CD68 (E3O7V) Mouse Chimeric mAb 41077T from Cell Signaling Technology

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Biological Research
January 28 2026

Fig 1: Elevated copper-induced cell death in the AS model. ApoE−/− mice were fed an HFD for 12 weeks to establish the AS model and their aortas were used for experiments. A A commercial kit was used to measure plasma levels of TC, TG, LDL-C and HDL-C. HDL-C: MeanControl = 4.128; MeanAS = 2.427; 95% CI [− 2.855, − 0.5484]. LDL-C: MeanControl = 2.115; MeanAS = 7.168; 95% CI [4.171, 5.936]. TC: MeanControl = 3.910; MeanAS = 13.32; 95% CI [7.415, 11.41]. TG: MeanControl = 2.608; MeanAS = 8.608; 95% CI [4.362, 7.638]. B Lipid accumulation in aortic plaques was analyzed by Oil Red O staining. MeanControl = 0.000; MeanAS = 15.81; 95% CI [9.120, 22.51]. C Plaque morphology, size and necrotic core area in the aortas were assessed by HE staining. MeanControl = 0.000; MeanAS = 6.285; 95% CI [3.876, 8.694]. D ROS levels were detected using the fluorescent probe DCFH-DA. MeanControl = 9.453; MeanAS = 22.27; 95% CI [5.498, 20.13]. E Immunohistochemistry was performed to evaluate the expression of α-SMA and CD68 in mouse aortas (200X). α-SMA: MeanControl = 8.767; MeanAS = 5.098; 95% CI [− 6.919, − 0.4181]. CD68: MeanControl = 0.7033; MeanAS = 15.76; 95% CI [9.006, 21.10]. F Copper ion content was measured using a dedicated assay kit. MeanControl = 32.10; MeanAS = 54.26; 95% CI [8.858, 35.47]. G WB was used to analyze the expression of copper-induced cell death-related genes (DLAT, SLC31A1, ATP7A, LIAS and FDX1) in mouse aortas. HAVSMCs were treated with the copper ionophore ES-Cu2+. DLAT: MeanControl = 1; MeanAS = 0.5003; 95% CI [− 0.5785, − 0.4208]. SLC31A1: MeanControl = 1; MeanAS = 1.864; 95% CI [0.5517, 1.177]. ATP7A: MeanControl = 1; MeanAS = 0.4682; 95% CI [− 0.6814, − 0.3821]. LIAS: MeanControl = 1; MeanAS = 0.6063; 95% CI [− 0.6198, − 0.1676]. FDX1: MeanControl = 1; MeanAS = 0.4903; 95% CI [− 0.6642, − 0.3553]. H Hoechst/PI staining was used to quantify the red/blue fluorescence intensity ratio (indicating cell death) in HAVSMCs. I ROS levels were detected using the DCFH-DA probe. J The activity of TCA cycle rate-limiting enzymes (α-ketoglutarate dehydrogenase and citrate synthase) in HAVSMCs was measured using assay kits. K WB was performed to assess the expression of copper detoxification-related genes (DLAT, SLC31A1, ATP7A, LIAS and FDX1) in HAVSMCs. *p < 0.05; **p < 0.01; ***p < 0.001 versus Control/Ethanol/Ethanol + Cholesterol/Ethanol + ES-Cu2+
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Biological Research
January 28 2026

Fig 2: Knockdown of U2AF2 has a stabilizing effect on plaques and delays the progression of atherosclerosis. ApoE−/− male mice were injected with lentivirus carrying sh-U2AF2 via the tail vein, followed by an HFD for 12 weeks after 4 weeks. Aortic tissues were collected for subsequent experiments. A qRT-PCR was used to detect the expression of U2AF2 and C1qbp mRNA in aortic tissues. U2AF2: MeanControl = 1.015; MeanAS = 3.319; MeanAS+LV-sh-NC = 3.480; MeanAS+LV-sh-U2AF2 = 1.748; 95% CIControl/AS [− 3.245, 3.264]; 95% CIAS+LV-sh-NC/AS+LV-sh-U2AF2 [0.7917, 2.673]; C1qbp: MeanControl = 1.016; MeanAS = 4.814; MeanAS+LV-sh-NC = 4.691; MeanAS+LV-sh-U2AF2 = 3.163; 95% CIControl/AS [− 5.030, − 2.566]; 95% CIAS+LV-sh-NC/AS+LV-sh-U2AF2 [0.2966, 2.761]. B, C Immunohistochemistry was performed to detect the protein expression of U2AF2 and C1qbp in aortic tissues (200X). U2AF2: MeanControl = 15.37; MeanAS = 32.36; MeanAS+LV-sh-NC = 31.96; MeanAS+LV-sh-U2AF2 = 20.04; 95% CIControl/AS [0.4048, 33.56]; 95% CIAS+LV-sh-NC/AS+LV-sh-U2AF2 [− 21.06, − 2.773]; C1qbp: MeanControl = 2.739; MeanAS = 22.2; MeanAS+LV-sh-NC = 23.20; MeanAS+LV-sh-U2AF2 = 14.55; 95% CIControl/AS [4.433, 34.43]; 95% CIAS+LV-sh-NC/AS+LV-sh-U2AF2 [− 17.14, − 0.1504]. D TUNEL staining was used to show dead cells in the fibrous cap of the plaque surface. MeanControl = 6.432; MeanAS = 47.72; MeanAS+LV-sh-NC = 46.46; MeanAS+LV-sh-U2AF2 = 25.77; 95% CIControl/AS [22.21, 60.36]; 95% CIAS+LV-sh-NC/AS+LV-sh-U2AF2 [− 41.35, − 0.048]. E Immunohistochemistry was used to detect the expression of α-SMA and CD68 in aortic tissues (200X). α-SMA: MeanControl = 12.01; MeanAS = 5.505; MeanAS+LV-sh-NC = 6.047; MeanAS+LV-sh-U2AF2 = 8.808; 95% CIControl/AS [− 12, − 1.011]; 95% CIAS+LV-sh-NC/AS+LV-sh-U2AF2 [0.0090, 5.514]; CD68: MeanControl = 0.525; MeanAS = 17.44; MeanAS+LV-sh-NC = 16.03; MeanAS+LV-sh-U2AF2 = 8.998; 95% CIControl/AS[6.959, 26.87]; 95% CIAS+LV-sh-NC/AS+LV-sh-U2AF2 [− 13.70, − 0.3661]. F HE staining was used to observe atherosclerotic plaques and foam cells in aortic tissues. MeanControl = 0; MeanAS = 11.13; MeanAS+LV-sh-NC = 10.59; MeanAS+LV-sh-U2AF2 = 5.783; 95% CIControl/AS [7.233, 15.02]; 95% CIAS+LV-sh-NC/AS+LV-sh-U2AF2 [− 9.37, − 0.24]. G Masson’s trichrome staining was used to measure collagen content. MeanControl = 12.02; MeanAS = 35.90; MeanAS+LV-sh-NC = 37.44; MeanAS+LV-sh-U2AF2 = 20.70; 95% CIControl/AS [13.82, 33.94]; 95% CIAS+LV-sh-NC/AS+LV-sh-U2AF2 [− 26.71, − 6.775]. H Oil Red O staining was performed to analyze lipid accumulation in the plaques. MeanControl = 0; MeanAS = 16.88; MeanAS+LV-sh-NC = 16.22; MeanAS+LV-sh-U2AF2 = 8.845; 95% CIControl/AS [9.303, 24.45]; 95% CIAS+LV-sh-NC/AS+LV-sh-U2AF2 [− 16.13, 0.6699]. I Kits were used to detect the levels of TC, TG, LDL-C and HDL-C in plasma. HDL-C: MeanControl = 4.355; Mean AS = 2.658; MeanAS+LV-sh-NC = 2.753; Mean AS+LV-sh-U2AF2 = 3.952; 95% CIControl/AS [− 2.939, − 0.4539]; 95% CIAS+LV-sh-NC/AS+LV-sh-U2AF2 [− 0.551, 2.342]; LDL-C: MeanControl = 2.325; MeanAS = 5.388; MeanAS+LV-sh-NC = 5.287; MeanAS+LV-sh-U2AF2 = 2.865; 95% CIControl/AS [1.962, 4.165]; 95% CIAS+LV-sh-NC/AS+LV-sh-U2AF2 [− 3.365, − 1.487]; TC: MeanControl = 4.147; MeanAS = 11.73; MeanAS+LV-sh-NC = 10.72; MeanAS+LV-sh-U2AF2 = 6.462; 95% CIControl/AS [5.343, 9.814]; 95% CIAS+LV-sh-NC/AS+LV-sh-U2AF2 [− 6.859, − 1.655]; TG:MeanControl = 2.608; MeanAS = 8.608; MeanAS+LV-sh-NC = 7.963; MeanAS+LV-sh-U2AF2 = 4.275; 95% CIControl/AS [4.362, 7.638]; 95% CIAS+LV-sh-NC/AS+LV-sh-U2AF2 [− 6.039, − 1.338]. *p < 0.05; **p < 0.01; ***p < 0.001 versuss Control/AS + LV-sh-NC. NC means negative control of LV-sh-U2AF2
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Cellular and Molecular Life Sciences
April 14 2026

Fig 3: GFPT2 knockdown ameliorated AS in vivo. (A–B) Body weight monitoring and serum lipid profile measurement, including TC, TG, LDL-C and HDL-C, revealing the effects of GFPT2 knockdown on weight gain and lipid profile change in AS mice. (C–D) WB and IF analyses were performed to assess the impact of GFPT2 knockdown on the expression of GFPT2, ACADL, and Arg1 in abdominal aortic tissues of AS mice. (E) IF double staining demonstrating the impact of GFPT2 knockdown on the co-localization of the macrophage marker CD68 with GFPT2 or ACADL. (F–I) H&E and Oil-red-O staining evaluating the effects of GFPT2 knockdown on plaque formation, foam cell accumulation, and lipid deposition in abdominal aortic tissues. (J–K) In vivo, fluorescence microscopy was employed to examine the influence of GFPT2 knockdown on efferocytosis function of primary peritoneal macrophages. (L–R) Flow cytometry, qRT-PCR and ELISA assays demonstrated that GFPT2 knockdown modulated CD36 and MerTK expression in surface of primary peritoneal macrophages from AS mice, as well as MCP-1 and IL-8 serum levels. ***p < 0.001, **p < 0.01, *p < 0.05 vs Con/ AS+sh-NC

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CD68 (E3O7V) Mouse Chimeric mAb

The CD68 (E3O7V) Mouse Chimeric mAb Antibody from Cell Signaling Technology is a Mouse Monoclonal antibody to CD68. This antibody recognizes Mouse, Rat, and Hamster antigen. The CD68 (E3O7V) Mouse Chimeric mAb Antibody has been shown to work in the following applications: Immunofluorescence.

Biological Research

Biological Research

Cellular and Molecular Life Sciences

CD68 (E3O7V) Mouse Chimeric mAb from Cell Signaling Technology

Cell Signaling Technology

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CD68 (E3O7V) Mouse Chimeric mAb from Cell Signaling Technology

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