pi3k p110γ (d55d5, 5405s) antibody  (Cell Signaling Technology Inc)

Journal: Journal of advanced research

Article Title: The fatty acid receptor CD36 promotes macrophage infiltration via p110γ signaling to stimulate metastasis.

doi: 10.1016/j.jare.2024.10.006

Figure Lengend Snippet: Fig. 7. CD36 promotes the recruitment of p110c to lipid rafts. A, B, The expression of p110c was determined by immunofluorescence staining along with the quantification in WT and Cd36-/- BMDMs (A), or NC and CD36 OE THP-1 cells (B) in the presence of TCM (n = 5). C, Representative histogram (left) and quantitative results of the MFI of p110c surface staining in BMDMs (n = 4). D, The expression of AKT and p110c in whole cell lysate (WCL), membrane (Mem), and cytoplasm (Cyto) in WT and Cd36-/- BMDMs was measured along with the quantification (n = 3). E, F, The expression of the lipid raft marker-Flotillin1 was determined by immunofluorescence staining along with the quantification in BMDMs (E) and THP-1 cells (F) (n = 5). G, Representative histogram (above) and quantitative results of the MFI of Flotillin1 surface staining in BMDMs (n = 4). H, The levels of p110c in the lipid rafts were detected in BMDMs and THP-1 cells along with the quantification (n = 3). Values for n represent biologically independent samples. Data are presented as mean ± SEM. *p < 0.05, ** p < 0.01, *** p < 0.001. Unpaired two-tailed t-test (A-H).

Article Snippet: Antibody information is listed as follows: anti-b-actin (1:5000, #bs-0061R, Bioss, Beijing China), anti-AKT (1:1000, #4691 T, Cell Signaling Technology, Inc., Danvers, MA, USA), anti-p-AKT (1:2000, #4060S, Cell Signaling Technology), anti-PI3K p85 (1:1000, #4257 T, Cell Signaling Technology), antip-PI3K p85 (1:500, #GTX132597, GeneTex, CA, USA), anti-PI3K p110c (1:1000, #sc-166365, Santa Cruz Biotechnology), Na/K ATPase (1:1000, #14418-1-AP, Proteintech), GAPDH (1:10000, #bs-10900R, Bioss) and anti-Flotillin1 (1:1000, #15571-1-AP, Proteintech).

Techniques: Expressing, Staining, Membrane, Marker, Two Tailed Test

Journal: Journal of advanced research

Article Title: The fatty acid receptor CD36 promotes macrophage infiltration via p110γ signaling to stimulate metastasis.

doi: 10.1016/j.jare.2024.10.006

Figure Lengend Snippet: Fig. 8. CD36-mediated lipid reprogramming induces the activation of lipid raft-associated p110c.A, B, Representative histogram (right) and quantitative results of the MFI of Flotillin1 (A) or p110c (B) surface staining in NC and CD36 OE THP-1 cells treated with MbCD (n = 4). C, The protein expression of P-AKT and AKT were determined in THP-1 cells treated with or without MbCD along with the quantification. D, E, Migration (D) or adhesion (E) assay was performed in THP-1 cells treated with or without MbCD (n = 5). F, The volcano diagram showed the difference of sphingolipids between WT and Cd36-/- BMDMs (n = 5). G, Enriched different lipid classes between WT and Cd36-/- BMDMs. H, I, Migration (H) or adhesion (I) assay was performed in BMDMs treated with or without ceramide (n = 3). J, K, The expression of Flotillin1 (J) and p110c (K) on the cell membrane was observed by confocal microscopy in WT and Cd36-/- BMDMs treated with or without ceramide (n = 3–4). Values for n represent biologically independent samples. Data are presented as mean ± SEM. *p < 0.05, ** p < 0.01, and *** p < 0.001 vs the control group; # p < 0.01, ## p < 0.01, and ### p < 0.001 vs the WT group. ANOVA (A-K).

Article Snippet: Antibody information is listed as follows: anti-b-actin (1:5000, #bs-0061R, Bioss, Beijing China), anti-AKT (1:1000, #4691 T, Cell Signaling Technology, Inc., Danvers, MA, USA), anti-p-AKT (1:2000, #4060S, Cell Signaling Technology), anti-PI3K p85 (1:1000, #4257 T, Cell Signaling Technology), antip-PI3K p85 (1:500, #GTX132597, GeneTex, CA, USA), anti-PI3K p110c (1:1000, #sc-166365, Santa Cruz Biotechnology), Na/K ATPase (1:1000, #14418-1-AP, Proteintech), GAPDH (1:10000, #bs-10900R, Bioss) and anti-Flotillin1 (1:1000, #15571-1-AP, Proteintech).

Techniques: Activation Assay, Staining, Expressing, Migration, Membrane, Confocal Microscopy, Control