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Image Search Results


Journal: Cell reports

Article Title: Mitochondrial reactive oxygen species regulate acetyl-CoA flux between cytokine production and fatty acid synthesis in effector T cells

doi: 10.1016/j.celrep.2025.115430

Figure Lengend Snippet:

Article Snippet: anti-mouse H3K4me3 Ab-PE (D1A9) , Cell Signaling , Cat# 55800S.

Techniques: FLAG-tag, Virus, Recombinant, Protease Inhibitor, Adjuvant, Staining, Isolation, Citrate Assay, Luminescence Assay, Chromatin Immunoprecipitation, Sample Prep, Plasmid Preparation, Software, Imaging, Microscopy, Transmission Assay, Gene Expression, Flow Cytometry, Mass Spectrometry

A–B, GTM-1 (6 mg/kg/day) or vehicle (VEH) was administered to five-month-old 3XTg-AD mice daily for 8 weeks. The average body weight (A) and total food consumed for 8 weeks (B) was recorded. C–D, F–G, 5-month-old 3XTg-AD mice (C, D) or 15-month-old 3XTg-AD mice (F, G) were treated with GTM-1 (3 mg/kg/day) daily for 8 weeks. The insoluble and soluble Aβ42 (C, D) levels were measured using a sandwich ELISA. E, Brain proteins were obtained from 8 different 3xTg-AD mice treated with GTM-1 and 8 different 3xTg-AD mice treated with vehicle after 8 weeks of treatment. The endogenous expression of APP, C99 and C83 were assessed using western blotting analyses. CT (control treatment) mice fed with a normal (vehicle) diet. Stars indicate significant differences between the model group and control or treatment groups for that time point. *P<0.05, **P<0.01. F, Five-month-old 3XTg-AD mice were treated with GTM-1 (6 mg/kg/day) or vehicle (PC, positive control) for 2 months. The brain sample from non-Tg mice with the same generic background was used as a negative control (NC). Soluble fractions extracted from brain samples were applied onto Hybond C-extra membrane. Next, the bound oligomeric Aβ and mono-Aβ on the membranes were detected using mono-Aβ specific antibodies, and oligomer-specific antibodies, respectively. Commercial soluble Aβ monomers and oligomeric Aβs produced from the monomer were spotted as indicated and used as another control. G, Densitometric analysis of the immune dot-blot experiments was performed using a high-resolution scanner, and the average intensity of each group was normalized using the average PC result. H, Five-month-old 3XTg-AD mice were treated as previously. Representative sections obtained from the brains of mice treated with GTM-1 and vehicle were immunostained using an Aβ-specific antibody.

Journal: PLoS ONE

Article Title: Induction of Autophagy by a Novel Small Molecule Improves Aβ Pathology and Ameliorates Cognitive Deficits

doi: 10.1371/journal.pone.0065367

Figure Lengend Snippet: A–B, GTM-1 (6 mg/kg/day) or vehicle (VEH) was administered to five-month-old 3XTg-AD mice daily for 8 weeks. The average body weight (A) and total food consumed for 8 weeks (B) was recorded. C–D, F–G, 5-month-old 3XTg-AD mice (C, D) or 15-month-old 3XTg-AD mice (F, G) were treated with GTM-1 (3 mg/kg/day) daily for 8 weeks. The insoluble and soluble Aβ42 (C, D) levels were measured using a sandwich ELISA. E, Brain proteins were obtained from 8 different 3xTg-AD mice treated with GTM-1 and 8 different 3xTg-AD mice treated with vehicle after 8 weeks of treatment. The endogenous expression of APP, C99 and C83 were assessed using western blotting analyses. CT (control treatment) mice fed with a normal (vehicle) diet. Stars indicate significant differences between the model group and control or treatment groups for that time point. *P<0.05, **P<0.01. F, Five-month-old 3XTg-AD mice were treated with GTM-1 (6 mg/kg/day) or vehicle (PC, positive control) for 2 months. The brain sample from non-Tg mice with the same generic background was used as a negative control (NC). Soluble fractions extracted from brain samples were applied onto Hybond C-extra membrane. Next, the bound oligomeric Aβ and mono-Aβ on the membranes were detected using mono-Aβ specific antibodies, and oligomer-specific antibodies, respectively. Commercial soluble Aβ monomers and oligomeric Aβs produced from the monomer were spotted as indicated and used as another control. G, Densitometric analysis of the immune dot-blot experiments was performed using a high-resolution scanner, and the average intensity of each group was normalized using the average PC result. H, Five-month-old 3XTg-AD mice were treated as previously. Representative sections obtained from the brains of mice treated with GTM-1 and vehicle were immunostained using an Aβ-specific antibody.

Article Snippet: Rabbit polyclonal anti-oligomer antibody A11 (cat. AHB0052) and mouse monoclonal antibody anti-mono Aβ (cat. AMB0062) were purchased from Invitrogen (Camarillo, CA).

Techniques: Sandwich ELISA, Expressing, Western Blot, Positive Control, Negative Control, Produced, Dot Blot