Mouse CD36/SR‑B3 Antibody

Detection of Mouse CD36/SR-B3 by Western Blot

Liver GADD45 beta controls liver fatty acid handling by cytosolic FABP1 retentionA, BMale GADD45 beta +/+ (WT; n = 16) or GADD45 beta −/− (KO; n = 15) mice fasted for 24 h (fasted) with (AV‐G45b OE) or without (AV‐NC) liver‐restricted GADD45 beta over‐expression (n = 7–8/group). Liver mRNA expression of Gadd45b (A) as well as fatty acid metabolic genes (B) encompassing transport (Slc28a2, Slc27a5, Cd36), intracellular binding (Fabp1, Dbi) and metabolism (Acly, Dgat1, Atgl, Hsl).CRepresentative immunoblots of FATP2, CD36, FABP1 and GADD45 beta from liver whole tissue lysate (W) as well as fractionated organelles/intracellular structures including nuclei (N), mitochondria (MT), microsomes (MS) and cytoplasm (C), from GADD45 beta +/+ (WT) and GADD45 beta −/− (KO) mice.DQuantified band densities of FABP1 enrichment from fractions in C (n = 4/group).ELiver fraction enrichment of FABP1 from male GADD45 beta +/+ (WT) or GADD45 beta −/− (KO) mice fasted for 24 h with (AD‐G45b OE) or without (AD‐NC) liver‐restricted GADD45 beta over‐expression (n = 4/group). Insert shows a representative FABP1 immunoblot.FLiver fraction enrichment of FABP1 from obese/diabetic male db/db mice fasted for 24 h with (AD‐G45b OE) or without (AD‐NC) liver‐restricted GADD45 beta over‐expression (n = 4/group). Insert shows a representative FABP1 immunoblot.GFABP1 and GADD45B immunoblots from Flag immunoprecipitations (IP‐FLAG) or mock IP (IP‐HA) from liver input samples from mice with (AD‐G45b OE) or without (AD‐NC) liver‐restricted GADD45 beta over‐expression. Shown is a representative immunoblot from 3 separate experiments using 3 different input samples per condition.H–JLiver tissue long‐chain acyl‐CoA (LC‐acyl‐CoA) concentrations were determined in GADD45 beta +/+ (WT) or GADD45 beta −/− (KO) mice (H; n = 6/group) with (AD‐G45b OE) or without (AD‐NC) liver‐restricted GADD45 beta over‐expression (I; n = 5/group). Liver LC‐acyl‐CoA concentrations were determined in wild‐type (WT; C57Bl/6J) or obese/diabetic (db/db; BKS.Cg‐m+/+ Lepr DB/J) mice with (AD‐G45b OE) or without (AD‐NC) liver‐restricted GADD45 beta over‐expression (J; n = 4/group).Data information: Data are mean ± SEM. Effect of genotype, *P < 0.05, **P < 0.01, ***P < 0.001. Effect of viral manipulation: #P < 0.05, ##P < 0.01, ###P < 0.001. The statistical test used and respective P‐value outputs can be found in Appendix Table S1. Image collected and cropped by CiteAb from the following publication (https://pubmed.ncbi.nlm.nih.gov/27137487), licensed under a CC-BY license. Not internally tested by R&D Systems.

Detection of Mouse CD36/SR-B3 by Western Blot

HIIT improves lipid metabolism of skeletal muscle in T2DM mice. (A,D) Protein expressions of ACC, HMGCR, CPT-1 alpha, CD36, and internal control alpha -tubulin in skeletal muscle. (B,C,E,F) Quantification of proteins described in (A,D) with normalization to protein levels of alpha -tubulin. All data are presented as mean ± SEM. n = 4 per group; *p < 0.05, **p < 0.01. Image collected and cropped by CiteAb from the following publication (https://pubmed.ncbi.nlm.nih.gov/32922365), licensed under a CC-BY license. Not internally tested by R&D Systems.

Detection of Mouse CD36/SR-B3 by Immunocytochemistry/ Immunofluorescence

Absence of Endo1 increases cell surface CD36 levels and lipid uptake in adipocytes.(A) Cell surface expression of CD36 in mature white adipocytes. **P < 0.01 versus WT. Results are expressed as mean ± SEM (n = 4). Two-tailed t test. (B) Total CD36 expression in gonadal adipose tissue (GAT) and s.c. adipose tissue (SAT). The molecular weights of protein markers are indicated (kDa). Results are expressed as mean ± SEM (n = 5). (C) Immunofluorescence images of CD36 cell surface expression in differentiated white adipocytes (left panel). Level of cellular fluorescence determined by corrected total cell fluorescence per area (CTCF/area). Results are expressed as mean ± SEM (n = 9). ***P < 0.005 versus WT. Two-tailed t test (right panel). Scale bar: 20 μm. (D) Lipid uptake in differentiated adipocytes, mature adipocytes, and differentiated myotubes. Results are expressed as mean ± SEM (n = 5–6). *P < 0.05; **P < 0.01; ****P < 0.001 versus basal. †P < 0.05; ††P < 0.01; ††††P < 0.001 versus WT. One-way ANOVA with Bonferroni correction. Image collected and cropped by CiteAb from the following open publication (https://insight.jci.org/articles/view/168418), licensed under a CC-BY license. Not internally tested by R&D Systems.

Detection of Mouse CD36/SR-B3 by Immunocytochemistry/ Immunofluorescence

Endospanin 1 directly interacts with CD36.(A) Detection of Flag-CD36 in 6Myc-Endo1 immunoprecipitate from HEK293T cells coexpressing 6Myc-Endo1 and Flag-CD36 compared with HEK293T cells transfected with Flag-CD36 alone. Representative blots of 3 independent experiments. (B) Detection of 6Myc-Endo1 after Flag-CD36 immunoprecipitation from HEK293T cells coexpressing 6Myc-Endo1 and Flag-CD36 compared with HEK293T cells transfected with 6Myc-Endo1 alone. Representative blots of 3 independent experiments. (C) Kinetics of Endo1 and CD36 protein expression in differentiated adipocytes during differentiation of adipocyte precursors isolated from the stromal vascular fraction of the s.c. adipose tissue of WT mice into mature white adipocytes. Results are expressed as mean ± SEM of 8 independent experiments. One representative Western blot is shown. (D) Confocal immunofluorescence detection and colocalization of Endo1 (rabbit anti-Endo1) and CD36 (goat anti-CD36) in differentiated adipocytes. Nuclei (blue) are stained with fluorescent DAPI dye. Scale bar: 20 μm. Representative images of 4 independent experiments. (E) Detection of endogenous Endo1 and CD36 after immunoprecipitation with Endo1 or CD36 antibodies from lysates of visceral adipose tissue (VAT), gonadal adipose tissue (GAT), and s.c. adipose tissue (SAT) of WT and KO mice. Endo1-KO adipocytes and tissues were used as negative controls. The molecular weights of protein markers are indicated (kDa). Representative blots of 2 independent experiments. Image collected and cropped by CiteAb from the following open publication (https://insight.jci.org/articles/view/168418), licensed under a CC-BY license. Not internally tested by R&D Systems.

Detection of CD36/SR-B3 by Western Blot

Induced levels of lipogenic proteins after insulin stimulation were lower in DKO hepatocytes.(A) Expression levels of FASN, ACC, and FAT/CD36 in hepatocytes at 360 min after insulin stimulation were analyzed by immunoblotting. (B) Expression levels of lipogenic molecules are presented by measuring band intensities after correction with those of beta -Actin. Open and closed bars indicate WT and DKO hepatocytes, respectively. The numbers of mice examined were WT, n = 3; DKO, n = 4. Data are expressed as means ± S.D. *P<0.05, **P<0.01 and ***P<0.001 as compared between WT and DKO hepatocytes. #P<0.05 and ##P<0.01 as compared between basal and insulin stimulation. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36827398), licensed under a CC-BY license. Not internally tested by R&D Systems.

Detection of CD36/SR-B3 by Western Blot

Induced levels of lipogenic proteins after insulin stimulation were lower in DKO hepatocytes.(A) Expression levels of FASN, ACC, and FAT/CD36 in hepatocytes at 360 min after insulin stimulation were analyzed by immunoblotting. (B) Expression levels of lipogenic molecules are presented by measuring band intensities after correction with those of beta -Actin. Open and closed bars indicate WT and DKO hepatocytes, respectively. The numbers of mice examined were WT, n = 3; DKO, n = 4. Data are expressed as means ± S.D. *P<0.05, **P<0.01 and ***P<0.001 as compared between WT and DKO hepatocytes. #P<0.05 and ##P<0.01 as compared between basal and insulin stimulation. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36827398), licensed under a CC-BY license. Not internally tested by R&D Systems.

Detection of Mouse CD36/SR-B3 by Western Blot

Impact of peroxisomal defect on the expression of phagocytosis-related genes in WT and mutant (Abcd1−/−Abcd2−/− and Acox1−/−) BV-2 cells. (A) Schematic representation of the main actors of phagocytosis. (B) Venn diagrams illustrating the up- and downregulated phagocytosis-related DEGs in Abcd1−/−Abcd2−/− and Acox1−/− non-stimulated BV-2 cells (DataSet GSE200022). Genes whose expression level was measured at the protein level are boxed. (C) Pie chart displaying the number of up- or downregulated phagocytosis-related DEGs after a 24-h LPS treatment (Log2FC > 1, AdjP Value < 0.05) in WT, Abcd1−/−Abcd2−/−, and Acox1−/− BV-2 cells (DataSet GSE237635). (D) Venn diagrams representing the LPS response of these DEGs (three independent batches of BV-2 cells for each genotype). (E) Heat map representing RNA-Seq gene expression of these DEGs at 24 h after LPS stimulation in WT, Abcd1−/−Abcd2−/−, and Acox1−/− BV-2 cells. (F) Representative image of Western blotting analysis (three independent experiments) of the expression levels of CD36, FCGR2B, MRC1, TLR2, and TLR4 in WT, Abcd1−/−Abcd2−/−, and Acox1−/− BV-2 cells untreated (–) or treated with LPS for 24 h (+). Expected molecular weights are indicated. Source data are available online for this figure. Image collected and cropped by CiteAb from the following open publication (https://www.frontiersin.org/articles/10.3389/fnmol.2023.1299314/full), licensed under a CC-BY license. Not internally tested by R&D Systems.