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Cell Signaling Technology Inc col i ab270993

Involvement of profibrotic macrophages in vascular regeneration after graft implantation in vivo . (a) UMAP of macrophages in native aortas and regenerated aortas across different time points after graft implantation in vivo . (b) Dot plots of profibrotic macrophage marker genes <t>(Ctsd,</t> <t>Spp1,</t> Gpnmb, Lgals3, and Fabp5) expressed in different subgroups of macrophages. (c) Percentage of cluster 2 (C2) macrophages in native aortas and regenerated aortas across different time points after graft implantation in vivo . (d) UMAP of expression of Ctsd, Spp1, Gpnmb, Lgals3, and Fabp5 in macrophages in native aortas and regenerated aortas across different time points after graft implantation in vivo . (e) Immunofluorescence staining of CD68 and CTSD in regenerated aortas across different time points after graft implantation in vivo . L indicates lumens. Arrow heads indicate double positively stained cells. (f) WB results of levels of CTSD and SPP1 in native and regenerated aortas across different time points after graft implantation in vivo and quantification of the levels of CTSD and SPP1. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different samples from five different animals were analyzed (n = 5).

Col I Ab270993, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 257 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Apolipoprotein E knockout attenuates vascular graft fibrosis by reducing profibrotic macrophage formation through low-density lipoprotein receptor related protein 1"

Article Title: Apolipoprotein E knockout attenuates vascular graft fibrosis by reducing profibrotic macrophage formation through low-density lipoprotein receptor related protein 1

Journal: Bioactive Materials

doi: 10.1016/j.bioactmat.2026.01.029

Figure Legend Snippet: Involvement of profibrotic macrophages in vascular regeneration after graft implantation in vivo . (a) UMAP of macrophages in native aortas and regenerated aortas across different time points after graft implantation in vivo . (b) Dot plots of profibrotic macrophage marker genes (Ctsd, Spp1, Gpnmb, Lgals3, and Fabp5) expressed in different subgroups of macrophages. (c) Percentage of cluster 2 (C2) macrophages in native aortas and regenerated aortas across different time points after graft implantation in vivo . (d) UMAP of expression of Ctsd, Spp1, Gpnmb, Lgals3, and Fabp5 in macrophages in native aortas and regenerated aortas across different time points after graft implantation in vivo . (e) Immunofluorescence staining of CD68 and CTSD in regenerated aortas across different time points after graft implantation in vivo . L indicates lumens. Arrow heads indicate double positively stained cells. (f) WB results of levels of CTSD and SPP1 in native and regenerated aortas across different time points after graft implantation in vivo and quantification of the levels of CTSD and SPP1. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different samples from five different animals were analyzed (n = 5).

Techniques Used: In Vivo, Marker, Expressing, Immunofluorescence, Staining

APOE KO reducing profibrotic macrophage formation during vascular regeneration. (a) UMAP of macrophages in native aortas from WT and Apoe −/− rats, heatmap of C2 scores in the UMAP of macrophages in the native aortas, and percentage of C2 cells in macrophages in the native aortas. UMAP of macrophages in regenerated aortas after graft implantation in WT and Apoe −/− rats, heatmap of C2 scores in the UMAP of macrophages in the regenerated aortas, and percentage of C2 cells in macrophages in the regenerated aortas on Day 30 (b) and Day 90 (c). (d) Immunofluorescence staining of CD68 and CTSD in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe−/− rats. (e) Quantification of CD68 and CTSD double positive cells in regenerated aortas on Day 30 and Day 90. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different images from five different samples were analyzed (n = 5). (f) WB results of APOE, CTSD and SPP1 levels in regenerated aortas after graft implantation in WT and Apoe −/− rats for 30 and 90 days. (g) Quantification of levels of APOE, CTSD and SPP1 in regenerated aortas on Day 30 and Day 90. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different samples from five different animals were analyzed (n = 5). (h) WB results of APOE, CTSD and SPP1 levels in WT and APOE KO macrophages after their culture on PCL scaffolds for 48 h. (i) Quantification of levels of APOE, CTSD and SPP1 in WT and APOE KO macrophages after their culture on PCL scaffolds for 48 h ∗ indicates p < 0.05, ∗∗ indicates p < 0.01, unpaired t -test. For each time point and each group, three different samples were analyzed (n = 3). (j) Immunofluorescence staining of APOE and CD68, CTSD and CD68, SPP1 and CD68, respectively, in WT and APOE KO macrophages after their culture on PCL scaffolds for 48 h.

Figure Legend Snippet: APOE KO reducing profibrotic macrophage formation during vascular regeneration. (a) UMAP of macrophages in native aortas from WT and Apoe −/− rats, heatmap of C2 scores in the UMAP of macrophages in the native aortas, and percentage of C2 cells in macrophages in the native aortas. UMAP of macrophages in regenerated aortas after graft implantation in WT and Apoe −/− rats, heatmap of C2 scores in the UMAP of macrophages in the regenerated aortas, and percentage of C2 cells in macrophages in the regenerated aortas on Day 30 (b) and Day 90 (c). (d) Immunofluorescence staining of CD68 and CTSD in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe−/− rats. (e) Quantification of CD68 and CTSD double positive cells in regenerated aortas on Day 30 and Day 90. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different images from five different samples were analyzed (n = 5). (f) WB results of APOE, CTSD and SPP1 levels in regenerated aortas after graft implantation in WT and Apoe −/− rats for 30 and 90 days. (g) Quantification of levels of APOE, CTSD and SPP1 in regenerated aortas on Day 30 and Day 90. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different samples from five different animals were analyzed (n = 5). (h) WB results of APOE, CTSD and SPP1 levels in WT and APOE KO macrophages after their culture on PCL scaffolds for 48 h. (i) Quantification of levels of APOE, CTSD and SPP1 in WT and APOE KO macrophages after their culture on PCL scaffolds for 48 h ∗ indicates p < 0.05, ∗∗ indicates p < 0.01, unpaired t -test. For each time point and each group, three different samples were analyzed (n = 3). (j) Immunofluorescence staining of APOE and CD68, CTSD and CD68, SPP1 and CD68, respectively, in WT and APOE KO macrophages after their culture on PCL scaffolds for 48 h.

Techniques Used: Immunofluorescence, Staining

APOE/LRP1 interaction promoting profibrotic macrophage formation during vascular regeneration after graft implantation in vivo . (a) Immunoprecipitation (IP) following mass spectrometry (MS) to screen potential receptors of APOE on surfaces of macrophages. (b) Co-immunoprecipitation (Co-IP) to confirm interaction between APOE and LRP1. (c) Immunofluorescence staining of CD68 and LRP1 in regenerated aortas across different time points. (d) Immunofluorescence staining of APOE and LRP1 in WT macrophages 48 h after their culture on PCL scaffolds. (e) WB results of LRP1, APOE, CTSD and SPP1 levels in WT macrophages cultured on tissue culture plates (negative control, NC) or PCL scaffolds (PCL) for 48 h prior to treatment with shRNA ADV-shRNA(NC) or ADV-shRNA(Lrp1) for 24 h. Quantification of levels of LRP1 (f), APOE (g), CTSD (h) and SPP1 (i) in WT macrophages cultured on tissue culture plates or PCL scaffolds treated with shRNA ADV-shRNA(NC) or ADV-shRNA(Lrp1). ∗ indicates p < 0.05, ∗∗ indicates p < 0.01, N.S. indicates non-significant. Tukey's post-hoc test. For each group, three different samples were analyzed (n = 3). (j) Flow cytometry analysis of CTSD positive cells in WT macrophages cultured on tissue culture plates (negative control, NC) or PCL scaffolds (PCL) for 48 h prior to treatment with ADV-shRNA(NC) or ADV-shRNA(Lrp1) for 24 h and quantification of percentage of CTSD positive cells in WT macrophages in each group. ∗ indicates p < 0.05, Tukey's post-hoc test. For each group, three independent experiments were repeated, and results were analyzed (n = 3).

Figure Legend Snippet: APOE/LRP1 interaction promoting profibrotic macrophage formation during vascular regeneration after graft implantation in vivo . (a) Immunoprecipitation (IP) following mass spectrometry (MS) to screen potential receptors of APOE on surfaces of macrophages. (b) Co-immunoprecipitation (Co-IP) to confirm interaction between APOE and LRP1. (c) Immunofluorescence staining of CD68 and LRP1 in regenerated aortas across different time points. (d) Immunofluorescence staining of APOE and LRP1 in WT macrophages 48 h after their culture on PCL scaffolds. (e) WB results of LRP1, APOE, CTSD and SPP1 levels in WT macrophages cultured on tissue culture plates (negative control, NC) or PCL scaffolds (PCL) for 48 h prior to treatment with shRNA ADV-shRNA(NC) or ADV-shRNA(Lrp1) for 24 h. Quantification of levels of LRP1 (f), APOE (g), CTSD (h) and SPP1 (i) in WT macrophages cultured on tissue culture plates or PCL scaffolds treated with shRNA ADV-shRNA(NC) or ADV-shRNA(Lrp1). ∗ indicates p < 0.05, ∗∗ indicates p < 0.01, N.S. indicates non-significant. Tukey's post-hoc test. For each group, three different samples were analyzed (n = 3). (j) Flow cytometry analysis of CTSD positive cells in WT macrophages cultured on tissue culture plates (negative control, NC) or PCL scaffolds (PCL) for 48 h prior to treatment with ADV-shRNA(NC) or ADV-shRNA(Lrp1) for 24 h and quantification of percentage of CTSD positive cells in WT macrophages in each group. ∗ indicates p < 0.05, Tukey's post-hoc test. For each group, three independent experiments were repeated, and results were analyzed (n = 3).

Techniques Used: In Vivo, Immunoprecipitation, Mass Spectrometry, Co-Immunoprecipitation Assay, Immunofluorescence, Staining, Cell Culture, Negative Control, shRNA, Flow Cytometry

Downregulation of APOE by AAV ameliorating fibrosis during vascular regeneration after graft implantation in vivo . (a) Illustration of a strategy of adventitial delivery of AAV-shRNA(Apoe) to inhibit APOE levels in regenerated aortas after graft implantation in vivo . Two weeks after graft implantation in vivo , AAV-shRNA(Apoe) were injected into the adventitia of the regenerated aortas, which were then harvested for analysis three weeks later. (b) M mode images of ultrasound detection of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. Arrow heads indicate movement of vascular walls. (c) Tensile tests of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. (d) Quantification of RI, PI, and compliance of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different images from six different animals were analyzed (n = 6). (e) Quantification of elastic modulus of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different images from six different animals were analyzed (n = 6). (f) H&E, MTC and EVG staining of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. (g) Immunofluorescence staining of COL I, COL III, elastin, αSMA, and eNOS in regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. L indicates lumens. Arrow heads indicate capillaries. Quantification of adventitia thickness (h), collagen positive areas according to MTC staining (i), elastin positive areas according to EVG staining (j), COL I positive areas (k), COL III positive areas (l), and number of capillaries (m) in adventitial areas of regenerated aortas. (n) Immunofluorescence staining of CTSD and CD68 in regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. (o) CD68 and CTSD double positive cells in regenerated aortas. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different samples from six different animals were analyzed (n = 6). (p) WB results of APOE, CTSD and SPP1 levels in regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks and quantification of levels of APOE, CTSD and SPP1 in regenerated aortas. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different samples from six different animals were analyzed (n = 6). (q) Quantification of IGF-1 concentrations in regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks by ELISA. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different samples from six different animals were analyzed (n = 3).

Figure Legend Snippet: Downregulation of APOE by AAV ameliorating fibrosis during vascular regeneration after graft implantation in vivo . (a) Illustration of a strategy of adventitial delivery of AAV-shRNA(Apoe) to inhibit APOE levels in regenerated aortas after graft implantation in vivo . Two weeks after graft implantation in vivo , AAV-shRNA(Apoe) were injected into the adventitia of the regenerated aortas, which were then harvested for analysis three weeks later. (b) M mode images of ultrasound detection of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. Arrow heads indicate movement of vascular walls. (c) Tensile tests of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. (d) Quantification of RI, PI, and compliance of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different images from six different animals were analyzed (n = 6). (e) Quantification of elastic modulus of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different images from six different animals were analyzed (n = 6). (f) H&E, MTC and EVG staining of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. (g) Immunofluorescence staining of COL I, COL III, elastin, αSMA, and eNOS in regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. L indicates lumens. Arrow heads indicate capillaries. Quantification of adventitia thickness (h), collagen positive areas according to MTC staining (i), elastin positive areas according to EVG staining (j), COL I positive areas (k), COL III positive areas (l), and number of capillaries (m) in adventitial areas of regenerated aortas. (n) Immunofluorescence staining of CTSD and CD68 in regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. (o) CD68 and CTSD double positive cells in regenerated aortas. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different samples from six different animals were analyzed (n = 6). (p) WB results of APOE, CTSD and SPP1 levels in regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks and quantification of levels of APOE, CTSD and SPP1 in regenerated aortas. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different samples from six different animals were analyzed (n = 6). (q) Quantification of IGF-1 concentrations in regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks by ELISA. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different samples from six different animals were analyzed (n = 3).

Techniques Used: In Vivo, shRNA, Injection, Staining, Immunofluorescence, Enzyme-linked Immunosorbent Assay

Membrane:

Article Title: Anticancer effect of piperine, a black pepper compound, regulating apoptosis mediated through extracellular vesicles and cathepsin D in acute leukemia.
Article Snippet: The proteins on the SDS polyacrylamide gel 433 were transferred to a PVDF membrane, which was blocked with 5% skim milk, 5% 434 BSA, or BlockPROTM protein-free blocking buffer (Visual Protein, Taiwan). .. Then, the 435 proteins on the PVDF membrane were incubated with primary antibodies against 436 CTSD, Bax, Caspase-3 (Cell Signaling Technology, USA), and α-tubulin 437 (Proteintech, USA) overnight at 4 °C. .. Next, the PVDF membrane (GVS Filter 438 Technology, Italy) was incubated with secondary antibodies, including mouse IgG 439 or rabbit IgG conjugated with horseradish peroxidase (HRP) (Cell Signaling 440 Technology, USA), depending on the source of the primary antibody.

Incubation:

Article Title: Disruption of FGL2 induces TFEB-dependent lysosomal degradation of PD-L1 and enhances the efficacy of anti-PD1 therapy in hepatocellular carcinoma
Article Snippet: .. Next, membranes were incubated with the following antibodies: FGL2 (1:500) (sc-100276, Santa Cruz Biotechnology), PD-L1 (1:4000) (66248-1-Ig, Proteintech), DDDDK-Tag (1:5000) (AE063, Abclonal), LAMP1 (1:10000) (67300-1-Ig, Proteintech), CTSD (1:10000) (21327-1-AP, Proteintech), TFEB (1:5000) (68632-1-Ig, Proteintech), phospho-TFEB (1:1000) (37681, CST), TFE3 (1:500) (A7936, Abclonal), MITF (1:1000) (13092-1-AP, Proteintech), GAPDH (1:50000) (60004-1-Ig, Proteintech), Histone H3 (1:5000) (17168-1-AP, Proteintech), p70S6K (1:1000) (2708, CST), phospho-p70S6K (1:1000) (9234, CST), 4EBP1 (1:1000) (9644, CST), phospho-4EBP1 (1:1000) (2855, CST), AKT (1:1000) (9272, CST), phospho-AKT (1:1000) (4060, CST), GSK3β(1:1000) (12456, CST), phospho-GSK3β (1:1000) (5558, CST), PKC (1:4000) (12919-1-AP, Proteintech), phospho-PKC (1:1000) (38938, CST), ERK1/2 (1:1000) (16443-1-AP, Proteintech), phospho-p44/42 MAPK (Erk1/2) (1:2000) (4370, CST), ATG5 (1:2000) (10181-2-AP, Proteintech), ATG7 (1:1000) (10088-2-AP, Proteintech), HRP goat anti-rabbit IgG (1:10000) (A21020, Abbkine) and HRP goat anti-mouse IgG (1:10000) (A21010, Abbkine). ..

Article Title: Apolipoprotein E knockout attenuates vascular graft fibrosis by reducing profibrotic macrophage formation through low-density lipoprotein receptor related protein 1
Article Snippet: .. Then, the cells were incubated with CTSD (CST, 74089S, 1:200 dilution) at room temperature for 1 h. After that, PBS was used to wash cells again, and the secondary antibodies were used to incubate the cells at room temperature for 1 h. Samples were analyzed using flow cytometer (BD, FACSCalibur). ..

Imaging:

Article Title: Autophagy across tissues of aging mice
Article Snippet: .. Primary antibodies: ATG2B (rabbit polyclonal, PA5-85718, Thermo Fisher); ATG5 (rabbit monoclonal, CST 12994, Cell Signalling Technology); ATG7 (rabbit monoclonal, CST8558, Cell Signalling Technology); ATG13 (rabbit monoclonal, CST 13273, Cell Signalling Technology); ATG16L1 (rabbit monoclonal, CST 8089, Cell Signalling Technology); BECN1 (mouse monoclonal, SC-48341, Santa Cruz); CD3 (clone: 17A2, rat monoclonal-FITC conjugate, CST 86603, Cell Signalling Technology); CD19 (clone: 1D3, rat monoclonal-PE conjugate, CST 82168, Cell Signalling Technology); CTSD (rabbit monoclonal, CST 74089, Cell Signalling Technology); F4/80 (clone: BM8.1, rat monoclonal-VioletFluor450 conjugate, CST 40781, Cell Signalling Technology); FIP200 (rabbit monoclonal, CST 12436, Cell Signalling Technology); GFAP (chicken polyclonal, ab4674, Abcam); GFP (rabbit polyclonal, A-6455, Thermo Fisher) IBA1 (goat polyclonal, ab48004, Abcam); LC3B (rabbit polyclonal, NB100-2220, Novus Biologicals); LMNB1 (rabbit monoclonal, CST 13435, Cell Signalling Technology); NBR1 (rabbit polyclonal, ab126175, Abcam); NeuN (clone: E4M5P, mouse monoclonal, CST 94403, Cell Signalling Technology); NDP52 (rabbit polyclonal, Ab68588, Abcam); SQSTM1/p62 (rabbit polyclonal, PM045, MBL Life Science (imaging) and mouse monoclonal, H00008878-M01, Novus Biologicals (Immunoblotting); ULK1 (rabbit monoclonal, CST 8054, Cell Signalling Technology). .. Secondary Antibodies: Alexa Fluor-488 donkey anti-goat IgG (705-545-003; Jackson ImmunoResearch); Alexa Fluor 488 donkey anti-mouse IgG (715-545-151; Jackson ImmunoResearch); Alexa Fluor 647-donkey anti-mouse IgG (715-605-150; Jackson ImmunoResearch); Alexa Fluor 647-donkey anti-rabbit IgG (711-605-152; Jackson ImmunoResearch); Cy3-donkey anti-chicken IgY/IgG (703-165-155; Jackson ImmunoResearch).

Article Title: Autophagy across tissues of aging mice.
Article Snippet: .. Primary antibodies: ATG2B (rabbit polyclonal, PA5-85718, Thermo Fisher); ATG5 (rabbit monoclonal, CST 12994, Cell Signalling Technology); ATG7 (rabbit monoclonal, CST8558, Cell Signalling Technology); ATG13 (rabbit monoclonal, CST 13273, Cell Signalling Technology); ATG16L1 (rabbit monoclonal, CST 8089, Cell Signalling Technology); BECN1 (mouse monoclonal, SC-48341, Santa Cruz); CD3 (clone: 17A2, rat monoclonal-FITC conjugate, CST 86603, Cell Signalling Technology); CD19 (clone: 1D3, rat monoclonal-PE conjugate, CST 82168, Cell Signalling Technology); CTSD (rabbit monoclonal, CST 74089, Cell Signalling Technology); F4/80 (clone: BM8.1, rat monoclonal-VioletFluor450 conjugate, CST 40781, Cell Signalling Technology); FIP200 (rabbit monoclonal, CST 12436, Cell Signalling Technology); GFAP (chicken polyclonal, ab4674, Abcam); GFP (rabbit polyclonal, A-6455, Thermo Fisher) IBA1 (goat polyclonal, ab48004, Abcam); LC3B (rabbit polyclonal, NB100-2220, Novus Biologicals); LMNB1 (rabbit monoclonal, CST 13435, Cell Signalling Technology); NBR1 (rabbit polyclonal, ab126175, Abcam); NeuN (clone: E4M5P, mouse monoclonal, CST 94403, Cell PLOS One | https://doi.org/10.1371/journal.pone.0325505 June 4, 2025 9 / 17 Signalling Technology); NDP52 (rabbit polyclonal, Ab68588, Abcam); SQSTM1/p62 (rabbit polyclonal, PM045, MBL Life Science (imaging) and mouse monoclonal, H00008878-M01, Novus Biologicals (Immunoblotting); ULK1 (rabbit monoclonal, CST 8054, Cell Signalling Technology). .. Secondary Antibodies: Alexa Fluor-488 donkey anti-goat IgG (705-545-003; Jackson ImmunoResearch); Alexa Fluor 488 donkey anti-mouse IgG (715-545-151; Jackson ImmunoResearch); Alexa Fluor 647-donkey anti-mouse IgG (715- 605-150; Jackson ImmunoResearch); Alexa Fluor 647-donkey anti-rabbit IgG (711-605-152; Jackson ImmunoResearch); Cy3-donkey anti-chicken IgY/IgG (703-165-155; Jackson ImmunoResearch).

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col i ab270993 (Cell Signaling Technology Inc)

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1) Product Images from "Apolipoprotein E knockout attenuates vascular graft fibrosis by reducing profibrotic macrophage formation through low-density lipoprotein receptor related protein 1"

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