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cytochrome c oxidase subunit 4  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc cytochrome c oxidase subunit 4
    Cytochrome C Oxidase Subunit 4, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 221 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mab/COX+IV+(4D11-B3-E8)+Mouse+mAb/pmc12816905-99-54-60
    Average 96 stars, based on 221 article reviews
    cytochrome c oxidase subunit 4 - by Bioz Stars, 2026-09
    96/100 stars

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    Related Articles

    Western Blot:

    Article Title: Faecalibacterium prausnitzii promotes anti-PD-L1 efficacy in natural killer/T-cell lymphoma by enhancing antitumor immunity.
    Article Snippet: Five percent BSA (Biofroxx, #4240GR500) was used to block nonspecific binding sites. .. The antibodies used for western blotting were as follows: anti-GADPH mAb (1:1,000, Proteintech, #60004–1-Ig) as an internal reference, and anti-Jak3 (D1H3) mAb (1:1,000, CST, #8827), antiphospho-JAK3 (Tyr980/981) pAb (1:1,000, Proteintech, #29101–1-AP), anti-STAT3 mAb (1:1,000, Proteintech, #60199–1-Ig), anti-phospho-STAT3 antibody (1:200, SANTA CRUZ, #sc-8059), and anti-PD-L1/CD274 mAb (1:1,000, Proteintech, #66248–1-Ig). .. The appropriate secondary antibodies were applied on the basis of the primary antibodies used: goat anti-mouse IgG, HRP-conjugated (1:2,000, CWBIO, #CW0102S) or goat anti-rabbit IgG, HRP-conjugated (1:2,000, CWBIO, #CW0103S).

    Recombinant:

    Article Title: Fortilin deficiency induces anti-atherosclerotic phenotypes in macrophages and protects hypercholesterolemic mice against atherosclerosis.
    Article Snippet: .. The following primary antibodies were used: • Rabbit anti-fortilin (MBL International,Woburn,MA,USA;Catalog #: PM017; 1:1,000 dilution; used for the experiments depicted in Fig. 1c); • Rabbit anti-fortilin (Abcam, Waltham, MA, USA; Clone EPR5540, ab133568; 1:2,000 dilution; Figs. 5g, S4a); • Mouse anti-GAPDH(Fitzgerald,Acton,MA,USA;Clone: 10R-G109a; 1:10,000 dilution; Fig. 1c); mouse anti-GAPDH (Santa Cruz Biotechnology, Inc. Dallas, TX, USA; Clone: 6C5; Catalog #: sc-32233; 1:1,000 dilution; Figs. 5g, S6e); • Rabbit anti-human calponin-1 (CNN1)mAb (Cell Signaling Technology (CST), Danvers, MA, USA; Clone D8L2T, Catalog #: 17819; 1:1,000 dilution; Fig. 5g); • Recombinant rabbit anti-human α-smooth muscle actin (SMA) antibody (Abcam, clone EPR5368, Catalog #: ab124964; 1:1,000 dilution; Fig. 5g); • Rabbit anti-human SM22α (Transgelin/TAGLN) polyclonal Ab (CST, Catalog #: 40471; 1:1,000 dilution; Fig. 5g); • Rabbit anti-human TGF-β1 polyclonal Ab (Abcam, Catalog #: ab92486; 1:1,000 dilution; Figs. 5g, S6e); • Rabbit anti-Mac2 (Galectin-3/LGALS3) mAb (CST, Clone: D4I2R, Catalog #: 8785; 1:1,000 dilution; Fig. 5g); • Rabbit anti-human CD68 mAb MultiMabTM(CST, multiple clones, Catalog #: 86985; 1:1,000 dilution; Fig. 5g). .. For the quantification of CD36 expression in THP1KO-fortilin and THP1WT-fortilin cells, we used JESSTM, a highly quantitative capillary-based western blot system (ProteinSimple®, San Jose, CA, USA)24.

    Article Title: ATF3-mediated inhibition of Trem2 by Toxoplasma gondii contributes to adverse pregnancy outcomes.
    Article Snippet: PVDF membranes were analyzed through enhanced chemiluminescence (ECL, Meilunbio, Dalian, China). .. The following antibodies were applied in the study: Trem2 antibody (1:3000, mouse monoclonal; R&D Systems, Minnesota, USA, no. AF1729), recombinant anti-ATF3 antibody (1:1000, rabbit monoclonal; Abcam, Cambridge, UK, EPR22610-19, no. ab254268), STAT6 (D3H4) mAb (1:1000, rabbit monoclonal; CST, Danvers, MA, USA, D3H4, no. 5397), GAPDH antibody (1:50,000, mouse monoclonal; 1E6D9, no. 60004-1-Ig), HRP-conjugated goat anti-mouse IgG (H + L) (1:5000, mouse monoclonal; no. SA00001-1) ordered from Proteintech (Rosemont, IL, USA), HRP-conjugated goat anti-rabbit IgG (H + L) (1:5000, rabbit monoclonal; Biosharp, Jiangsu, China, no. BL003A). .. Mouse placenta from E17.5 mice was fixed in 4% paraformaldehyde (PFA, biosharp, BL539A) for 24 h at 4 °C, dehydrated in graded ethanol (70% → 100%, 1 h/step), cleared in xylene (2 × 30 min), and paraffin-embedded.

    Article Title: ATF3-mediated inhibition of Trem2 by Toxoplasma gondii contributes to adverse pregnancy outcomes
    Article Snippet: PVDF membranes were analyzed through enhanced chemiluminescence (ECL, Meilunbio, Dalian, China). .. The following antibodies were applied in the study: Trem2 antibody (1:3000, mouse monoclonal; R&D Systems, Minnesota, USA, no. AF1729), recombinant anti-ATF3 antibody (1:1000, rabbit monoclonal; Abcam, Cambridge, UK, EPR22610-19, no. ab254268), STAT6 (D3H4) mAb (1:1000, rabbit monoclonal; CST, Danvers, MA, USA, D3H4, no. 5397), GAPDH antibody (1:50,000, mouse monoclonal; 1E6D9, no. 60004-1-Ig), HRP-conjugated goat anti-mouse IgG (H + L) (1:5000, mouse monoclonal; no. SA00001-1) ordered from Proteintech (Rosemont, IL, USA), HRP-conjugated goat anti-rabbit IgG (H + L) (1:5000, rabbit monoclonal; Biosharp, Jiangsu, China, no. BL003A). .. Mouse placenta from E17.5 mice was fixed in 4% paraformaldehyde (PFA, biosharp, BL539A) for 24 h at 4 °C, dehydrated in graded ethanol (70% → 100%, 1 h/step), cleared in xylene (2 × 30 min), and paraffin-embedded.

    Article Title: Fortilin deficiency induces anti-atherosclerotic phenotypes in macrophages and protects hypercholesterolemic mice against atherosclerosis
    Article Snippet: .. The following primary antibodies were used: Rabbit anti-fortilin (MBL International, Woburn, MA, USA; Catalog #: PM017; 1:1,000 dilution; used for the experiments depicted in Fig. ); Rabbit anti-fortilin (Abcam, Waltham, MA, USA; Clone EPR5540, ab133568; 1:2,000 dilution; Figs. , ); Mouse anti-GAPDH (Fitzgerald, Acton, MA, USA; Clone: 10R-G109a; 1:10,000 dilution; Fig. ); mouse anti-GAPDH (Santa Cruz Biotechnology, Inc. Dallas, TX, USA; Clone: 6C5; Catalog #: sc-32233; 1:1,000 dilution; Figs. , ); Rabbit anti-human calponin-1 (CNN1) mAb (Cell Signaling Technology (CST), Danvers, MA, USA; Clone D8L2T, Catalog #: 17819; 1:1,000 dilution; Fig. ); Recombinant rabbit anti-human α-smooth muscle actin (SMA) antibody (Abcam, clone EPR5368, Catalog #: ab124964; 1:1,000 dilution; Fig. ); Rabbit anti-human SM22α (Transgelin/TAGLN) polyclonal Ab (CST, Catalog #: 40471; 1:1,000 dilution; Fig. ); Rabbit anti-human TGF-β1 polyclonal Ab (Abcam, Catalog #: ab92486; 1:1,000 dilution; Figs. , ); Rabbit anti-Mac2 (Galectin-3/LGALS3) mAb (CST, Clone: D4I2R, Catalog #: 8785; 1:1,000 dilution; Fig. ); Rabbit anti-human CD68 mAb MultiMabTM(CST, multiple clones, Catalog #: 86985; 1:1,000 dilution; Fig. ). .. For the quantification of CD36 expression in THP1 KO-fortilin and THP1 WT-fortilin cells, we used JESSTM, a highly quantitative capillary-based western blot system (ProteinSimple®, San Jose, CA, USA) .

    Clone Assay:

    Article Title: Fortilin deficiency induces anti-atherosclerotic phenotypes in macrophages and protects hypercholesterolemic mice against atherosclerosis.
    Article Snippet: .. The following primary antibodies were used: • Rabbit anti-fortilin (MBL International,Woburn,MA,USA;Catalog #: PM017; 1:1,000 dilution; used for the experiments depicted in Fig. 1c); • Rabbit anti-fortilin (Abcam, Waltham, MA, USA; Clone EPR5540, ab133568; 1:2,000 dilution; Figs. 5g, S4a); • Mouse anti-GAPDH(Fitzgerald,Acton,MA,USA;Clone: 10R-G109a; 1:10,000 dilution; Fig. 1c); mouse anti-GAPDH (Santa Cruz Biotechnology, Inc. Dallas, TX, USA; Clone: 6C5; Catalog #: sc-32233; 1:1,000 dilution; Figs. 5g, S6e); • Rabbit anti-human calponin-1 (CNN1)mAb (Cell Signaling Technology (CST), Danvers, MA, USA; Clone D8L2T, Catalog #: 17819; 1:1,000 dilution; Fig. 5g); • Recombinant rabbit anti-human α-smooth muscle actin (SMA) antibody (Abcam, clone EPR5368, Catalog #: ab124964; 1:1,000 dilution; Fig. 5g); • Rabbit anti-human SM22α (Transgelin/TAGLN) polyclonal Ab (CST, Catalog #: 40471; 1:1,000 dilution; Fig. 5g); • Rabbit anti-human TGF-β1 polyclonal Ab (Abcam, Catalog #: ab92486; 1:1,000 dilution; Figs. 5g, S6e); • Rabbit anti-Mac2 (Galectin-3/LGALS3) mAb (CST, Clone: D4I2R, Catalog #: 8785; 1:1,000 dilution; Fig. 5g); • Rabbit anti-human CD68 mAb MultiMabTM(CST, multiple clones, Catalog #: 86985; 1:1,000 dilution; Fig. 5g). .. For the quantification of CD36 expression in THP1KO-fortilin and THP1WT-fortilin cells, we used JESSTM, a highly quantitative capillary-based western blot system (ProteinSimple®, San Jose, CA, USA)24.

    Article Title: Fortilin deficiency induces anti-atherosclerotic phenotypes in macrophages and protects hypercholesterolemic mice against atherosclerosis
    Article Snippet: .. The following primary antibodies were used: Rabbit anti-fortilin (MBL International, Woburn, MA, USA; Catalog #: PM017; 1:1,000 dilution; used for the experiments depicted in Fig. ); Rabbit anti-fortilin (Abcam, Waltham, MA, USA; Clone EPR5540, ab133568; 1:2,000 dilution; Figs. , ); Mouse anti-GAPDH (Fitzgerald, Acton, MA, USA; Clone: 10R-G109a; 1:10,000 dilution; Fig. ); mouse anti-GAPDH (Santa Cruz Biotechnology, Inc. Dallas, TX, USA; Clone: 6C5; Catalog #: sc-32233; 1:1,000 dilution; Figs. , ); Rabbit anti-human calponin-1 (CNN1) mAb (Cell Signaling Technology (CST), Danvers, MA, USA; Clone D8L2T, Catalog #: 17819; 1:1,000 dilution; Fig. ); Recombinant rabbit anti-human α-smooth muscle actin (SMA) antibody (Abcam, clone EPR5368, Catalog #: ab124964; 1:1,000 dilution; Fig. ); Rabbit anti-human SM22α (Transgelin/TAGLN) polyclonal Ab (CST, Catalog #: 40471; 1:1,000 dilution; Fig. ); Rabbit anti-human TGF-β1 polyclonal Ab (Abcam, Catalog #: ab92486; 1:1,000 dilution; Figs. , ); Rabbit anti-Mac2 (Galectin-3/LGALS3) mAb (CST, Clone: D4I2R, Catalog #: 8785; 1:1,000 dilution; Fig. ); Rabbit anti-human CD68 mAb MultiMabTM(CST, multiple clones, Catalog #: 86985; 1:1,000 dilution; Fig. ). .. For the quantification of CD36 expression in THP1 KO-fortilin and THP1 WT-fortilin cells, we used JESSTM, a highly quantitative capillary-based western blot system (ProteinSimple®, San Jose, CA, USA) .

    Immunofluorescence:

    Article Title: Deficient AMPK-SENP1-Sirt3 signaling impairs mitochondrial complex I function in Parkinson's disease model.
    Article Snippet: For immunofluorescence, chicken TH polyclonal antibody (anti-TH, Abcam, 76442; 1:1000) and ionized calcium-binding adapter molecule 1 (IBA1) (anti-IBA1, Wako, 01919741; 1:1000; Richmond, VA) were used. .. Secondary antibodies used in this study included Goat Anti-Rabbit IgG (H + L) Antibody (1:10,000; Cell Signaling, 35401), Goat Anti-Mouse IgG (H + L) Antibody (1:10,000; Abcam, 205719) and Mouse Anti-Rabbit IgG (Conformation Specific) (L27A9) mAb (1:3000; Cell Signaling, 5127); as well as Goat Anti-Rabbit IgG H&L (Alexa Fluor® 488) (1:1000; Abcam, 150077) and Goat AntiChicken IgY H&L (Alexa Fluor® 594) (1:1000; Abcam, 150172) for immunofluorescence. .. A cohort of 3-month-old male Sirt3 K223R mice and their WT littermates were intraperitoneally injected with either MPTP/HCl (30 mg/kg of body weight, Sigma, M0896; St. Louis, MO) or an equivalent volume of 0.9% saline for 5 consecutive days.

    Incubation:

    Article Title: Alternative antigen retention by a gp96-fusion approach induces long-lasting and broad immunity in mice
    Article Snippet: .. The primary antibodies for incubation are respectively RBD mAb (1:500, Abclonal, A23771), GRP94 (GP96) mAb (1:1000, CST, 20292 T), and LRP1 mAb (1:200, Abcam, ab92544). .. The incubation ratio of the primary antibody, HPV18 L1 mAb (Abcam, ab267404), for the detection of HPV-infected cell lines in the Western Blot assay is 1:500.

    other:

    Article Title: Glucoprivation-induced nutrient preference relies on distinct NPY neurons that project to the paraventricular nucleus of the hypothalamus.
    Article Snippet: This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record.. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article.. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.



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    Cell Signaling Technology Inc β actin 13e5 rabbit mab
    TAPC interacts with VEGFR2 and modulates downstream signaling. (a) Cell viability assay of MC38 cells treated with increasing concentrations of TAPC. (b) Immunoblot analysis of VEGFR2 and key regulators of the PI3K–AKT signaling pathway (PI3K, AKT, and STAT3) in MC38 cells treated with PEG-PO or TAPC (5 and 10 μM). <t>β-Actin</t> was used as a loading control. (c) Pull-down assay of VEGFR2 from MC38 cell lysates using biotinylated TAPC, beads-only sample served as control. (d) Confocal IF imaging of MC38 cells incubated with Cy5.5-labeled TAPC and stained for VEGFR2, nuclei counterstained with DAPI. Scale bars: 20 μm. (e) BLI analysis of TAPC binding to recombinant VEGFR2 using serial concentrations (100, 66.7, 44.4, 29.6, 19.8, 13.2, and 8.8 μM). (f) Molecular dynamics simulations showing predicted protein–ligand complexes (top) and binding pocket visualizations (bottom) of VEGFR2 with TAPC, NDMPFI, MBAMF, and TPFE. (g) Binding free energy calculations of these complexes, including van der Waals, electrostatic, solvation, and total energy components. (h) Extracellular acidification rate (ECAR) of MC38 cells treated with control (0 μM), TAPC (2.5 μM), or TAPC (10 μM), with sequential addition of glucose, oligomycin, and 2-deoxyglucose (2-DG). (i) Quantification of glycolysis and glycolytic capacity in MC38 cells treated with control (0 μM), TAPC (2.5 μM), or TAPC (10 μM) (n = 8). Data are presented as mean ± SEM. Statistical significance was assessed using one-way ANOVA with Tukey's multiple comparisons test; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.
    β Actin 13e5 Rabbit Mab, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    cst 9664s  (Cell Signaling Technology Inc)
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    Cell Signaling Technology Inc cst 9664s
    TAPC interacts with VEGFR2 and modulates downstream signaling. (a) Cell viability assay of MC38 cells treated with increasing concentrations of TAPC. (b) Immunoblot analysis of VEGFR2 and key regulators of the PI3K–AKT signaling pathway (PI3K, AKT, and STAT3) in MC38 cells treated with PEG-PO or TAPC (5 and 10 μM). <t>β-Actin</t> was used as a loading control. (c) Pull-down assay of VEGFR2 from MC38 cell lysates using biotinylated TAPC, beads-only sample served as control. (d) Confocal IF imaging of MC38 cells incubated with Cy5.5-labeled TAPC and stained for VEGFR2, nuclei counterstained with DAPI. Scale bars: 20 μm. (e) BLI analysis of TAPC binding to recombinant VEGFR2 using serial concentrations (100, 66.7, 44.4, 29.6, 19.8, 13.2, and 8.8 μM). (f) Molecular dynamics simulations showing predicted protein–ligand complexes (top) and binding pocket visualizations (bottom) of VEGFR2 with TAPC, NDMPFI, MBAMF, and TPFE. (g) Binding free energy calculations of these complexes, including van der Waals, electrostatic, solvation, and total energy components. (h) Extracellular acidification rate (ECAR) of MC38 cells treated with control (0 μM), TAPC (2.5 μM), or TAPC (10 μM), with sequential addition of glucose, oligomycin, and 2-deoxyglucose (2-DG). (i) Quantification of glycolysis and glycolytic capacity in MC38 cells treated with control (0 μM), TAPC (2.5 μM), or TAPC (10 μM) (n = 8). Data are presented as mean ± SEM. Statistical significance was assessed using one-way ANOVA with Tukey's multiple comparisons test; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.
    Cst 9664s, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    Resistance exercise exceeds the benefits of endurance exercise in ameliorating metabolic dysfunction. Following 8 weeks of diet and exercise interventions, all mice were assessed for their metabolic function by GTT, ITT, and skeletal muscle response of Akt and AS160 phosphorylation to injection of insulin measured by Western blot. (A–C) HOMA-IR taken after an overnight fast for baseline glucose and insulin. (D and E) GTT from 0–120 min and calculated AUC; colored * indicates significant difference from NC-SED. (F and G) ITT from 0–60 min and calculated AUC; colored * indicates significant difference from NC-SED. (H–N) pAkt stimulation, AS160 S318, and AS160 T642 in hindlimb muscles before and after insulin injection and the pre–post ∆ in phosphorylation. (O and P) Total and phosphorylated 4E-BP1. (Q–T) Western results for Raptor, COX4, LC3 II/I, and ubiquitin staining. Representative western blot images inset right. Data presented as mean ± standard error of the mean. Statistical analysis performed by analysis of variance between groups: * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. NC-SED n : 8–16 (white); HFD-SED n : 8–18 (red); HFD-R EX n : 8–16 (blue); HFD-E EX n : 8–15 (green). 4E-BP1 = Eukaryotic translation initiation factor 4E binding protein; Akt = protein kinase B; AS160 = Akt substrate 160; COX4 = cytochrome c oxidase 4; CS = citrate sythase; E EX = endurance exercise; GAPDH = glyceraldehyde 3 phosphate dehydrogenase; GTT = glucose tolerance test; HFD = high fat diet; HOMA-IR = homeostatic model assessment for insulin resistance; iAUC = integrated area under the curve; ITT = insulin tolerance test; LC3 II/I = microtubule-associated protein light chain 3; NC = normal chow; pAkt = phospho-Akt; R EX = resistance exercise; SED = sedentary; Ub = ubiquitin.

    Journal: Journal of Sport and Health Science

    Article Title: Weightlifting outperforms voluntary wheel running for improving adiposity and insulin sensitivity in obese mice

    doi: 10.1016/j.jshs.2025.101100

    Figure Lengend Snippet: Resistance exercise exceeds the benefits of endurance exercise in ameliorating metabolic dysfunction. Following 8 weeks of diet and exercise interventions, all mice were assessed for their metabolic function by GTT, ITT, and skeletal muscle response of Akt and AS160 phosphorylation to injection of insulin measured by Western blot. (A–C) HOMA-IR taken after an overnight fast for baseline glucose and insulin. (D and E) GTT from 0–120 min and calculated AUC; colored * indicates significant difference from NC-SED. (F and G) ITT from 0–60 min and calculated AUC; colored * indicates significant difference from NC-SED. (H–N) pAkt stimulation, AS160 S318, and AS160 T642 in hindlimb muscles before and after insulin injection and the pre–post ∆ in phosphorylation. (O and P) Total and phosphorylated 4E-BP1. (Q–T) Western results for Raptor, COX4, LC3 II/I, and ubiquitin staining. Representative western blot images inset right. Data presented as mean ± standard error of the mean. Statistical analysis performed by analysis of variance between groups: * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. NC-SED n : 8–16 (white); HFD-SED n : 8–18 (red); HFD-R EX n : 8–16 (blue); HFD-E EX n : 8–15 (green). 4E-BP1 = Eukaryotic translation initiation factor 4E binding protein; Akt = protein kinase B; AS160 = Akt substrate 160; COX4 = cytochrome c oxidase 4; CS = citrate sythase; E EX = endurance exercise; GAPDH = glyceraldehyde 3 phosphate dehydrogenase; GTT = glucose tolerance test; HFD = high fat diet; HOMA-IR = homeostatic model assessment for insulin resistance; iAUC = integrated area under the curve; ITT = insulin tolerance test; LC3 II/I = microtubule-associated protein light chain 3; NC = normal chow; pAkt = phospho-Akt; R EX = resistance exercise; SED = sedentary; Ub = ubiquitin.

    Article Snippet: Primary antibodies used for analysis were from Cell Signaling Technologies (Danvers, MA, USA) and diluted 1:1000 unless otherwise stated as follows: protein kinase B (Akt; 1:500; #4691; Cell Signaling Technologies), phospho-Akt (pAkt) S473 (1:500; #9271; Cell Signaling Technologies), Ubiquitin (#3933; Cell Signaling Technologies), microtubule-associated protein light chain 3 (LC3 II/I; #4018; Cell Signaling Technologies), cytochrome c oxidase subunit 4(COX4; #11967; Cell Signaling Technologies), Akt substrate 160 (AS160 S318; #8619; Cell Signaling Technologies), AS160 T642 (#8881; Cell Signaling Technologies), eukaryotic translation initiation factor 4E binding protein (4E-BP1; #9452; Cell Signaling Technologies), and glyceraldehyde 3 phosphate dehydrogenase (GAPDH; #2118; Cell Signaling Technologies).

    Techniques: Phospho-proteomics, Injection, Western Blot, Muscles, Ubiquitin Proteomics, Staining, Binding Assay

    Resistance exercise exceeds the benefits of endurance exercise in ameliorating metabolic dysfunction. Following 8 weeks of diet and exercise interventions, all mice were assessed for their metabolic function by GTT, ITT, and skeletal muscle response of Akt and AS160 phosphorylation to injection of insulin measured by Western blot. (A–C) HOMA-IR taken after an overnight fast for baseline glucose and insulin. (D and E) GTT from 0–120 min and calculated AUC; colored * indicates significant difference from NC-SED. (F and G) ITT from 0–60 min and calculated AUC; colored * indicates significant difference from NC-SED. (H–N) pAkt stimulation, AS160 S318, and AS160 T642 in hindlimb muscles before and after insulin injection and the pre–post ∆ in phosphorylation. (O and P) Total and phosphorylated 4E-BP1. (Q–T) Western results for Raptor, COX4, LC3 II/I, and ubiquitin staining. Representative western blot images inset right. Data presented as mean ± standard error of the mean. Statistical analysis performed by analysis of variance between groups: * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. NC-SED n : 8–16 (white); HFD-SED n : 8–18 (red); HFD-R EX n : 8–16 (blue); HFD-E EX n : 8–15 (green). 4E-BP1 = Eukaryotic translation initiation factor 4E binding protein; Akt = protein kinase B; AS160 = Akt substrate 160; COX4 = cytochrome c oxidase 4; CS = citrate sythase; E EX = endurance exercise; GAPDH = glyceraldehyde 3 phosphate dehydrogenase; GTT = glucose tolerance test; HFD = high fat diet; HOMA-IR = homeostatic model assessment for insulin resistance; iAUC = integrated area under the curve; ITT = insulin tolerance test; LC3 II/I = microtubule-associated protein light chain 3; NC = normal chow; pAkt = phospho-Akt; R EX = resistance exercise; SED = sedentary; Ub = ubiquitin.

    Journal: Journal of Sport and Health Science

    Article Title: Weightlifting outperforms voluntary wheel running for improving adiposity and insulin sensitivity in obese mice

    doi: 10.1016/j.jshs.2025.101100

    Figure Lengend Snippet: Resistance exercise exceeds the benefits of endurance exercise in ameliorating metabolic dysfunction. Following 8 weeks of diet and exercise interventions, all mice were assessed for their metabolic function by GTT, ITT, and skeletal muscle response of Akt and AS160 phosphorylation to injection of insulin measured by Western blot. (A–C) HOMA-IR taken after an overnight fast for baseline glucose and insulin. (D and E) GTT from 0–120 min and calculated AUC; colored * indicates significant difference from NC-SED. (F and G) ITT from 0–60 min and calculated AUC; colored * indicates significant difference from NC-SED. (H–N) pAkt stimulation, AS160 S318, and AS160 T642 in hindlimb muscles before and after insulin injection and the pre–post ∆ in phosphorylation. (O and P) Total and phosphorylated 4E-BP1. (Q–T) Western results for Raptor, COX4, LC3 II/I, and ubiquitin staining. Representative western blot images inset right. Data presented as mean ± standard error of the mean. Statistical analysis performed by analysis of variance between groups: * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. NC-SED n : 8–16 (white); HFD-SED n : 8–18 (red); HFD-R EX n : 8–16 (blue); HFD-E EX n : 8–15 (green). 4E-BP1 = Eukaryotic translation initiation factor 4E binding protein; Akt = protein kinase B; AS160 = Akt substrate 160; COX4 = cytochrome c oxidase 4; CS = citrate sythase; E EX = endurance exercise; GAPDH = glyceraldehyde 3 phosphate dehydrogenase; GTT = glucose tolerance test; HFD = high fat diet; HOMA-IR = homeostatic model assessment for insulin resistance; iAUC = integrated area under the curve; ITT = insulin tolerance test; LC3 II/I = microtubule-associated protein light chain 3; NC = normal chow; pAkt = phospho-Akt; R EX = resistance exercise; SED = sedentary; Ub = ubiquitin.

    Article Snippet: Primary antibodies used for analysis were from Cell Signaling Technologies (Danvers, MA, USA) and diluted 1:1000 unless otherwise stated as follows: protein kinase B (Akt; 1:500; #4691; Cell Signaling Technologies), phospho-Akt (pAkt) S473 (1:500; #9271; Cell Signaling Technologies), Ubiquitin (#3933; Cell Signaling Technologies), microtubule-associated protein light chain 3 (LC3 II/I; #4018; Cell Signaling Technologies), cytochrome c oxidase subunit 4(COX4; #11967; Cell Signaling Technologies), Akt substrate 160 (AS160 S318; #8619; Cell Signaling Technologies), AS160 T642 (#8881; Cell Signaling Technologies), eukaryotic translation initiation factor 4E binding protein (4E-BP1; #9452; Cell Signaling Technologies), and glyceraldehyde 3 phosphate dehydrogenase (GAPDH; #2118; Cell Signaling Technologies).

    Techniques: Phospho-proteomics, Injection, Western Blot, Muscles, Ubiquitin Proteomics, Staining, Binding Assay

    Resistance exercise exceeds the benefits of endurance exercise in ameliorating metabolic dysfunction. Following 8 weeks of diet and exercise interventions, all mice were assessed for their metabolic function by GTT, ITT, and skeletal muscle response of Akt and AS160 phosphorylation to injection of insulin measured by Western blot. (A–C) HOMA-IR taken after an overnight fast for baseline glucose and insulin. (D and E) GTT from 0–120 min and calculated AUC; colored * indicates significant difference from NC-SED. (F and G) ITT from 0–60 min and calculated AUC; colored * indicates significant difference from NC-SED. (H–N) pAkt stimulation, AS160 S318, and AS160 T642 in hindlimb muscles before and after insulin injection and the pre–post ∆ in phosphorylation. (O and P) Total and phosphorylated 4E-BP1. (Q–T) Western results for Raptor, COX4, LC3 II/I, and ubiquitin staining. Representative western blot images inset right. Data presented as mean ± standard error of the mean. Statistical analysis performed by analysis of variance between groups: * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. NC-SED n : 8–16 (white); HFD-SED n : 8–18 (red); HFD-R EX n : 8–16 (blue); HFD-E EX n : 8–15 (green). 4E-BP1 = Eukaryotic translation initiation factor 4E binding protein; Akt = protein kinase B; AS160 = Akt substrate 160; COX4 = cytochrome c oxidase 4; CS = citrate sythase; E EX = endurance exercise; GAPDH = glyceraldehyde 3 phosphate dehydrogenase; GTT = glucose tolerance test; HFD = high fat diet; HOMA-IR = homeostatic model assessment for insulin resistance; iAUC = integrated area under the curve; ITT = insulin tolerance test; LC3 II/I = microtubule-associated protein light chain 3; NC = normal chow; pAkt = phospho-Akt; R EX = resistance exercise; SED = sedentary; Ub = ubiquitin.

    Journal: Journal of Sport and Health Science

    Article Title: Weightlifting outperforms voluntary wheel running for improving adiposity and insulin sensitivity in obese mice

    doi: 10.1016/j.jshs.2025.101100

    Figure Lengend Snippet: Resistance exercise exceeds the benefits of endurance exercise in ameliorating metabolic dysfunction. Following 8 weeks of diet and exercise interventions, all mice were assessed for their metabolic function by GTT, ITT, and skeletal muscle response of Akt and AS160 phosphorylation to injection of insulin measured by Western blot. (A–C) HOMA-IR taken after an overnight fast for baseline glucose and insulin. (D and E) GTT from 0–120 min and calculated AUC; colored * indicates significant difference from NC-SED. (F and G) ITT from 0–60 min and calculated AUC; colored * indicates significant difference from NC-SED. (H–N) pAkt stimulation, AS160 S318, and AS160 T642 in hindlimb muscles before and after insulin injection and the pre–post ∆ in phosphorylation. (O and P) Total and phosphorylated 4E-BP1. (Q–T) Western results for Raptor, COX4, LC3 II/I, and ubiquitin staining. Representative western blot images inset right. Data presented as mean ± standard error of the mean. Statistical analysis performed by analysis of variance between groups: * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. NC-SED n : 8–16 (white); HFD-SED n : 8–18 (red); HFD-R EX n : 8–16 (blue); HFD-E EX n : 8–15 (green). 4E-BP1 = Eukaryotic translation initiation factor 4E binding protein; Akt = protein kinase B; AS160 = Akt substrate 160; COX4 = cytochrome c oxidase 4; CS = citrate sythase; E EX = endurance exercise; GAPDH = glyceraldehyde 3 phosphate dehydrogenase; GTT = glucose tolerance test; HFD = high fat diet; HOMA-IR = homeostatic model assessment for insulin resistance; iAUC = integrated area under the curve; ITT = insulin tolerance test; LC3 II/I = microtubule-associated protein light chain 3; NC = normal chow; pAkt = phospho-Akt; R EX = resistance exercise; SED = sedentary; Ub = ubiquitin.

    Article Snippet: Primary antibodies used for analysis were from Cell Signaling Technologies (Danvers, MA, USA) and diluted 1:1000 unless otherwise stated as follows: protein kinase B (Akt; 1:500; #4691; Cell Signaling Technologies), phospho-Akt (pAkt) S473 (1:500; #9271; Cell Signaling Technologies), Ubiquitin (#3933; Cell Signaling Technologies), microtubule-associated protein light chain 3 (LC3 II/I; #4018; Cell Signaling Technologies), cytochrome c oxidase subunit 4(COX4; #11967; Cell Signaling Technologies), Akt substrate 160 (AS160 S318; #8619; Cell Signaling Technologies), AS160 T642 (#8881; Cell Signaling Technologies), eukaryotic translation initiation factor 4E binding protein (4E-BP1; #9452; Cell Signaling Technologies), and glyceraldehyde 3 phosphate dehydrogenase (GAPDH; #2118; Cell Signaling Technologies).

    Techniques: Phospho-proteomics, Injection, Western Blot, Muscles, Ubiquitin Proteomics, Staining, Binding Assay

    In vivo therapeutic efficacy of advanced BAITs in a postoperative tumor model. (A) Schematic of in vivo experimental design. LLC tumors were surgically resected, and mice were re-challenged with LLC cells. Mice then received BAIT treatments. (B) Photographs of tumors and tumor weights at day 16 for each group (n = 5; ∗ is P < 0.05, ∗∗ is P < 0.01, ∗∗∗ is P < 0.001 by one-way ANOVA with Bonferroni post-hoc test). (C) Individual tumor growth curves over time (n = 5; ∗∗ is P < 0.01, ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (D) H&E-stained tumor sections. (E) TUNEL staining of tumor sections (brown, apoptotic cells). Black arrowheads mark TUNEL + areas. (F) Quantification of TUNEL + apoptotic cells (n = 5; ∗∗∗∗ is P < 0.0001 by one-way ANOVA with Bonferroni post-hoc test). (G) Representative immunofluorescence for Ki67 (green) in tumor tissues (nuclei in blue). The Apo-BAIT group shows greatly reduced Ki67 + proliferating cells. (H) Quantification of Ki67 + cell density (n = 5; ∗ is P < 0.05, ∗∗ is P < 0.01, ∗∗∗∗ is P < 0.0001 by one-way ANOVA with Bonferroni post-hoc test). Data are presented as mean ± SD.

    Journal: Bioactive Materials

    Article Title: Countering postoperative immune suppression with a self-assembling dendritic cell nanovaccine

    doi: 10.1016/j.bioactmat.2026.05.005

    Figure Lengend Snippet: In vivo therapeutic efficacy of advanced BAITs in a postoperative tumor model. (A) Schematic of in vivo experimental design. LLC tumors were surgically resected, and mice were re-challenged with LLC cells. Mice then received BAIT treatments. (B) Photographs of tumors and tumor weights at day 16 for each group (n = 5; ∗ is P < 0.05, ∗∗ is P < 0.01, ∗∗∗ is P < 0.001 by one-way ANOVA with Bonferroni post-hoc test). (C) Individual tumor growth curves over time (n = 5; ∗∗ is P < 0.01, ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (D) H&E-stained tumor sections. (E) TUNEL staining of tumor sections (brown, apoptotic cells). Black arrowheads mark TUNEL + areas. (F) Quantification of TUNEL + apoptotic cells (n = 5; ∗∗∗∗ is P < 0.0001 by one-way ANOVA with Bonferroni post-hoc test). (G) Representative immunofluorescence for Ki67 (green) in tumor tissues (nuclei in blue). The Apo-BAIT group shows greatly reduced Ki67 + proliferating cells. (H) Quantification of Ki67 + cell density (n = 5; ∗ is P < 0.05, ∗∗ is P < 0.01, ∗∗∗∗ is P < 0.0001 by one-way ANOVA with Bonferroni post-hoc test). Data are presented as mean ± SD.

    Article Snippet: Anti-Ki67 mouse mAb (Cat# GB121141-100), anti-CD3 mouse mAb (Cat# GB15014-100), FITC-conjugated goat anti-mouse IgG (H + L) (Cat# GB22301), and Cy5-conjugated goat anti-mouse IgG (H + L) (Cat# GB27301) for immunofluorescence assays, and DAB (SA-HRP) TUNEL apoptosis detection kit were supplied by Servicebio (Wuhan, China).

    Techniques: In Vivo, Drug discovery, Staining, TUNEL Assay, Immunofluorescence

    TAPC interacts with VEGFR2 and modulates downstream signaling. (a) Cell viability assay of MC38 cells treated with increasing concentrations of TAPC. (b) Immunoblot analysis of VEGFR2 and key regulators of the PI3K–AKT signaling pathway (PI3K, AKT, and STAT3) in MC38 cells treated with PEG-PO or TAPC (5 and 10 μM). β-Actin was used as a loading control. (c) Pull-down assay of VEGFR2 from MC38 cell lysates using biotinylated TAPC, beads-only sample served as control. (d) Confocal IF imaging of MC38 cells incubated with Cy5.5-labeled TAPC and stained for VEGFR2, nuclei counterstained with DAPI. Scale bars: 20 μm. (e) BLI analysis of TAPC binding to recombinant VEGFR2 using serial concentrations (100, 66.7, 44.4, 29.6, 19.8, 13.2, and 8.8 μM). (f) Molecular dynamics simulations showing predicted protein–ligand complexes (top) and binding pocket visualizations (bottom) of VEGFR2 with TAPC, NDMPFI, MBAMF, and TPFE. (g) Binding free energy calculations of these complexes, including van der Waals, electrostatic, solvation, and total energy components. (h) Extracellular acidification rate (ECAR) of MC38 cells treated with control (0 μM), TAPC (2.5 μM), or TAPC (10 μM), with sequential addition of glucose, oligomycin, and 2-deoxyglucose (2-DG). (i) Quantification of glycolysis and glycolytic capacity in MC38 cells treated with control (0 μM), TAPC (2.5 μM), or TAPC (10 μM) (n = 8). Data are presented as mean ± SEM. Statistical significance was assessed using one-way ANOVA with Tukey's multiple comparisons test; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

    Journal: Bioactive Materials

    Article Title: Aminated fullerene-based nanoplatform enables synergistic VEGFR2-targeted anti-angiogenesis and tumor immunotherapy

    doi: 10.1016/j.bioactmat.2026.03.016

    Figure Lengend Snippet: TAPC interacts with VEGFR2 and modulates downstream signaling. (a) Cell viability assay of MC38 cells treated with increasing concentrations of TAPC. (b) Immunoblot analysis of VEGFR2 and key regulators of the PI3K–AKT signaling pathway (PI3K, AKT, and STAT3) in MC38 cells treated with PEG-PO or TAPC (5 and 10 μM). β-Actin was used as a loading control. (c) Pull-down assay of VEGFR2 from MC38 cell lysates using biotinylated TAPC, beads-only sample served as control. (d) Confocal IF imaging of MC38 cells incubated with Cy5.5-labeled TAPC and stained for VEGFR2, nuclei counterstained with DAPI. Scale bars: 20 μm. (e) BLI analysis of TAPC binding to recombinant VEGFR2 using serial concentrations (100, 66.7, 44.4, 29.6, 19.8, 13.2, and 8.8 μM). (f) Molecular dynamics simulations showing predicted protein–ligand complexes (top) and binding pocket visualizations (bottom) of VEGFR2 with TAPC, NDMPFI, MBAMF, and TPFE. (g) Binding free energy calculations of these complexes, including van der Waals, electrostatic, solvation, and total energy components. (h) Extracellular acidification rate (ECAR) of MC38 cells treated with control (0 μM), TAPC (2.5 μM), or TAPC (10 μM), with sequential addition of glucose, oligomycin, and 2-deoxyglucose (2-DG). (i) Quantification of glycolysis and glycolytic capacity in MC38 cells treated with control (0 μM), TAPC (2.5 μM), or TAPC (10 μM) (n = 8). Data are presented as mean ± SEM. Statistical significance was assessed using one-way ANOVA with Tukey's multiple comparisons test; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

    Article Snippet: Antibodies were listed as follows: Anti-VEGF Receptor 2 antibody [EPRER16Y] (Abcam, Cat: ab134191), Anti-PI 3 Kinase catalytic subunit gamma (Abcam, Cat: ab302958), Anti-AKT (phosphor T308) antibody (Abcam, Cat: ab38449), Anti-STAT3 antibody [EPR787Y] (Abcam, Cat: ab68153), β-Actin (13E5) rabbit mAb (CST, Cat: #4970), Anti-CD31 antibody [EPR17260-263] (Abcam, Cat: ab222783), FITC anti-mouse CD45 (Biolegend, Cat: 103108), PerCP/Cyanine5.5 anti-mouse CD4 (Biolegend, Cat: 100434), FOXP3 Monoclonal Antibody (NRRF-30), PE, eBioscience (Thermo, Cat: 12-4771-82), CD3 (Abcam, Cat: ab16669), CD4 (Servicebio, Cat: GB15064).

    Techniques: Viability Assay, Western Blot, Control, Pull Down Assay, Imaging, Incubation, Labeling, Staining, Binding Assay, Recombinant

    In vivo anti-tumor and anti-angiogenic effects of TAPC@CNPs. (a) Schematic illustration of the therapeutic study in Balb/c mice bearing subcutaneous MC38 tumors (n = 7). (b) Body weights of mice during treatment. (c) Photographs of excised tumors collected at endpoint. (d) Tumor growth curves during treatment. Tumor volume was calculated using the formula (length × width 2 )/2. (e) Tumor weights measured at endpoint. (f) Immunoblot analysis of VEGFR2 expression in tumor lysates from different treatment groups, β-actin was used as a reference protein. (g) IHC staining of CD31 in tumor sections from different treatment groups. Scale bar, 100 μm. (h) H&E staining of major organs (heart, liver, spleen, lung, kidney) and tumor tissues. (i) Serum ALT and AST levels measured at endpoint. Data are presented as mean ± SEM. Statistical analysis was performed by one-way ANOVA with Tukey's multiple comparisons test, ns indicates not significant, ∗p < 0.05, ∗∗p < 0.01, ∗∗∗∗p < 0.0001.

    Journal: Bioactive Materials

    Article Title: Aminated fullerene-based nanoplatform enables synergistic VEGFR2-targeted anti-angiogenesis and tumor immunotherapy

    doi: 10.1016/j.bioactmat.2026.03.016

    Figure Lengend Snippet: In vivo anti-tumor and anti-angiogenic effects of TAPC@CNPs. (a) Schematic illustration of the therapeutic study in Balb/c mice bearing subcutaneous MC38 tumors (n = 7). (b) Body weights of mice during treatment. (c) Photographs of excised tumors collected at endpoint. (d) Tumor growth curves during treatment. Tumor volume was calculated using the formula (length × width 2 )/2. (e) Tumor weights measured at endpoint. (f) Immunoblot analysis of VEGFR2 expression in tumor lysates from different treatment groups, β-actin was used as a reference protein. (g) IHC staining of CD31 in tumor sections from different treatment groups. Scale bar, 100 μm. (h) H&E staining of major organs (heart, liver, spleen, lung, kidney) and tumor tissues. (i) Serum ALT and AST levels measured at endpoint. Data are presented as mean ± SEM. Statistical analysis was performed by one-way ANOVA with Tukey's multiple comparisons test, ns indicates not significant, ∗p < 0.05, ∗∗p < 0.01, ∗∗∗∗p < 0.0001.

    Article Snippet: Antibodies were listed as follows: Anti-VEGF Receptor 2 antibody [EPRER16Y] (Abcam, Cat: ab134191), Anti-PI 3 Kinase catalytic subunit gamma (Abcam, Cat: ab302958), Anti-AKT (phosphor T308) antibody (Abcam, Cat: ab38449), Anti-STAT3 antibody [EPR787Y] (Abcam, Cat: ab68153), β-Actin (13E5) rabbit mAb (CST, Cat: #4970), Anti-CD31 antibody [EPR17260-263] (Abcam, Cat: ab222783), FITC anti-mouse CD45 (Biolegend, Cat: 103108), PerCP/Cyanine5.5 anti-mouse CD4 (Biolegend, Cat: 100434), FOXP3 Monoclonal Antibody (NRRF-30), PE, eBioscience (Thermo, Cat: 12-4771-82), CD3 (Abcam, Cat: ab16669), CD4 (Servicebio, Cat: GB15064).

    Techniques: In Vivo, Western Blot, Expressing, Immunohistochemistry, Staining