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cd80  (Miltenyi Biotec)


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    Miltenyi Biotec cd80
    Proposed model illustrating the effects of EZH2 inhibition across multiple joint compartments in osteoarthritis. In OA fibroblast-like synoviocytes (FLS), increased EZH2 and H3K27me3 levels were associated with inflammatory and catabolic responses, which were reduced by pharmacological EZH2 inhibition with EPZ-6438. In human OA FLS, EPZ-6438 decreased inflammatory, catabolic and pain-associated mediators, including IL1B, MMP13, NGF and NTN1, reduced LDHA expression and increased autophagy-associated responses. Proteomic and ChIP-seq analyses further identified inflammatory, metabolic and axon guidance-related pathways, including inflammation-dependent EZH2 recruitment at the PAX6 locus. EZH2 inhibition also reduced inflammatory activation of macrophages and osteoclastogenesis in OA-derived bone marrow cells. Collectively, these findings support a broader role for EZH2 in inflammatory, catabolic and osteoimmune responses across multiple OA-relevant cellular compartments. The identification of PAX6, NTN1 and axon guidance-related pathways highlights neuro-associated molecular programs that may be relevant to pain-associated responses, although their direct contribution to pain or sensory nerve remodeling was not assessed in this study. The reduced structural joint damage and pain-related behaviors observed following EZH2 inhibition in the MIA-induced OA model are consistent with this multicellular framework
    Cd80, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 94/100, based on 37 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/cd80/CD80+Antibody%2C+anti-mouse%2C+REAfinity/pmc13694607-279-21-25
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    1) Product Images from "EZH2 coordinates inflammatory and pain-associated pathways across joint compartments in osteoarthritis"

    Article Title: EZH2 coordinates inflammatory and pain-associated pathways across joint compartments in osteoarthritis

    Journal: Molecular Biomedicine

    doi: 10.1186/s43556-026-00643-w

    Proposed model illustrating the effects of EZH2 inhibition across multiple joint compartments in osteoarthritis. In OA fibroblast-like synoviocytes (FLS), increased EZH2 and H3K27me3 levels were associated with inflammatory and catabolic responses, which were reduced by pharmacological EZH2 inhibition with EPZ-6438. In human OA FLS, EPZ-6438 decreased inflammatory, catabolic and pain-associated mediators, including IL1B, MMP13, NGF and NTN1, reduced LDHA expression and increased autophagy-associated responses. Proteomic and ChIP-seq analyses further identified inflammatory, metabolic and axon guidance-related pathways, including inflammation-dependent EZH2 recruitment at the PAX6 locus. EZH2 inhibition also reduced inflammatory activation of macrophages and osteoclastogenesis in OA-derived bone marrow cells. Collectively, these findings support a broader role for EZH2 in inflammatory, catabolic and osteoimmune responses across multiple OA-relevant cellular compartments. The identification of PAX6, NTN1 and axon guidance-related pathways highlights neuro-associated molecular programs that may be relevant to pain-associated responses, although their direct contribution to pain or sensory nerve remodeling was not assessed in this study. The reduced structural joint damage and pain-related behaviors observed following EZH2 inhibition in the MIA-induced OA model are consistent with this multicellular framework
    Figure Legend Snippet: Proposed model illustrating the effects of EZH2 inhibition across multiple joint compartments in osteoarthritis. In OA fibroblast-like synoviocytes (FLS), increased EZH2 and H3K27me3 levels were associated with inflammatory and catabolic responses, which were reduced by pharmacological EZH2 inhibition with EPZ-6438. In human OA FLS, EPZ-6438 decreased inflammatory, catabolic and pain-associated mediators, including IL1B, MMP13, NGF and NTN1, reduced LDHA expression and increased autophagy-associated responses. Proteomic and ChIP-seq analyses further identified inflammatory, metabolic and axon guidance-related pathways, including inflammation-dependent EZH2 recruitment at the PAX6 locus. EZH2 inhibition also reduced inflammatory activation of macrophages and osteoclastogenesis in OA-derived bone marrow cells. Collectively, these findings support a broader role for EZH2 in inflammatory, catabolic and osteoimmune responses across multiple OA-relevant cellular compartments. The identification of PAX6, NTN1 and axon guidance-related pathways highlights neuro-associated molecular programs that may be relevant to pain-associated responses, although their direct contribution to pain or sensory nerve remodeling was not assessed in this study. The reduced structural joint damage and pain-related behaviors observed following EZH2 inhibition in the MIA-induced OA model are consistent with this multicellular framework

    Techniques Used: Inhibition, Expressing, ChIP-sequencing, Activation Assay, Derivative Assay

    Related Articles

    other:

    Article Title: Tissue-resident natural killer cells support survival in pancreatic cancer through promotion of cDC1-CD8 T activity
    Article Snippet: CD80 , REA983 , APC , Miltenyi Biotech, 130-116-46 , 1:100.

    Article Title: Dynamic stimulation promotes functional tissue-like organization of a 3D human lymphoid microenvironment model in vitro
    Article Snippet: Images used for the analysis were obtained from sections stained with Hoechst 33342 (Cat. No. 23491-52-3; Merck KGaA, Darmstadt, Germany; 1:2000).


    Immune Cell:

    Article Title: EZH2 coordinates inflammatory and pain-associated pathways across joint compartments in osteoarthritis
    Article Snippet: For intracellular staining, cells were fixed and permeabilized using the Inside Stain kit according to the manufacturer’s instructions (Miltenyi Biotec) before intracellular antibody staining. .. The following antibodies were used for immune cell characterization: CD11b (REA592 VioBlue, 130–113–810, Miltenyi Biotec), F4/80 (REA126 PE-Vio770, 130–118–459, Miltenyi Biotec), CD80 (REA983 APC-Vio770, 130–116–463, Miltenyi Biotec), CD86 (REA1190 PE, 130–122–129, Miltenyi Biotec), MHC-II (REA813 FITC, 130–112–386, Miltenyi Biotec), CD38 (REA616 PerCP-Vio700, 130–109–260, Miltenyi Biotec), and iNOS (REA982 APC, 130–116–423, Miltenyi Biotec). ..

    Immunopeptidomics:

    Article Title: EZH2 coordinates inflammatory and pain-associated pathways across joint compartments in osteoarthritis
    Article Snippet: For intracellular staining, cells were fixed and permeabilized using the Inside Stain kit according to the manufacturer’s instructions (Miltenyi Biotec) before intracellular antibody staining. .. The following antibodies were used for immune cell characterization: CD11b (REA592 VioBlue, 130–113–810, Miltenyi Biotec), F4/80 (REA126 PE-Vio770, 130–118–459, Miltenyi Biotec), CD80 (REA983 APC-Vio770, 130–116–463, Miltenyi Biotec), CD86 (REA1190 PE, 130–122–129, Miltenyi Biotec), MHC-II (REA813 FITC, 130–112–386, Miltenyi Biotec), CD38 (REA616 PerCP-Vio700, 130–109–260, Miltenyi Biotec), and iNOS (REA982 APC, 130–116–423, Miltenyi Biotec). ..



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    Proposed model illustrating the effects of EZH2 inhibition across multiple joint compartments in osteoarthritis. In OA fibroblast-like synoviocytes (FLS), increased EZH2 and H3K27me3 levels were associated with inflammatory and catabolic responses, which were reduced by pharmacological EZH2 inhibition with EPZ-6438. In human OA FLS, EPZ-6438 decreased inflammatory, catabolic and pain-associated mediators, including IL1B, MMP13, NGF and NTN1, reduced LDHA expression and increased autophagy-associated responses. Proteomic and ChIP-seq analyses further identified inflammatory, metabolic and axon guidance-related pathways, including inflammation-dependent EZH2 recruitment at the PAX6 locus. EZH2 inhibition also reduced inflammatory activation of macrophages and osteoclastogenesis in OA-derived bone marrow cells. Collectively, these findings support a broader role for EZH2 in inflammatory, catabolic and osteoimmune responses across multiple OA-relevant cellular compartments. The identification of PAX6, NTN1 and axon guidance-related pathways highlights neuro-associated molecular programs that may be relevant to pain-associated responses, although their direct contribution to pain or sensory nerve remodeling was not assessed in this study. The reduced structural joint damage and pain-related behaviors observed following EZH2 inhibition in the MIA-induced OA model are consistent with this multicellular framework
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    Image Search Results


    Proposed model illustrating the effects of EZH2 inhibition across multiple joint compartments in osteoarthritis. In OA fibroblast-like synoviocytes (FLS), increased EZH2 and H3K27me3 levels were associated with inflammatory and catabolic responses, which were reduced by pharmacological EZH2 inhibition with EPZ-6438. In human OA FLS, EPZ-6438 decreased inflammatory, catabolic and pain-associated mediators, including IL1B, MMP13, NGF and NTN1, reduced LDHA expression and increased autophagy-associated responses. Proteomic and ChIP-seq analyses further identified inflammatory, metabolic and axon guidance-related pathways, including inflammation-dependent EZH2 recruitment at the PAX6 locus. EZH2 inhibition also reduced inflammatory activation of macrophages and osteoclastogenesis in OA-derived bone marrow cells. Collectively, these findings support a broader role for EZH2 in inflammatory, catabolic and osteoimmune responses across multiple OA-relevant cellular compartments. The identification of PAX6, NTN1 and axon guidance-related pathways highlights neuro-associated molecular programs that may be relevant to pain-associated responses, although their direct contribution to pain or sensory nerve remodeling was not assessed in this study. The reduced structural joint damage and pain-related behaviors observed following EZH2 inhibition in the MIA-induced OA model are consistent with this multicellular framework

    Journal: Molecular Biomedicine

    Article Title: EZH2 coordinates inflammatory and pain-associated pathways across joint compartments in osteoarthritis

    doi: 10.1186/s43556-026-00643-w

    Figure Lengend Snippet: Proposed model illustrating the effects of EZH2 inhibition across multiple joint compartments in osteoarthritis. In OA fibroblast-like synoviocytes (FLS), increased EZH2 and H3K27me3 levels were associated with inflammatory and catabolic responses, which were reduced by pharmacological EZH2 inhibition with EPZ-6438. In human OA FLS, EPZ-6438 decreased inflammatory, catabolic and pain-associated mediators, including IL1B, MMP13, NGF and NTN1, reduced LDHA expression and increased autophagy-associated responses. Proteomic and ChIP-seq analyses further identified inflammatory, metabolic and axon guidance-related pathways, including inflammation-dependent EZH2 recruitment at the PAX6 locus. EZH2 inhibition also reduced inflammatory activation of macrophages and osteoclastogenesis in OA-derived bone marrow cells. Collectively, these findings support a broader role for EZH2 in inflammatory, catabolic and osteoimmune responses across multiple OA-relevant cellular compartments. The identification of PAX6, NTN1 and axon guidance-related pathways highlights neuro-associated molecular programs that may be relevant to pain-associated responses, although their direct contribution to pain or sensory nerve remodeling was not assessed in this study. The reduced structural joint damage and pain-related behaviors observed following EZH2 inhibition in the MIA-induced OA model are consistent with this multicellular framework

    Article Snippet: The following antibodies were used for immune cell characterization: CD11b (REA592 VioBlue, 130–113–810, Miltenyi Biotec), F4/80 (REA126 PE-Vio770, 130–118–459, Miltenyi Biotec), CD80 (REA983 APC-Vio770, 130–116–463, Miltenyi Biotec), CD86 (REA1190 PE, 130–122–129, Miltenyi Biotec), MHC-II (REA813 FITC, 130–112–386, Miltenyi Biotec), CD38 (REA616 PerCP-Vio700, 130–109–260, Miltenyi Biotec), and iNOS (REA982 APC, 130–116–423, Miltenyi Biotec).

    Techniques: Inhibition, Expressing, ChIP-sequencing, Activation Assay, Derivative Assay