CD36 Antibody - BSA Free

Western Blot: CD36 AntibodyBSA Free [NB400-144]

Western Blot: CD36 Antibody [NB400-144] - Mouse primary muscle cell lysate. Western blot image submitted by a verified customer review.

Immunocytochemistry/ Immunofluorescence: CD36 Antibody - BSA Free [NB400-144]

Immunocytochemistry/Immunofluorescence: CD36 Antibody [NB400-144] - Bone marrrow derived mouse macrophages stained with CD36 antibody. ICC/IF image submitted by a verified customer review.

Western Blot: CD36 AntibodyBSA Free [NB400-144]

Western Blot: CD36 Antibody [NB400-144] - Detection of CD36 in human adipocyte extract (30 ug). Lane 1: 0.5 ug/ml NB 400-144; lane 2: 2 ug/ml NB 400-144. ECL: 3 second exposure.

Western Blot: CD36 Antibody - BSA Free [NB400-144] -

ATM activation by chloroquine alleviates senescence.(a) Immunoblots showing protein levels of ATM, NBS1, and RAP80 in human skin fibroblasts (HSFs). A gradually increased level of p16 indicates cellular senescence, while elevated gammaH2AX level indicates accumulated DNA damage. (b) Immunoblots showing protein levels of ATM, NBS1, and RAP80 in mouse embryonic fibroblasts (MEFs). (c) Immunoblots showing protein levels of ATM, NBS1, and RAP80 in brain tissues isolated from 3-, 10-, and 18-month-old male mice. (d) SA-beta -Gal staining in HSFs treated with sh-ATM or scramble shRNA. Scale bar, 100 µm. (e) Quantification of SA-beta -Gal-positive staining of (d) from five views randomly captured for each group. Data represent means ± SEM. ***p<0.001. (f) Immunoblots showing increased gammaH2AX and unaffected LC3I/II in HSFs treated with sh-ATM or scramble shRNA. (g) Immunoblots showing protein levels of pS1981 ATM, gammaH2AX, and cleaved caspase-3 in HSFs treated with 10 μM of CQ for indicated time. (h) SA-beta -Gal staining in HSFs expressing either scramble or ATM shRNA treated with 1 μM CQ or DMSO (12 hr). Scale bar, 100 µm. (i) Quantification of SA-beta -Gal-positive staining of (h) from five views randomly captured for each group. Data represent means ± SEM. ***p<0.001; ‘N.S.’ indicates no significant difference. (j) HSFs at passage 20 were continuously cultured with 1 μM CQ or DMSO, and cell number was calculated at each passage. Data represent means ± SEM. ***p<0.01. (k) Immunoblots showing protein levels of gammaH2AX, p62, and LC3 in MEFs treated with 1 μM CQ or DMSO. Note that CQ had little effect on the expression levels of p62 and LC3. (l) MEFs at passage one were continuously cultured in 20% O2 with 1 μM CQ or DMSO, and cell number was determined at each passage. Data represent means ± SEM. ***p<0.01.10.7554/eLife.34836.006Figure 1—source data 1.Statistical analysis for SA-beta -Gal positive staining.10.7554/eLife.34836.007Figure 1—source data 2.Statistical analysis for EdU positive staining.Statistical analysis for SA-beta -Gal positive staining.Statistical analysis for EdU positive staining.Decline of ATM-centered DNA repair machinery during senescence.(a) Real-time PCR analysis showing progressively elevated mRNA level of p21 in continuously cultured human endothelial cells (HUVEC). **p<0.01. (b) SA-beta -Gal staining of HUVEC cells at indicated passages. Scale bar, 100 µm. (c) HUVEC cells at P21, P18, P12, and P7 were subjected to transcriptome analysis. A minimum average rpkm value of 1.0 and maximum 10% fluctuation in young cells (P7 Vs P12) was set as the threshold. Genes were downregulated by more than 20% in pre-senescent, and senescent cells compared with young cells (P21/P18 Vs P12/P7) were selected. (d) Pathway analysis of genes identified in (c) by STRING v10. (e) Downregulation of ATM-related DNA repair genes during senescence.ATM regulates replicative senescence.(a) Representative images showing cells treated with Scramble (sh-NC) or sh-ATM. (b) Percent EdU-positive cells in sh-NC or sh-ATM treated HSFs. Views were randomly captured and at least 100 cells were included in each group. Data represent means ± SEM. ***p<0.001. (c) Immunoblots showing protein levels of pS1981 ATM and gammaH2AX in HSFs treated with 10 μM chloroquine (CQ) or 0.4 μM CPT (4 hr). Note that CQ activated ATM (pS1981) without increasing gammaH2AX, while CPT activated ATM accompanied by increased gammaH2AX. (d) SA-beta -Gal staining in primary MEFs treated with 1 μM CQ or DMSO. Scale bar, 100 µm. (e) Quantification of SA-beta -Gal-positive staining of (d) from five views randomly captured for each group. Data represent means ± SEM. ***p<0.001. (f) Percent EdU-positive cells in HSFs treated with DMSO, 1 μM or 10 μM CQ. Views were randomly captured and at least 100 cells were included in each group. Data represent means ± SEM. ***p<0.001. (g) Representative images showing proliferative HSFs treated with different doses of CQ for the indicated time points. (h) Immunoblots showing LC3B levels in HSFs treated with indicated dose of CQ for indicated period of time. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/29717979), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: Rabbit Polyclonal CD36 Antibody [NB400-144] -

Western Blot: Rabbit Polyclonal CD36 Antibody [NB400-144] - The western blot was conducted on avian (passerine) skeletal muscle tissue homogenate. 6ug of total protein was loaded and GAPDH was probed to ensure total protein loads were similar across samples. Rabbit polyclonal CD36 antibody (NB400-144) was used at 1:5000 dilution (diluted in 5% milk). CD36 and GAPDH were probed sequentially - not multiplexed. CD36 produced a band above 40kDa and GAPDH at 36kDa. Image from a verified customer review.

Immunocytochemistry/ Immunofluorescence: CD36 Antibody - BSA Free [NB400-144] -

Immunocytochemistry/ Immunofluorescence: CD36 Antibody - BSA Free [NB400-144] - Timp4-deficiency results in defective lipid digestion & absorption. Fecal triglyceride (TG) content (Ai) in chow- or HFD-fed WT & Timp4−/− mice. Fecal lipid analysis by thin layer chromatography in chow-fed (Aii) & HFD-fed (iii) WT & Timp4−/− mice. (B) Immunostaining for CD36 in small intestine (proximal region) of chow-fed & HFD-fed WT & Timp4−/− mice. Western blot (C) & mRNA (D) levels for CD36 in enterocyte fraction of chow-fed & HFD-fed WT & Timp4−/− mice (collected from the proximal small intestine). (E) Triglyceride levels in enterocytes collected from the proximal small intestine. Averaged data are presented as mean ± S.E.M & analyzed by ANOVA. * indicates significance (p < 0.05). Image collected & cropped by CiteAb from the following publication (https://www.nature.com/articles/s41598-017-05951-4), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: CD36 Antibody - BSA Free [NB400-144] -

Western Blot: CD36 Antibody - BSA Free [NB400-144] - Timp4-deficiency results in defective lipid digestion & absorption. Fecal triglyceride (TG) content (Ai) in chow- or HFD-fed WT & Timp4−/− mice. Fecal lipid analysis by thin layer chromatography in chow-fed (Aii) & HFD-fed (iii) WT & Timp4−/− mice. (B) Immunostaining for CD36 in small intestine (proximal region) of chow-fed & HFD-fed WT & Timp4−/− mice. Western blot (C) & mRNA (D) levels for CD36 in enterocyte fraction of chow-fed & HFD-fed WT & Timp4−/− mice (collected from the proximal small intestine). (E) Triglyceride levels in enterocytes collected from the proximal small intestine. Averaged data are presented as mean ± S.E.M & analyzed by ANOVA. * indicates significance (p < 0.05). Image collected & cropped by CiteAb from the following publication (https://www.nature.com/articles/s41598-017-05951-4), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: CD36 Antibody - BSA Free [NB400-144] -

Western Blot: CD36 Antibody - BSA Free [NB400-144] - MiR-29a inhibits the expression of fatty acid translocase CD36 by targeting 3’ untranslated region (UTR). (A) qPCR analysis of Cd36 in live tissue. (B) Representative immunoblotting bands & densitometric results of CD36 in liver tissue. (C) qPCR analysis of cd36 expression of HepG2 cells in vitro after 48h transfection of scramble sequence or miR-29a-mimic. Data obtained from six independent experiments. (D) Upper panel, sequence information, & mutual pairing status of CD36-3’UTR, mmu-miR29a, & CD36-3’UTR Mut. Note that red characters represent mismatching sites. HepG2 was first transfected with CD36-3’UTR or CD36-3’UTR mutant luciferase reporter construct then treated with control medium (ctrl), miRNA-scramble, or miR-29a mimic, & finally lysed to detect the luciferase signal. Data are expressed as mean ± SE. * p < 0.05, ** p < 0.01, & *** p < 0.001 between the indicated groups. WT, wild type mice. HFD, high-fat diet. miR-29a, mice harboring overexpression of miR-29a. mmu-miR29a, mouse-origin miR-29a. ctrl, control. Mut, mutant. UTR, untranslated region. Image collected & cropped by CiteAb from the following publication (https://pubmed.ncbi.nlm.nih.gov/31652636), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Immunohistochemistry: CD36 Antibody - BSA Free [NB400-144] -

Immunohistochemistry: CD36 Antibody - BSA Free [NB400-144] - Integrin beta3 modulates SMC transdifferentiation. a–c Mice were fed a HFD for 6 or 16 weeks as indicated, & then transverse aortic root sections were stained. In a, b sections from ApoE(−/−), SMMHC-CreERT2, ROSA26R(mTmG/+) mice were stained for SMA, GFP (fate marker), nuclei (DAPI), & either integrin beta3 (a) or CD36 (b). Dashed yellow lines separate cap from core (a, b) & core from media (b). n = 5. In c sections from ApoE(−/−) mice that were also wild type or null for Itgb3 were stained for SMMHC, CD68, & nuclei (DAPI). n = 3. Boxed regions (a, c) are shown as close-ups on right; in c CD68+SMMHC+ cells in the media (arrowheads) & plaque (arrows) of the Itgb3 null atherosclerotic aorta are indicated. Med, tunica media; Lu, lumen; Pl, plaque. Scale bars, 25 μm. d–h Aortic SMCs were isolated from ApoE(−/−) mice & then subjected to siRNA-mediated knockdown with si-Itgb3 vs. scrambled (Scr; d–f) or with si-Itgb3, si-Tlr4 vs. si-Itgb3 (g, h). Levels of indicated transcripts from qRT-PCR are relative to Gapdh & normalized to either Scr in d, f or to si-Itgb3 in g, h. For d, g, n = 4–5 in duplicate. In e silenced SMCs were cultured with DiI-conjugated ox-LDL for 10 h & stained with DAPI; n = 5. In f, h silenced SMCs were exposed to soluble cholesterol:methyl-beta -cyclodextrin complexes for 3 days, & then mRNA levels were assessed; n = 4–7 in duplicate. *, **, ***, ^, **** vs. control (Scr in d, f & si-Itgb3 in g, h), p < 0.05, p < 0.01, p < 0.005, p < 0.001, & p < 0.0005, respectively. NS, not significant. Student’s t-test was used, & error bars represent standard deviations. i Schematic of the effect of beta3 reduction via TLR4 & CD36 in SMCs on transdifferentiation Image collected & cropped by CiteAb from the following publication (https://www.nature.com/articles/s41467-018-04447-7), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: CD36 Antibody - BSA Free [NB400-144] -

Western Blot: CD36 Antibody - BSA Free [NB400-144] - The increase in CD36 levels caused by lipids in Sirt3-deficient hepatocytes is mediated by Nrf2. VLDLR mRNA abundance (a) & protein levels of VLDLR & NQO1, an Nrf-2-target gene, (b) were assessed in Huh-7 cells incubated with fatty acid free-BSA or BSA-palmitate (0.3 mM) & exposed to either vehicle or the Sirt3 inhibitor AAPBO (100 μM) for 16 h. a, p < 0.05 vs. CT. b, p < 0.05 vs. CT cells incubated with palmitate. c, p < 0.05 vs. CT cells treated with AAPBO. c, fatty acid uptake in Huh-7 cells incubated with fatty acid free-BSA or BSA-palmitate (0.3 mM) & exposed to either vehicle or the Sirt3 inhibitor AAPBO (100 μM) for 16 h was measured by the uptake of BODIPY-C16. a, p < 0.05 vs. CT. b, p < 0.05 vs. CT cells incubated with palmitate. c, p < 0.05 vs. CT cells treated with AAPBO. mRNA abundance (d) & protein levels of VLDLR (e) in Huh-7 cells transfected with control (CT) or SIRT3 siRNA & incubated in the presence or absence 0.3 mM palmitate (Pal) for 24 h. Protein levels of CD36 (f), NQO1 (g) & PPAR gamma (h) in Huh-7 cells transfected with control (CT) or SIRT3 siRNA & incubated in the presence or absence 0.3 mM palmitate (Pal) or the Nrf2 inhibitor ML385 (10 μM) for 24 h. a, p < 0.05 vs. CT siRNA cells. b, p < 0.05 vs. CT siRNA cells incubated with palmitate. c, p < 0.05 vs. SIRT3 siRNA cells. d, p < 0.05 vs. CT siRNA cells incubated with palmitate & ML385 Image collected & cropped by CiteAb from the following publication (https://pubmed.ncbi.nlm.nih.gov/32912335), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: CD36 Antibody - BSA Free [NB400-144] -

Western Blot: CD36 Antibody - BSA Free [NB400-144] - The increase in CD36 levels caused by lipids in Sirt3-deficient hepatocytes is mediated by Nrf2. VLDLR mRNA abundance (a) & protein levels of VLDLR & NQO1, an Nrf-2-target gene, (b) were assessed in Huh-7 cells incubated with fatty acid free-BSA or BSA-palmitate (0.3 mM) & exposed to either vehicle or the Sirt3 inhibitor AAPBO (100 μM) for 16 h. a, p < 0.05 vs. CT. b, p < 0.05 vs. CT cells incubated with palmitate. c, p < 0.05 vs. CT cells treated with AAPBO. c, fatty acid uptake in Huh-7 cells incubated with fatty acid free-BSA or BSA-palmitate (0.3 mM) & exposed to either vehicle or the Sirt3 inhibitor AAPBO (100 μM) for 16 h was measured by the uptake of BODIPY-C16. a, p < 0.05 vs. CT. b, p < 0.05 vs. CT cells incubated with palmitate. c, p < 0.05 vs. CT cells treated with AAPBO. mRNA abundance (d) & protein levels of VLDLR (e) in Huh-7 cells transfected with control (CT) or SIRT3 siRNA & incubated in the presence or absence 0.3 mM palmitate (Pal) for 24 h. Protein levels of CD36 (f), NQO1 (g) & PPAR gamma (h) in Huh-7 cells transfected with control (CT) or SIRT3 siRNA & incubated in the presence or absence 0.3 mM palmitate (Pal) or the Nrf2 inhibitor ML385 (10 μM) for 24 h. a, p < 0.05 vs. CT siRNA cells. b, p < 0.05 vs. CT siRNA cells incubated with palmitate. c, p < 0.05 vs. SIRT3 siRNA cells. d, p < 0.05 vs. CT siRNA cells incubated with palmitate & ML385 Image collected & cropped by CiteAb from the following publication (https://pubmed.ncbi.nlm.nih.gov/32912335), licensed under a CC-BY license. Not internally tested by Novus Biologicals.