multiple sclerosis Search Results


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Sanguine Biosciences Inc multiple sclerosis
Multiple Sclerosis, supplied by Sanguine Biosciences Inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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TargetMol chemokine inhibitor library
Fig. 4 CXCL1EV-dead induces macrophage M2 polarization by activating PD-L1 expression. A <t>Chemokine</t> array assay was conducted to characterize the differences in chemokine content between EV-dead and EV-alive. An ELISA assay was conducted to compare the relative CXCL1 content in EV-dead and EV-alive. B Changes in M2 phenotype polarization of Raw264.7 macrophages when treated with 10 ng/ml murine CXCL1, 50 μg/ ml EV-dead, 50 μg/ml EV-deadshCXCL1, 5 μg/ml CXCL1 neutralizing antibody (NA), or EV-dead and CXCL1-NA combination for 48 h. C Representative images of Transwell assay. Raw264.7 macrophages were treated as indicated for 48 h and then co-cultured with 4 T1 cells. Scale bar: 200 μm. D–F Expression changes of CXCL1 and PD-L1 in Raw264.7 macrophages when treated as indicated for 48 h. Scale bar: 10 μm. G The results of the flow cytometry assay suggested that 50 μg/ml EV-dead treatment for 48 h induced the M2 polarization of Raw264.7 macrophages by activating PD-L1 expression; n = 3. Data are presented as mean ± SD. *p < 0.05, **p < 0.01
Chemokine Inhibitor Library, supplied by TargetMol, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Novus Biologicals human brain lysates
Fig. 4 CXCL1EV-dead induces macrophage M2 polarization by activating PD-L1 expression. A <t>Chemokine</t> array assay was conducted to characterize the differences in chemokine content between EV-dead and EV-alive. An ELISA assay was conducted to compare the relative CXCL1 content in EV-dead and EV-alive. B Changes in M2 phenotype polarization of Raw264.7 macrophages when treated with 10 ng/ml murine CXCL1, 50 μg/ ml EV-dead, 50 μg/ml EV-deadshCXCL1, 5 μg/ml CXCL1 neutralizing antibody (NA), or EV-dead and CXCL1-NA combination for 48 h. C Representative images of Transwell assay. Raw264.7 macrophages were treated as indicated for 48 h and then co-cultured with 4 T1 cells. Scale bar: 200 μm. D–F Expression changes of CXCL1 and PD-L1 in Raw264.7 macrophages when treated as indicated for 48 h. Scale bar: 10 μm. G The results of the flow cytometry assay suggested that 50 μg/ml EV-dead treatment for 48 h induced the M2 polarization of Raw264.7 macrophages by activating PD-L1 expression; n = 3. Data are presented as mean ± SD. *p < 0.05, **p < 0.01
Human Brain Lysates, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Novus Biologicals human brain whole tissue lysates
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Human Brain Whole Tissue Lysates, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Ms Performance Test (Mspt), supplied by Biogen Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Clinical Trials In Multiple Sclerosis, supplied by Novartis, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Multiple Sclerosis (Ms) Diseasemodifying Therapies, supplied by Johns Hopkins HealthCare, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Novartis multiple sclerosis drug
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Multiple Sclerosis Drug, supplied by Novartis, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Fig. 4 CXCL1EV-dead induces macrophage M2 polarization by activating PD-L1 expression. A Chemokine array assay was conducted to characterize the differences in chemokine content between EV-dead and EV-alive. An ELISA assay was conducted to compare the relative CXCL1 content in EV-dead and EV-alive. B Changes in M2 phenotype polarization of Raw264.7 macrophages when treated with 10 ng/ml murine CXCL1, 50 μg/ ml EV-dead, 50 μg/ml EV-deadshCXCL1, 5 μg/ml CXCL1 neutralizing antibody (NA), or EV-dead and CXCL1-NA combination for 48 h. C Representative images of Transwell assay. Raw264.7 macrophages were treated as indicated for 48 h and then co-cultured with 4 T1 cells. Scale bar: 200 μm. D–F Expression changes of CXCL1 and PD-L1 in Raw264.7 macrophages when treated as indicated for 48 h. Scale bar: 10 μm. G The results of the flow cytometry assay suggested that 50 μg/ml EV-dead treatment for 48 h induced the M2 polarization of Raw264.7 macrophages by activating PD-L1 expression; n = 3. Data are presented as mean ± SD. *p < 0.05, **p < 0.01

Journal: Journal of experimental & clinical cancer research : CR

Article Title: Chemotherapy-elicited extracellular vesicle CXCL1 from dying cells promotes triple-negative breast cancer metastasis by activating TAM/PD-L1 signaling.

doi: 10.1186/s13046-024-03050-7

Figure Lengend Snippet: Fig. 4 CXCL1EV-dead induces macrophage M2 polarization by activating PD-L1 expression. A Chemokine array assay was conducted to characterize the differences in chemokine content between EV-dead and EV-alive. An ELISA assay was conducted to compare the relative CXCL1 content in EV-dead and EV-alive. B Changes in M2 phenotype polarization of Raw264.7 macrophages when treated with 10 ng/ml murine CXCL1, 50 μg/ ml EV-dead, 50 μg/ml EV-deadshCXCL1, 5 μg/ml CXCL1 neutralizing antibody (NA), or EV-dead and CXCL1-NA combination for 48 h. C Representative images of Transwell assay. Raw264.7 macrophages were treated as indicated for 48 h and then co-cultured with 4 T1 cells. Scale bar: 200 μm. D–F Expression changes of CXCL1 and PD-L1 in Raw264.7 macrophages when treated as indicated for 48 h. Scale bar: 10 μm. G The results of the flow cytometry assay suggested that 50 μg/ml EV-dead treatment for 48 h induced the M2 polarization of Raw264.7 macrophages by activating PD-L1 expression; n = 3. Data are presented as mean ± SD. *p < 0.05, **p < 0.01

Article Snippet: CXCL1 secretion inhibitor screening To screen the potential CXCL1 secretion inhibitor of 4 T1 cells from the Chemokine Inhibitor Library (L7600, TOPSCIENCE, Shanghai, China), 4 T1 cells were treated with 80 types of chemokine inhibitors (1 μM) for 48 h. Subsequently, the concentration of CXCL1 in cell culture supernatants was detected using the Mouse CXCL1 ELISA Kit.

Techniques: Expressing, Enzyme-linked Immunosorbent Assay, Transwell Assay, Cell Culture, Flow Cytometry

Patient description and tumor sample characteristics

Journal: Experimental Neurobiology

Article Title: LGR5 and Downstream Intracellular Signaling Proteins Play Critical Roles in the Cell Proliferation of Neuroblastoma, Meningioma and Pituitary Adenoma

doi: 10.5607/en.2019.28.5.628

Figure Lengend Snippet: Patient description and tumor sample characteristics

Article Snippet: Human brain whole tissue lysates and brain tissue slides from normal adults were obtained from Novus Biologicals (Littleton, CO, USA).

Techniques: Concentration Assay

Expression of LGR5, hnRNPA2B1, and hnRNPH3 proteins in human normal, benign meningioma, and pituitary adenoma tissues, and immunohistochemistry for LGR5 and hnRNPH3 in meningioma and pituitary adenoma tissues with immunofluorescence confocal microscopy. (A) Comparison of expression levels of LGR5, hnRNPA2B1, and hnRNPH3 between normal, benign meningioma, and pituitary adenoma by western blotting. (B) Confocal images of the human normal brain (top), meningioma (middle) and pituitary adenoma (bottom) tissues stained with antibodies against LGR5 (green) and hnRNPH3 (red). Scale bar: 20 μm. The number of LGR5 + /hnRNPH3 + cells per DAPI positive cells and hnRNPH3 + cells per LGR5 positive cells was counted and expressed as %.

Journal: Experimental Neurobiology

Article Title: LGR5 and Downstream Intracellular Signaling Proteins Play Critical Roles in the Cell Proliferation of Neuroblastoma, Meningioma and Pituitary Adenoma

doi: 10.5607/en.2019.28.5.628

Figure Lengend Snippet: Expression of LGR5, hnRNPA2B1, and hnRNPH3 proteins in human normal, benign meningioma, and pituitary adenoma tissues, and immunohistochemistry for LGR5 and hnRNPH3 in meningioma and pituitary adenoma tissues with immunofluorescence confocal microscopy. (A) Comparison of expression levels of LGR5, hnRNPA2B1, and hnRNPH3 between normal, benign meningioma, and pituitary adenoma by western blotting. (B) Confocal images of the human normal brain (top), meningioma (middle) and pituitary adenoma (bottom) tissues stained with antibodies against LGR5 (green) and hnRNPH3 (red). Scale bar: 20 μm. The number of LGR5 + /hnRNPH3 + cells per DAPI positive cells and hnRNPH3 + cells per LGR5 positive cells was counted and expressed as %.

Article Snippet: Human brain whole tissue lysates and brain tissue slides from normal adults were obtained from Novus Biologicals (Littleton, CO, USA).

Techniques: Expressing, Immunohistochemistry, Immunofluorescence, Confocal Microscopy, Comparison, Western Blot, Staining