal cord lysates of mice with the indicated genotypes. (e) BODIPY 493/503 (BD493) staining of lipid droplets in N2A cells treated with DMSO or Arf1 inhibitor GCA. Scale bar: 10 μm. (f) Malondialdehyde (MDA, a lipid peroxidation marker) in N2A cells treated with DMSO or GCA (n = 4). (g) ATP levels in culture medium of N2A cells treated with DMSO, GCA, or BFA for 24 hours (n = 5). (h) Immunoblot with anti-ApoE antibody to demonstrate that ApoE shRNA effectively knocked down ApoE protein expression in N2A cells. (i) Neuronal N2A cells were transfected with the indicated shRNAs, cocultured with microglial EOC 20 cells for 48 hours, and assayed for IL-1β by ELISA (n = 5 per group). (j) Western blot using antibodies of caspase-1 (Cas-1), IL-1β, and Arf1 to show that Arf1 ablation in N2A neuronal cells increased IL-1β expression and Cas-1 activation (p20) in cocultured microglial EOC 20 cells. (k–m) Nlrp3 deficiency almost completely suppressed the neurodegenerative phenotypes of Arf1-ablated mice, including neurological score (k), induction of IL-1β (l), and induction of IFNγ, (m) (n = 5 per group). Data are represented as mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001 using two-tailed t-test.

Journal: bioRxiv

Article Title: Arf1-Ablation-Induced Neuronal Damage Promotes Neurodegeneration Through an NLRP3 Inflammasome–Meningeal γδ T cell–IFNγ-Reactive Astrocyte Pathway

doi: 10.1101/2020.03.27.012526

Figure Lengend Snippet: Control ( UBC-CreER/Arf1 f/+ , WT), Nlrp3 -deficient ( Nlrp3 -/- ), Arf1-ablated ( UBC-CreER/Arf1 f/f , Arf1 -/- ), and Arf1-ablated in an Nlrp3 -deficient background (UBC-CreER/Arf1 f/f /Nlrp3 -/- , Arf1 -/- Nlrp3 -/- ) mice were assayed on the following indicated phenotypes. (a) Immunofluorescence staining for BODIPY 581/591 C11 (BD-C11), IBA1, and Hoechst in the brain sections and spinal cords from mice with the indicated genotypes. Scale bar: 100 μm (upper panel), 10 μm (bottom panel). (b) Quantification of BD-C11 level in the different brain regions and spinal cords of control and Arf1-ablated mice. (c) Quantification of ATP amount in the spinal cord lysates of mice with the indicated genotypes (n = 5 mice per group). (d) Increased chemokine levels in the spinal cord lysates of mice with the indicated genotypes. (e) BODIPY 493/503 (BD493) staining of lipid droplets in N2A cells treated with DMSO or Arf1 inhibitor GCA. Scale bar: 10 μm. (f) Malondialdehyde (MDA, a lipid peroxidation marker) in N2A cells treated with DMSO or GCA (n = 4). (g) ATP levels in culture medium of N2A cells treated with DMSO, GCA, or BFA for 24 hours (n = 5). (h) Immunoblot with anti-ApoE antibody to demonstrate that ApoE shRNA effectively knocked down ApoE protein expression in N2A cells. (i) Neuronal N2A cells were transfected with the indicated shRNAs, cocultured with microglial EOC 20 cells for 48 hours, and assayed for IL-1β by ELISA (n = 5 per group). (j) Western blot using antibodies of caspase-1 (Cas-1), IL-1β, and Arf1 to show that Arf1 ablation in N2A neuronal cells increased IL-1β expression and Cas-1 activation (p20) in cocultured microglial EOC 20 cells. (k–m) Nlrp3 deficiency almost completely suppressed the neurodegenerative phenotypes of Arf1-ablated mice, including neurological score (k), induction of IL-1β (l), and induction of IFNγ, (m) (n = 5 per group). Data are represented as mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001 using two-tailed t-test.

Article Snippet: We further assessed lipid peroxidation using the BODIPY 581/591 C11 lipid peroxidation sensor (BD-C11).

Techniques: Immunofluorescence, Staining, Marker, Western Blot, shRNA, Expressing, Transfection, Enzyme-linked Immunosorbent Assay, Activation Assay, Two Tailed Test