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anti mouse cd47 monoclonal antibodies (Bio X Cell)

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Bio X Cell anti mouse cd47 monoclonal antibodies

Real‐time monitoring of tumor progression and <t>anti‐CD47</t> therapeutic efficiency. (A) Female BALB/c mice aged 8–10 weeks were implanted with dorsal skinfold window chambers. 4T1_PB3R‐RFP TNBC cells were transplanted into the subcutaneous tissue, and tumors were monitored using intravital imaging. (B) Detailed visualization of angiogenesis and tumor nodule formation in TNBC skinfold models compared with the isotype control group. (C, D) Conventional whole‐body bioluminescence imaging of mice bearing 4T1_PB3R‐RFP‐luc tumors revealed considerably decreased signals following anti‐CD47 immunotherapy administered over 5 days, beginning on day 9 for 5 days ( n = 7, p < 0.0001, 10 mg/kg, intravenous injection). Data are presented as the mean ± standard deviation (SD).

Anti Mouse Cd47 Monoclonal Antibodies, supplied by Bio X Cell, used in various techniques. Bioz Stars score: 96/100, based on 114 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+cd47/InVivoMAb+anti-mouse+CD47/pmc13650256-56-17-29
Average 96 stars, based on 114 article reviews

anti mouse cd47 monoclonal antibodies - by Bioz Stars, 2026-10

96/100 stars

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1) Product Images from "In Vivo Immunoscoring Technique to Monitor Anti‐ CD47 Immunotherapy Efficacy in Triple‐Negative Breast Cancer"

Article Title: In Vivo Immunoscoring Technique to Monitor Anti‐ CD47 Immunotherapy Efficacy in Triple‐Negative Breast Cancer

Journal: Cancer Medicine

doi: 10.1002/cam4.72232

Real‐time monitoring of tumor progression and anti‐CD47 therapeutic efficiency. (A) Female BALB/c mice aged 8–10 weeks were implanted with dorsal skinfold window chambers. 4T1_PB3R‐RFP TNBC cells were transplanted into the subcutaneous tissue, and tumors were monitored using intravital imaging. (B) Detailed visualization of angiogenesis and tumor nodule formation in TNBC skinfold models compared with the isotype control group. (C, D) Conventional whole‐body bioluminescence imaging of mice bearing 4T1_PB3R‐RFP‐luc tumors revealed considerably decreased signals following anti‐CD47 immunotherapy administered over 5 days, beginning on day 9 for 5 days ( n = 7, p < 0.0001, 10 mg/kg, intravenous injection). Data are presented as the mean ± standard deviation (SD).

Figure Legend Snippet: Real‐time monitoring of tumor progression and anti‐CD47 therapeutic efficiency. (A) Female BALB/c mice aged 8–10 weeks were implanted with dorsal skinfold window chambers. 4T1_PB3R‐RFP TNBC cells were transplanted into the subcutaneous tissue, and tumors were monitored using intravital imaging. (B) Detailed visualization of angiogenesis and tumor nodule formation in TNBC skinfold models compared with the isotype control group. (C, D) Conventional whole‐body bioluminescence imaging of mice bearing 4T1_PB3R‐RFP‐luc tumors revealed considerably decreased signals following anti‐CD47 immunotherapy administered over 5 days, beginning on day 9 for 5 days ( n = 7, p < 0.0001, 10 mg/kg, intravenous injection). Data are presented as the mean ± standard deviation (SD).

Techniques Used: Real-time Monitoring, Tissue, Imaging, Control, Injection, Standard Deviation

In vivo and in vitro validation of TNBC targeting by Dextran‐AF680. (A–C) The signals emitted by Dextran‐AF680 at various time intervals following intravenous injections exhibited significant differences between 10 and 180 min and between 180 and 360 min. (D, E) Dextran‐AF680 can be administrated for TNBC imaging with photoacoustic tomography, and the optimal imaging time is 3 h after dextran injection, indicating its potential as an imaging probe for enhancing TNBC visualization ( n = 7, p = 0.024, p = 0.004). (F, G) Longitudinal conventional fluorescence imaging of the anti‐CD47 immunotherapeutic response, in comparison with the isotype control treatment, demonstrated a significant change in the average radiant efficiency of Dextran AF680 following 5 days of treatment ( n = 12, p = 0.0022). (H, I) An evident shift in the population of Dextran‐AF680+ and RFP+ cells was observed after anti‐CD47 mAb immunotherapies ( n = 10, p = 0.0079). Data are presented as the mean ± standard deviation (SD).

Figure Legend Snippet: In vivo and in vitro validation of TNBC targeting by Dextran‐AF680. (A–C) The signals emitted by Dextran‐AF680 at various time intervals following intravenous injections exhibited significant differences between 10 and 180 min and between 180 and 360 min. (D, E) Dextran‐AF680 can be administrated for TNBC imaging with photoacoustic tomography, and the optimal imaging time is 3 h after dextran injection, indicating its potential as an imaging probe for enhancing TNBC visualization ( n = 7, p = 0.024, p = 0.004). (F, G) Longitudinal conventional fluorescence imaging of the anti‐CD47 immunotherapeutic response, in comparison with the isotype control treatment, demonstrated a significant change in the average radiant efficiency of Dextran AF680 following 5 days of treatment ( n = 12, p = 0.0022). (H, I) An evident shift in the population of Dextran‐AF680+ and RFP+ cells was observed after anti‐CD47 mAb immunotherapies ( n = 10, p = 0.0079). Data are presented as the mean ± standard deviation (SD).

Techniques Used: In Vivo, In Vitro, Biomarker Discovery, Imaging, Micro-PAT, Injection, Fluorescence, Comparison, Control, Standard Deviation

Intravital imaging of M2 macrophage targeting by Dextran‐AF680. (A) Dynamic in vivo distribution of intravenously injected Dextran‐AF680 in representative blood vessels of a skinfold TNBC model. The Dextran‐AF680 signal peaked at 3 h and dissipated from the vessels within 24 h. (B) Substantial colocalization was observed between Dextran‐AF680 targeted cells (red) and CD206‐FITC+ cells (green). (C) Antibody‐dependent cellular phagocytosis (ADCP) occured in rapid, brief waves between Dextran‐AF680‐labeled macrophages and CD47 inhibitor‐treated tumor cells in a skinfold TNBC model. (D) CD47 inhibitor‐treated cancer cells (green) were engulfed by macrophages labeled with the pan‐macrophage marker F4/80‐PE (red), underscoring the highly phagocytic nature of macrophages (scale bars, 25 μm). (E) Intravital imaging of the robust phagocytic capacity of F4/80+ macrophages (red) toward CD47 inhibitor‐treated tumor cells (green).

Figure Legend Snippet: Intravital imaging of M2 macrophage targeting by Dextran‐AF680. (A) Dynamic in vivo distribution of intravenously injected Dextran‐AF680 in representative blood vessels of a skinfold TNBC model. The Dextran‐AF680 signal peaked at 3 h and dissipated from the vessels within 24 h. (B) Substantial colocalization was observed between Dextran‐AF680 targeted cells (red) and CD206‐FITC+ cells (green). (C) Antibody‐dependent cellular phagocytosis (ADCP) occured in rapid, brief waves between Dextran‐AF680‐labeled macrophages and CD47 inhibitor‐treated tumor cells in a skinfold TNBC model. (D) CD47 inhibitor‐treated cancer cells (green) were engulfed by macrophages labeled with the pan‐macrophage marker F4/80‐PE (red), underscoring the highly phagocytic nature of macrophages (scale bars, 25 μm). (E) Intravital imaging of the robust phagocytic capacity of F4/80+ macrophages (red) toward CD47 inhibitor‐treated tumor cells (green).

Techniques Used: Imaging, In Vivo, Injection, Labeling, Marker

In vivo and in vitro validation of TNBC targeting by MCP1‐FITC. (A, B) Following intravenous injection of MCP1‐FITC, fluorescence signals in TNBC tissue peaked at 4 min and rapidly declined within 2 h ( n = 6, p = 0.0313). (C, D) Ex vivo imaging of dissected organs from subcutaneous xenograft models revealed a noticeable difference in fluorescence signal intensity between TNBC tumors and normal organs at 4 min after intravenous injection of MCP1‐FITC ( n = 6, p = 0.0095). (E, F) The average radiant efficiency of MCP1‐FITC in resected TNBC tissues was quantitively compared between the anti‐CD47 monoclonal antibody (mAb) and isotype control (ISO) treatment groups ( n = 16, p = 0.0499). (G) A significant difference in the M1/M2 ratio, based on the average radiant efficiency, was observed between anti‐CD47 mAb‐treated and ISO‐treated mice ( n = 12, p = 0.0022). (H) A pronounced shift in the population of MCP1‐FITC targeted cells was observed following repeated immunotherapy. (I, J) Significant differences in the M1/M2 ratio, based on the MCP‐1 FITC+ cells, is observed between anti‐CD47 mAb‐treated and ISO‐treated mice ( n = 16, p = 0.0104), ( n = 10, p = 0.0079). (K) A correlation analysis indicated that there is a strong correlation between the flow cytometry‐derived M1/M2 ratio and the imaging‐derived M1/M2 ratio. Data are presented as the mean ± standard deviation (SD).

Figure Legend Snippet: In vivo and in vitro validation of TNBC targeting by MCP1‐FITC. (A, B) Following intravenous injection of MCP1‐FITC, fluorescence signals in TNBC tissue peaked at 4 min and rapidly declined within 2 h ( n = 6, p = 0.0313). (C, D) Ex vivo imaging of dissected organs from subcutaneous xenograft models revealed a noticeable difference in fluorescence signal intensity between TNBC tumors and normal organs at 4 min after intravenous injection of MCP1‐FITC ( n = 6, p = 0.0095). (E, F) The average radiant efficiency of MCP1‐FITC in resected TNBC tissues was quantitively compared between the anti‐CD47 monoclonal antibody (mAb) and isotype control (ISO) treatment groups ( n = 16, p = 0.0499). (G) A significant difference in the M1/M2 ratio, based on the average radiant efficiency, was observed between anti‐CD47 mAb‐treated and ISO‐treated mice ( n = 12, p = 0.0022). (H) A pronounced shift in the population of MCP1‐FITC targeted cells was observed following repeated immunotherapy. (I, J) Significant differences in the M1/M2 ratio, based on the MCP‐1 FITC+ cells, is observed between anti‐CD47 mAb‐treated and ISO‐treated mice ( n = 16, p = 0.0104), ( n = 10, p = 0.0079). (K) A correlation analysis indicated that there is a strong correlation between the flow cytometry‐derived M1/M2 ratio and the imaging‐derived M1/M2 ratio. Data are presented as the mean ± standard deviation (SD).

Techniques Used: In Vivo, In Vitro, Biomarker Discovery, Injection, Fluorescence, Tissue, Ex Vivo, Imaging, Xenograft Assay, Control, Analysis, Flow Cytometry, Derivative Assay, Standard Deviation

Control:

Article Title: NNMT inhibition in cancer-associated fibroblasts restores antitumour immunity.
Article Snippet: For CD8-depletion experiments, mice were i.p. injected with 12.5 mg per kg anti-CD8 antibody (BioXCell, BP0004-1) or an isotype control (BioXCell, BP0089) at the indicated timepoints. .. For ICB, mice received 10 mg per kg of anti-PD-1 or anti-CD47 (BioXCell, BP0146 (anti-PD-1), BP0283 (anti-CD47)) antibody or an isotype control (BioXCell, BP0089 (control for anti-PD-1), BP0083 (control for anti-CD47)) at the indicated timepoints. ..

Article Title: Oncolytic Newcastle-disease-virus-mediated CD47 blockade in preclinical melanoma and pancreatic cancer models
Article Snippet: .. For both models, when tumors were approximately 5 × 5 mm, mice were either PBS treated or received one of the following: three consecutive intratumoral doses of 1 × 10 8 PFU NDV-Luciferase, NDV-αCD47, NDV-SIRPα-Fc, NDV-Luc plus 50 μg anti-CD47 (BE0270, BioXCell, CT), 50 μg anti-CD47 only, or 50 μg of a rat isotype control (BE0089, BioXCell, CT) ( n = 6–8 per treatment group). ..

Article Title: Oncolytic Newcastle Disease Virus-Mediated CD47 Blockade in Preclinical Melanoma and Pancreatic Cancer Models
Article Snippet: .. For both models, when tumors were approximately 5 × 5 mm, mice were either PBS treated or received one of the following: three consecutive intratumoral doses of 1 × 10 8 PFU NDV-Luciferase, NDV-αCD47, NDV-SIRPα-Fc, NDV-Luc plus 50 μg anti-CD47 (BE0270, BioXCell, CT), 50 μg anti-CD47 only, or 50 μg of a rat isotype control (BE0089, BioXCell, CT) (n = 6–8 per treatment group). ..

Concentration Assay:

Article Title: Resolvin D2 limits senescent cell accumulation in atherosclerotic plaques.
Article Snippet: Atherosclerosis is a non-resolving inflammatory disease, and mechanisms to promote inflammation resolution, reduce vascular injury and promote repair in atherosclerosis are unmet needs.. Specialized pro-resolving mediators (SPMs) like Resolvins, in part, mediate inflammation resolution and limit atherosclerosis progression.. Uncovering processes associated with their protective actions are of interest.

Injection:

Article Title: Inhibition of Macrophage ARID3A Alleviates Myocardial Ischemia-Reperfusion Injury After Heart Transplantation by Reducing THBS1/CD47 Signaling-Mediated Neutrophil Extracellular Traps Formation.
Article Snippet: Recipient mice were injected with clodronate liposomes (200 μL, 5 μg μL−1, Liposoma BV, Amsterdam, the Netherlands) or control/empty liposomes by tail vein 24 h prior to receiving HT. .. In addition, anti-CD47 (200 μg/mouse/time, BioXcell), anti-THBS1 (100 μg/mouse/time, BioXcell) and anti-Ly6G (50 μg/mouse/time, BioXcell) were injected into the recipient mice via the tail vein 24 h before mice receivedHT and 2 h after reperfusion. .. Anti-IgG (BioXcell, USA), the isotype control, was administered at the same time, with the same dose and in the samemanner as themodelmice to exclude the interference of non-specific antibody epitopes.

Article Title: Monitoring Response to Combinatorial Immunotherapies by Tracking both T Cells and Natural Killer Cells In Vivo via ImmunoPET-Raman Multimodal Gold Nanostars
Article Snippet: .. Immunotherapy combination treatment consisted of 200 μg of anti-PD-L1 (BioXcell, clone B7–H1) and 120 μg of anti-CD47 (BioXcell, clone MIAP301) delivered via IP injection every other day for 3 doses for 4T1 and 4 dose for CT26. ..

Article Title: Inhibition of Macrophage ARID3A Alleviates Myocardial Ischemia‐Reperfusion Injury After Heart Transplantation by Reducing THBS1/CD47 Signaling‐Mediated Neutrophil Extracellular Traps Formation
Article Snippet: Recipient mice were injected with clodronate liposomes (200 μL, 5 μg μL −1 , Liposoma BV, Amsterdam, the Netherlands) or control/empty liposomes by tail vein 24 h prior to receiving HT. .. In addition, anti‐CD47 (200 μg/mouse/time, BioXcell), anti‐THBS1 (100 μg/mouse/time, BioXcell) and anti‐Ly6G (50 μg/mouse/time, BioXcell) were injected into the recipient mice via the tail vein 24 h before mice received HT and 2 h after reperfusion. .. Anti‐IgG (BioXcell, USA), the isotype control, was administered at the same time, with the same dose and in the same manner as the model mice to exclude the interference of non‐specific antibody epitopes.

Image Search Results

Journal: Cancer Medicine

Article Title: In Vivo Immunoscoring Technique to Monitor Anti‐ CD47 Immunotherapy Efficacy in Triple‐Negative Breast Cancer

doi: 10.1002/cam4.72232

Figure Lengend Snippet: Real‐time monitoring of tumor progression and anti‐CD47 therapeutic efficiency. (A) Female BALB/c mice aged 8–10 weeks were implanted with dorsal skinfold window chambers. 4T1_PB3R‐RFP TNBC cells were transplanted into the subcutaneous tissue, and tumors were monitored using intravital imaging. (B) Detailed visualization of angiogenesis and tumor nodule formation in TNBC skinfold models compared with the isotype control group. (C, D) Conventional whole‐body bioluminescence imaging of mice bearing 4T1_PB3R‐RFP‐luc tumors revealed considerably decreased signals following anti‐CD47 immunotherapy administered over 5 days, beginning on day 9 for 5 days ( n = 7, p < 0.0001, 10 mg/kg, intravenous injection). Data are presented as the mean ± standard deviation (SD).

Article Snippet: To evaluate the performance of the in vivo immunoscoring technique for the monitoring of anti‐CD47 immunotherapy efficacy, anti‐mouse CD47 monoclonal antibodies (specifically, anti‐CD47 mAbs, clone MIAP301, Rat IgG2a, κ, BioXcell, USA) and an IgG2a mAbs isotype control (clone 2A3, Rat IgG2a, κ, BioXcell, USA) were systemically and intravenously (IV) injected at a dosage of 10 mg/kg once a day for a duration of five consecutive days.

Techniques: Real-time Monitoring, Tissue, Imaging, Control, Injection, Standard Deviation

Journal: Cancer Medicine

Article Title: In Vivo Immunoscoring Technique to Monitor Anti‐ CD47 Immunotherapy Efficacy in Triple‐Negative Breast Cancer

doi: 10.1002/cam4.72232

Figure Lengend Snippet: In vivo and in vitro validation of TNBC targeting by Dextran‐AF680. (A–C) The signals emitted by Dextran‐AF680 at various time intervals following intravenous injections exhibited significant differences between 10 and 180 min and between 180 and 360 min. (D, E) Dextran‐AF680 can be administrated for TNBC imaging with photoacoustic tomography, and the optimal imaging time is 3 h after dextran injection, indicating its potential as an imaging probe for enhancing TNBC visualization ( n = 7, p = 0.024, p = 0.004). (F, G) Longitudinal conventional fluorescence imaging of the anti‐CD47 immunotherapeutic response, in comparison with the isotype control treatment, demonstrated a significant change in the average radiant efficiency of Dextran AF680 following 5 days of treatment ( n = 12, p = 0.0022). (H, I) An evident shift in the population of Dextran‐AF680+ and RFP+ cells was observed after anti‐CD47 mAb immunotherapies ( n = 10, p = 0.0079). Data are presented as the mean ± standard deviation (SD).

Techniques: In Vivo, In Vitro, Biomarker Discovery, Imaging, Micro-PAT, Injection, Fluorescence, Comparison, Control, Standard Deviation

Journal: Cancer Medicine

Article Title: In Vivo Immunoscoring Technique to Monitor Anti‐ CD47 Immunotherapy Efficacy in Triple‐Negative Breast Cancer

doi: 10.1002/cam4.72232

Figure Lengend Snippet: Intravital imaging of M2 macrophage targeting by Dextran‐AF680. (A) Dynamic in vivo distribution of intravenously injected Dextran‐AF680 in representative blood vessels of a skinfold TNBC model. The Dextran‐AF680 signal peaked at 3 h and dissipated from the vessels within 24 h. (B) Substantial colocalization was observed between Dextran‐AF680 targeted cells (red) and CD206‐FITC+ cells (green). (C) Antibody‐dependent cellular phagocytosis (ADCP) occured in rapid, brief waves between Dextran‐AF680‐labeled macrophages and CD47 inhibitor‐treated tumor cells in a skinfold TNBC model. (D) CD47 inhibitor‐treated cancer cells (green) were engulfed by macrophages labeled with the pan‐macrophage marker F4/80‐PE (red), underscoring the highly phagocytic nature of macrophages (scale bars, 25 μm). (E) Intravital imaging of the robust phagocytic capacity of F4/80+ macrophages (red) toward CD47 inhibitor‐treated tumor cells (green).

Techniques: Imaging, In Vivo, Injection, Labeling, Marker

Journal: Cancer Medicine

Article Title: In Vivo Immunoscoring Technique to Monitor Anti‐ CD47 Immunotherapy Efficacy in Triple‐Negative Breast Cancer

doi: 10.1002/cam4.72232

Figure Lengend Snippet: In vivo and in vitro validation of TNBC targeting by MCP1‐FITC. (A, B) Following intravenous injection of MCP1‐FITC, fluorescence signals in TNBC tissue peaked at 4 min and rapidly declined within 2 h ( n = 6, p = 0.0313). (C, D) Ex vivo imaging of dissected organs from subcutaneous xenograft models revealed a noticeable difference in fluorescence signal intensity between TNBC tumors and normal organs at 4 min after intravenous injection of MCP1‐FITC ( n = 6, p = 0.0095). (E, F) The average radiant efficiency of MCP1‐FITC in resected TNBC tissues was quantitively compared between the anti‐CD47 monoclonal antibody (mAb) and isotype control (ISO) treatment groups ( n = 16, p = 0.0499). (G) A significant difference in the M1/M2 ratio, based on the average radiant efficiency, was observed between anti‐CD47 mAb‐treated and ISO‐treated mice ( n = 12, p = 0.0022). (H) A pronounced shift in the population of MCP1‐FITC targeted cells was observed following repeated immunotherapy. (I, J) Significant differences in the M1/M2 ratio, based on the MCP‐1 FITC+ cells, is observed between anti‐CD47 mAb‐treated and ISO‐treated mice ( n = 16, p = 0.0104), ( n = 10, p = 0.0079). (K) A correlation analysis indicated that there is a strong correlation between the flow cytometry‐derived M1/M2 ratio and the imaging‐derived M1/M2 ratio. Data are presented as the mean ± standard deviation (SD).

Techniques: In Vivo, In Vitro, Biomarker Discovery, Injection, Fluorescence, Tissue, Ex Vivo, Imaging, Xenograft Assay, Control, Analysis, Flow Cytometry, Derivative Assay, Standard Deviation

$a The synthetic process and the structure diagram of MAzyme (created in BioRender. Huang, H. (2026) https://BioRender.com/glo0g6v ). b TEM image of MAzyme and a magnification image (inset). c The high-resolution TEM image of MAzyme. d , e Elemental mapping images of MAzyme. f The structural changes of the initial and final states of the composite system in different models during the simulation process. g Temporal evolution of the self-aggregation supramolecular structure for MAzyme by MSD. h Fourier transform infrared (FTIR) spectrum of MAzyme. i High-resolution Cu 2 p X-ray photoelectron spectroscopy (XPS) results of MAzyme. j X-ray diffraction (XRD) pattern of MAzyme. k N 2 adsorption/desorption isotherms of MAzyme and the corresponding pore-size distribution curve calculated by non-local density functional theory (NLDFT, inset). l TEM image of biomimetic MMAzyme, indicating a cytomembrane layer coated on the surface of MAzyme. m Characteristic protein bands of CD36, CD47, and CCR2 on MAzyme, MMAzyme, and MM by Western blotting. n Zeta potentials and o particle diameter of MAzyme and MMAzyme analyzed by dynamic light scattering (DLS) ( n = 3 independent samples). Data in ( n , o ) were expressed as mean ± S.D. Source data are provided as a file.$

Journal: Nature Communications

Article Title: Bioinspired porous metal-amino acid nanozymes enable multi-pathway treatment of atherosclerosis through anti-oxidation and pro-efferocytosis

doi: 10.1038/s41467-026-75509-4

Figure Lengend Snippet: a The synthetic process and the structure diagram of MAzyme (created in BioRender. Huang, H. (2026) https://BioRender.com/glo0g6v ). b TEM image of MAzyme and a magnification image (inset). c The high-resolution TEM image of MAzyme. d , e Elemental mapping images of MAzyme. f The structural changes of the initial and final states of the composite system in different models during the simulation process. g Temporal evolution of the self-aggregation supramolecular structure for MAzyme by MSD. h Fourier transform infrared (FTIR) spectrum of MAzyme. i High-resolution Cu 2 p X-ray photoelectron spectroscopy (XPS) results of MAzyme. j X-ray diffraction (XRD) pattern of MAzyme. k N 2 adsorption/desorption isotherms of MAzyme and the corresponding pore-size distribution curve calculated by non-local density functional theory (NLDFT, inset). l TEM image of biomimetic MMAzyme, indicating a cytomembrane layer coated on the surface of MAzyme. m Characteristic protein bands of CD36, CD47, and CCR2 on MAzyme, MMAzyme, and MM by Western blotting. n Zeta potentials and o particle diameter of MAzyme and MMAzyme analyzed by dynamic light scattering (DLS) ( n = 3 independent samples). Data in ( n , o ) were expressed as mean ± S.D. Source data are provided as a file.

Article Snippet: The following primary antibodies were used in this study: CD47 Rabbit pAb (A1838, ABclonal,1:750), CD36/SR-B3 Rabbit pAb (A5792, ABclonal,1:2500), CCR2 Rabbit pAb (A2855, ABclonal,1:750), Na-K-ATP Rabbit pAb (GB11400, Servicebio,1:2000), MERTK Rabbit pAb (A5443, ABclonal,1:750), LXRα Rabbit mAb (A3974, ABclonal,1:3000), ABCG1 Rabbit mAb (A17907, ABclonal,1:1500), PPARγ Rabbit pAb (WL01800, Wanleibio,1:1000), Anti-ABCA1 antibody ( AB307536 , Abcam,1:1000), GAPDH Rabbit pAb (AC001, ABclonal,1:20000), p-SHP1 (8849, Cell Signaling Technology, 1:1000), HRP-conjugated Goat anti-Rabbit IgG (H+L) (AS014, ABclonal,1:5000).

Techniques: Fourier Transform Infrared Spectroscopy, Spectroscopy, Adsorption, Pore Size, Functional Assay, Western Blot

a Schematic illustration of the pro-efferocytosis property of MMAzyme-S. (Created in BioRender. Huang, H. (2026) https://BioRender.com/7l5dwq4 ). b CLSM images depicting phagocytosis of CD47-overexpressed ACs in proinflammatory-phenotype macrophages pretreated with different samples. FCM results ( c ) and the corresponding quantitative analysis ( d ) of efferocytosis towards CD47-overexpressed ACs by proinflammatory phenotype macrophages pretreated with different samples ( n = 3 independent biological samples). e The quantitative results of the Western blotting of Mertk in macrophages under different treatments ( n = 3 independent biological samples. Samples in different blots were derived from the same experiment. All gels/blots were processed in parallel. f Schematics illustration for the mechanism of promoting cholesterol efflux mediated by MMAzyme-S (created in BioRender. Huang, H. (2026) https://BioRender.com/o3x56t5 ). g Optical microscopy images of induced foamy cell formation in macrophages under different treatments. h Cholesterol content in the supernatant of foamy cells under different treatments ( n = 4 independent biological samples). i Western blotting analysis of Mertk, PPARγ, LXRα, ABCA1, and ABCG1 in macrophages under different treatments. Corresponding quantitative results of the Western blotting of PPARγ ( j ), LXRα ( k ), ABCA1 ( l ), and ABCG1 ( m ) in macrophages under different treatments ( n = 3 independent biological samples. Samples in different blots were derived from the same experiment. All gels/blots were processed in parallel). Data in ( d , e , h , j – m ) were expressed as mean ± S.D. Significance in ( d , e , h , j – m ) was calculated using one-way ANOVA followed by Tukey’s post hoc test for multiple comparisons. Although the individual values of Group ii and Group iii in ( l ) do not overlap, the statistical analysis does not indicate a significant difference, possibly due to the limited sample size. Source data are provided as a file.

Journal: Nature Communications

Article Title: Bioinspired porous metal-amino acid nanozymes enable multi-pathway treatment of atherosclerosis through anti-oxidation and pro-efferocytosis

doi: 10.1038/s41467-026-75509-4

Figure Lengend Snippet: a Schematic illustration of the pro-efferocytosis property of MMAzyme-S. (Created in BioRender. Huang, H. (2026) https://BioRender.com/7l5dwq4 ). b CLSM images depicting phagocytosis of CD47-overexpressed ACs in proinflammatory-phenotype macrophages pretreated with different samples. FCM results ( c ) and the corresponding quantitative analysis ( d ) of efferocytosis towards CD47-overexpressed ACs by proinflammatory phenotype macrophages pretreated with different samples ( n = 3 independent biological samples). e The quantitative results of the Western blotting of Mertk in macrophages under different treatments ( n = 3 independent biological samples. Samples in different blots were derived from the same experiment. All gels/blots were processed in parallel. f Schematics illustration for the mechanism of promoting cholesterol efflux mediated by MMAzyme-S (created in BioRender. Huang, H. (2026) https://BioRender.com/o3x56t5 ). g Optical microscopy images of induced foamy cell formation in macrophages under different treatments. h Cholesterol content in the supernatant of foamy cells under different treatments ( n = 4 independent biological samples). i Western blotting analysis of Mertk, PPARγ, LXRα, ABCA1, and ABCG1 in macrophages under different treatments. Corresponding quantitative results of the Western blotting of PPARγ ( j ), LXRα ( k ), ABCA1 ( l ), and ABCG1 ( m ) in macrophages under different treatments ( n = 3 independent biological samples. Samples in different blots were derived from the same experiment. All gels/blots were processed in parallel). Data in ( d , e , h , j – m ) were expressed as mean ± S.D. Significance in ( d , e , h , j – m ) was calculated using one-way ANOVA followed by Tukey’s post hoc test for multiple comparisons. Although the individual values of Group ii and Group iii in ( l ) do not overlap, the statistical analysis does not indicate a significant difference, possibly due to the limited sample size. Source data are provided as a file.

Techniques: Western Blot, Derivative Assay, Microscopy

miR‐18a regulates the TGF‐β signaling pathway to confer CD8 + T cell tolerance by targeting THBS1 . (A) Volcano plot showing differential expression of TGF‐β pathway genes, with miR‐18a‐5p targets (diamonds) and miR‐18a‐3p targets (triangles) highlighted and THBS1 labeled. (B) Western blot of THBS1 in A375‐Cas9 (control) and miR‐18a KO cells. (C) Dual‐luciferase reporter assay showing miR‐18a‐5p mimics suppress WT THBS1 3′UTR activity but not MUT 3′UTR. NC: scrambled mimic control. (D) Western blot confirming siRNA‐mediated THBS1 knockdown (438, 1955, and 2095) in miR‐18a KO A375 cells. Control: scrambled RNA. (E) Cell proliferation of A375‐Cas9 (control) and miR‐18a KO cells co‐cultured with CD8 + T cells at various T:E ratios with scrambled RNA (NC) or si THBS1 (2095). (F) Schematic of C57BL/6 murine tumor model with miR‐18a‐5p mimic treatment. Mice were inoculated with miR‐18a KO YUMM1.7 cells and subsequently injected with 20 µL of scrambled mimic control or miR‐18a‐5p mimics. (G) Representative tumor images and tumor growth curves in miR‐18a‐5p mimic‐treated versus control mice. (H) Single‐cell UMAP of tumor tissues from control and miR‐18a‐5p mimic‐treated mice. (I) Hallmark pathway enrichment of DEGs (miR‐18a‐5p mimic versus control), showing TGF‐β suppression. FDTs: Fibroblast‐Derived Tumor cells; EDTs: Epithelial‐Derived Tumor cells. (J) Signaling interactions between FDTs and CD8 + T cells in control versus miR‐18a‐5p mimic‐treated mice. (K) Thbs1 expression across cell types in control and miR‐18a‐5p mimic‐treated mice. (L) Cell proliferation of A375‐Cas9 (control) and miR‐18a KO A375 cells with/without CD8 + T cell and CD47 inhibitor (magrolimab; isotype IgG control). (M, N) Representative IHC images (M) and quantification (N) of Ki67, Cd47, and Thbs1 in murine tumor tissues. Data represent means ± SD; n = 3 biologically independent samples for panels C and E, n = 6 for panel L, and n = 7 for panels G and N. Two‐way ANOVA followed by Tukey's post hoc test is used to calculate P ‐values in panel G and unpaired two‐tailed Student's t ‐test is used to calculate P ‐values in panels C, E, L, and N: *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001; ns, not significant.

Journal: Advanced Science

Article Title: Genome‐Wide CRISPR Screen Identifies a microRNA Orchestrating Pleiotropic Resistance to Targeted Therapy and T Cell Immunity in Melanoma

doi: 10.1002/advs.202515158

Figure Lengend Snippet: miR‐18a regulates the TGF‐β signaling pathway to confer CD8 + T cell tolerance by targeting THBS1 . (A) Volcano plot showing differential expression of TGF‐β pathway genes, with miR‐18a‐5p targets (diamonds) and miR‐18a‐3p targets (triangles) highlighted and THBS1 labeled. (B) Western blot of THBS1 in A375‐Cas9 (control) and miR‐18a KO cells. (C) Dual‐luciferase reporter assay showing miR‐18a‐5p mimics suppress WT THBS1 3′UTR activity but not MUT 3′UTR. NC: scrambled mimic control. (D) Western blot confirming siRNA‐mediated THBS1 knockdown (438, 1955, and 2095) in miR‐18a KO A375 cells. Control: scrambled RNA. (E) Cell proliferation of A375‐Cas9 (control) and miR‐18a KO cells co‐cultured with CD8 + T cells at various T:E ratios with scrambled RNA (NC) or si THBS1 (2095). (F) Schematic of C57BL/6 murine tumor model with miR‐18a‐5p mimic treatment. Mice were inoculated with miR‐18a KO YUMM1.7 cells and subsequently injected with 20 µL of scrambled mimic control or miR‐18a‐5p mimics. (G) Representative tumor images and tumor growth curves in miR‐18a‐5p mimic‐treated versus control mice. (H) Single‐cell UMAP of tumor tissues from control and miR‐18a‐5p mimic‐treated mice. (I) Hallmark pathway enrichment of DEGs (miR‐18a‐5p mimic versus control), showing TGF‐β suppression. FDTs: Fibroblast‐Derived Tumor cells; EDTs: Epithelial‐Derived Tumor cells. (J) Signaling interactions between FDTs and CD8 + T cells in control versus miR‐18a‐5p mimic‐treated mice. (K) Thbs1 expression across cell types in control and miR‐18a‐5p mimic‐treated mice. (L) Cell proliferation of A375‐Cas9 (control) and miR‐18a KO A375 cells with/without CD8 + T cell and CD47 inhibitor (magrolimab; isotype IgG control). (M, N) Representative IHC images (M) and quantification (N) of Ki67, Cd47, and Thbs1 in murine tumor tissues. Data represent means ± SD; n = 3 biologically independent samples for panels C and E, n = 6 for panel L, and n = 7 for panels G and N. Two‐way ANOVA followed by Tukey's post hoc test is used to calculate P ‐values in panel G and unpaired two‐tailed Student's t ‐test is used to calculate P ‐values in panels C, E, L, and N: *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001; ns, not significant.

Article Snippet: Primary antibodies used were as follows: phospho‐MEK (Cell Signaling Technology, 3958S, RRID: AB_2138014; 1:1,000), total MEK (Cell Signaling Technology, 4694S, RRID: AB_10695868; 1:2,000), phospho‐AKT (Cell Signaling Technology, 4060S, RRID: AB_2315049; 1:1,000), total AKT (Cell Signaling Technology, 2920S, RRID: AB_1147620; 1:2,000), phospho‐ERK (Cell Signaling Technology, 4377S, RRID: AB_331775; 1:1,000), total ERK (Cell Signaling Technology, 4695S, RRID: AB_390779; 1:2,000), AJUBA (ABclonal, A22039, RRID: AB_3719524; 1:2,000), CD47 (ABclonal, A11382, RRID: AB_2861554; 1:2,000), THBS1 (ABclonal, A2125, RRID: AB_2764144; 1:2,000), and hnRNP A1 (ABclonal, A11564, RRID: AB_2861599; 1:2,000). β‐actin (ABclonal, AC026, RRID: AB_2768234; 1:10,000) or GAPDH (ABclonal, AC001, RRID: AB_2619673; 1:10,000) served as loading controls.

Techniques: Quantitative Proteomics, Labeling, Western Blot, Control, Luciferase, Reporter Assay, Activity Assay, Knockdown, Cell Culture, Injection, Single Cell, Derivative Assay, Expressing, Two Tailed Test

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anti mouse cd47 monoclonal antibodies (Bio X Cell)

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1) Product Images from "In Vivo Immunoscoring Technique to Monitor Anti‐ CD47 Immunotherapy Efficacy in Triple‐Negative Breast Cancer"

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