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cluster differentiation 68 (cd68  (Agilent technologies)


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    Agilent technologies cluster differentiation 68 (cd68
    Functional phenotype of iMGL derived from the ALSP-CSF1R patient with a c.2350G > A (p.V784M) CSF1R variant. All iMGL were generated using the 2.9 protocol. Quantification ( A ) and images ( B ) of iMGL migratory activity toward ADP assessed by Boyden chamber assay. Cells were concomitantly treated or not with PSB0739. Kruskal–Wallis tests followed by Dunn’s multiple comparison tests were performed. n = 6 healthy control lines and 6 batches of a single ALSP patient line, differentiated side-by-side. White = Hoechst 33342, scale bar = 75 μm in ( B ). Quantification of green fluorescence intensity per cell ( C ) and representative images ( D ) of iMGL exposed to vehicle or pHrodo.™ Green-labelled myelin, opsonized red blood cells (IgG-RBC) or E. coli for three hours and then counterstained with Hoescht 33342. T-tests were performed. n = 3 healthy control lines and 3 batches of a single ALSP patient line, differentiated side-by-side, * p < 0.05. Scale bar = 250 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\mu m$$\end{document} μ m in ( D ). Quantification of mean fluorescence intensities (MFI; E ) and representative images ( F ) of LAMP1, <t>CD68</t> and IBA1 immunostaining of iMGL. T-tests were performed. n = 3 healthy control lines and 3 batches of a single ALSP patient line, differentiated side-by-side, ** p < 0.01, *** p < 0.001. Scale bar = 100 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\mu m$$\end{document} μ m in ( F ). G Cytokine secretion assessed in cell supernatants following a 24-h treatment with vehicle, LPS (100 ng/mL) or Pam 3 CSK 4 (100 ng/mL). A two-way ANOVA was performed, followed by Tukey’s post hoc test. n = 4 healthy control lines and 4 batches of a single ALSP patient line, differentiated side-by-side, *** p < 0.001, ns = non-significant. H qRT-PCR performed after three hours of Pam 3 CSK 4 (100 ng/mL) vs. vehicle treatment. T-tests were performed. n = 3 healthy control lines and 3 batches of a single ALSP patient line, differentiated side-by-side, * p < 0.05
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    Images

    1) Product Images from "An adapted protocol to derive microglia from stem cells and its application in the study of CSF1R-related disorders"

    Article Title: An adapted protocol to derive microglia from stem cells and its application in the study of CSF1R-related disorders

    Journal: Molecular Neurodegeneration

    doi: 10.1186/s13024-024-00723-x

    Functional phenotype of iMGL derived from the ALSP-CSF1R patient with a c.2350G > A (p.V784M) CSF1R variant. All iMGL were generated using the 2.9 protocol. Quantification ( A ) and images ( B ) of iMGL migratory activity toward ADP assessed by Boyden chamber assay. Cells were concomitantly treated or not with PSB0739. Kruskal–Wallis tests followed by Dunn’s multiple comparison tests were performed. n = 6 healthy control lines and 6 batches of a single ALSP patient line, differentiated side-by-side. White = Hoechst 33342, scale bar = 75 μm in ( B ). Quantification of green fluorescence intensity per cell ( C ) and representative images ( D ) of iMGL exposed to vehicle or pHrodo.™ Green-labelled myelin, opsonized red blood cells (IgG-RBC) or E. coli for three hours and then counterstained with Hoescht 33342. T-tests were performed. n = 3 healthy control lines and 3 batches of a single ALSP patient line, differentiated side-by-side, * p < 0.05. Scale bar = 250 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\mu m$$\end{document} μ m in ( D ). Quantification of mean fluorescence intensities (MFI; E ) and representative images ( F ) of LAMP1, CD68 and IBA1 immunostaining of iMGL. T-tests were performed. n = 3 healthy control lines and 3 batches of a single ALSP patient line, differentiated side-by-side, ** p < 0.01, *** p < 0.001. Scale bar = 100 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\mu m$$\end{document} μ m in ( F ). G Cytokine secretion assessed in cell supernatants following a 24-h treatment with vehicle, LPS (100 ng/mL) or Pam 3 CSK 4 (100 ng/mL). A two-way ANOVA was performed, followed by Tukey’s post hoc test. n = 4 healthy control lines and 4 batches of a single ALSP patient line, differentiated side-by-side, *** p < 0.001, ns = non-significant. H qRT-PCR performed after three hours of Pam 3 CSK 4 (100 ng/mL) vs. vehicle treatment. T-tests were performed. n = 3 healthy control lines and 3 batches of a single ALSP patient line, differentiated side-by-side, * p < 0.05
    Figure Legend Snippet: Functional phenotype of iMGL derived from the ALSP-CSF1R patient with a c.2350G > A (p.V784M) CSF1R variant. All iMGL were generated using the 2.9 protocol. Quantification ( A ) and images ( B ) of iMGL migratory activity toward ADP assessed by Boyden chamber assay. Cells were concomitantly treated or not with PSB0739. Kruskal–Wallis tests followed by Dunn’s multiple comparison tests were performed. n = 6 healthy control lines and 6 batches of a single ALSP patient line, differentiated side-by-side. White = Hoechst 33342, scale bar = 75 μm in ( B ). Quantification of green fluorescence intensity per cell ( C ) and representative images ( D ) of iMGL exposed to vehicle or pHrodo.™ Green-labelled myelin, opsonized red blood cells (IgG-RBC) or E. coli for three hours and then counterstained with Hoescht 33342. T-tests were performed. n = 3 healthy control lines and 3 batches of a single ALSP patient line, differentiated side-by-side, * p < 0.05. Scale bar = 250 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\mu m$$\end{document} μ m in ( D ). Quantification of mean fluorescence intensities (MFI; E ) and representative images ( F ) of LAMP1, CD68 and IBA1 immunostaining of iMGL. T-tests were performed. n = 3 healthy control lines and 3 batches of a single ALSP patient line, differentiated side-by-side, ** p < 0.01, *** p < 0.001. Scale bar = 100 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\mu m$$\end{document} μ m in ( F ). G Cytokine secretion assessed in cell supernatants following a 24-h treatment with vehicle, LPS (100 ng/mL) or Pam 3 CSK 4 (100 ng/mL). A two-way ANOVA was performed, followed by Tukey’s post hoc test. n = 4 healthy control lines and 4 batches of a single ALSP patient line, differentiated side-by-side, *** p < 0.001, ns = non-significant. H qRT-PCR performed after three hours of Pam 3 CSK 4 (100 ng/mL) vs. vehicle treatment. T-tests were performed. n = 3 healthy control lines and 3 batches of a single ALSP patient line, differentiated side-by-side, * p < 0.05

    Techniques Used: Functional Assay, Derivative Assay, Variant Assay, Generated, Activity Assay, Boyden Chamber Assay, Comparison, Fluorescence, Immunostaining, Quantitative RT-PCR

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    Article Snippet: Histiocytic sarcoma is a rare neoplasm of mature histiocytes with an aggressive clinical course and poor response to treatment.. Primary gastric histiocytic sarcoma is rarer and just reported sporadically.Histiocytic sarcoma is a rare neoplasm of mature histiocytes with an aggressive clinical course and poor response to treatment.. Primary gastric histiocytic sarcoma is rarer and just reported sporadically.

    Article Title: Surgical intervention combined with weight-bearing walking training promotes recovery in patients with chronic spinal cord injury: a randomized controlled study
    Article Snippet: Paraformaldehye-fixed paraffin-embedded spinal cord tissue samples were shipped to Shanghai Jiao Tong University School of Medicine, where sections (4 μm) were stained with mouse anti-human CD68 (KP1, Dako, Glostrup, Denmark).

    Article Title: Dynamic changes in immune cells in humanized liver metastasis and subcutaneous xenograft mouse models
    Article Snippet: Antibodies against the following factors were used: CD7 (1:100 dilution; catalog no. M7255; DAKO, Glostrup, Denmark), CD4 (1:100 dilution; catalog no. NCL-L-CD4_368; Novocastra, Newcastle, UK), CD8 (ready to use; catalog no. PA0183; Novocastra), Granzyme B (1:50 dilution; catalog no. M7235; DAKO), CD79a (1:300 dilution; catalog no. 179 M-95; Cell Marque, Rocklin, CA, USA), CD56 (1:400 dilution; catalog no. M7304; DAKO), CD68 (1:100 dilution; catalog no. MO814; DAKO), and human leukocyte antigens (HLAs) (1:300 dilution; catalog no. ab70328; Abcam, Cambridge, UK).

    Article Title: l-Arginine-Loaded Oxidized Isabgol/Chitosan-Based Biomimetic Composite Scaffold Accelerates Collagen Synthesis, Vascularization, and Re-epithelialization during Wound Healing in Diabetic Rats.
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    Article Title: The Impact of TIGAR on Prognosis in Hepatocellular Carcinoma; Association with Tumor Microenvironment and Ferroptosis
    Article Snippet: The tissue sections were incubated with anti-TIGAR antibody (Abcam, Cambridge, UK), anti-cluster of differentiation (CD) 8 antibody (Clone C8/144B; Agilent Technologies), anti-CD68 antibody (PG-M1, DAKO), anti-programmed death-ligand 1 (PD-L1) antibody (Abcam), anti-CD34 antibody (QBEnd/10, Santa Cruz Biotechnology), and anti-phospho-nuclear factor erythroid 2-related factor 2 (NRF2) antibody (Abcam) overnight at 4°C.

    Immunostaining:

    Article Title: Expression of CD163 and major histocompatibility complex class I as diagnostic markers for idiopathic inflammatory myopathies
    Article Snippet: .. BenchMark XT Autostainer (Ventana Medical Systems, Inc., Tucson, AZ, USA) was used for immunostaining using antibodies against CD3 (1:100, Rabbit monoclonal, clone POLY, catalog No.A0452, DAKO, Denmark, Glostrup), CD4 (1:16, Rabbit monoclonal, clone SP35, catalog No.790–4423, VENTANA, Tusan, USA), CD8 (1:400, Mouse monoclonal, clone C8/144B, catalog No.M7103, CELL MARQUE, CA, USA), CD20 (1:400, Mouse monoclonal, clone L26, catalog No.M0755, DAKO, Denmark, Glostrup), CD68 (1:2000, Mouse monoclonal, clone KP1, catalog No.M0814, DAKO, Denmark, Glostrup), CD163 (1:400, Mouse monoclonal, clone MRQ-26, catalog No.163 M-16, CELL MARQUE, CA, USA), MX1 (1:500, Rabbit polyclonal, clone N2C2, catalog No. GTX110256, GENETEX, CA, USA), HLA Class I ABC (1:10000, clone EMR8-5, catalog No. ab70328, Abcam, Inc., Cambridge, UK), HLA-DR + DP + DQ (1:2500, clone CR3/43, catalog No. ab7856, Abcam, Inc., Cambridge, UK), and HLA-DR (1:5000, clone TAL 1B5, catalog No. ab20181, Abcam, Inc., Cambridge, UK). ..

    Incubation:

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    Functional phenotype of iMGL derived from the ALSP-CSF1R patient with a c.2350G > A (p.V784M) CSF1R variant. All iMGL were generated using the 2.9 protocol. Quantification ( A ) and images ( B ) of iMGL migratory activity toward ADP assessed by Boyden chamber assay. Cells were concomitantly treated or not with PSB0739. Kruskal–Wallis tests followed by Dunn’s multiple comparison tests were performed. n = 6 healthy control lines and 6 batches of a single ALSP patient line, differentiated side-by-side. White = Hoechst 33342, scale bar = 75 μm in ( B ). Quantification of green fluorescence intensity per cell ( C ) and representative images ( D ) of iMGL exposed to vehicle or pHrodo.™ Green-labelled myelin, opsonized red blood cells (IgG-RBC) or E. coli for three hours and then counterstained with Hoescht 33342. T-tests were performed. n = 3 healthy control lines and 3 batches of a single ALSP patient line, differentiated side-by-side, * p < 0.05. Scale bar = 250 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\mu m$$\end{document} μ m in ( D ). Quantification of mean fluorescence intensities (MFI; E ) and representative images ( F ) of LAMP1, <t>CD68</t> and IBA1 immunostaining of iMGL. T-tests were performed. n = 3 healthy control lines and 3 batches of a single ALSP patient line, differentiated side-by-side, ** p < 0.01, *** p < 0.001. Scale bar = 100 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\mu m$$\end{document} μ m in ( F ). G Cytokine secretion assessed in cell supernatants following a 24-h treatment with vehicle, LPS (100 ng/mL) or Pam 3 CSK 4 (100 ng/mL). A two-way ANOVA was performed, followed by Tukey’s post hoc test. n = 4 healthy control lines and 4 batches of a single ALSP patient line, differentiated side-by-side, *** p < 0.001, ns = non-significant. H qRT-PCR performed after three hours of Pam 3 CSK 4 (100 ng/mL) vs. vehicle treatment. T-tests were performed. n = 3 healthy control lines and 3 batches of a single ALSP patient line, differentiated side-by-side, * p < 0.05
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    Functional phenotype of iMGL derived from the ALSP-CSF1R patient with a c.2350G > A (p.V784M) CSF1R variant. All iMGL were generated using the 2.9 protocol. Quantification ( A ) and images ( B ) of iMGL migratory activity toward ADP assessed by Boyden chamber assay. Cells were concomitantly treated or not with PSB0739. Kruskal–Wallis tests followed by Dunn’s multiple comparison tests were performed. n = 6 healthy control lines and 6 batches of a single ALSP patient line, differentiated side-by-side. White = Hoechst 33342, scale bar = 75 μm in ( B ). Quantification of green fluorescence intensity per cell ( C ) and representative images ( D ) of iMGL exposed to vehicle or pHrodo.™ Green-labelled myelin, opsonized red blood cells (IgG-RBC) or E. coli for three hours and then counterstained with Hoescht 33342. T-tests were performed. n = 3 healthy control lines and 3 batches of a single ALSP patient line, differentiated side-by-side, * p < 0.05. Scale bar = 250 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\mu m$$\end{document} μ m in ( D ). Quantification of mean fluorescence intensities (MFI; E ) and representative images ( F ) of LAMP1, <t>CD68</t> and IBA1 immunostaining of iMGL. T-tests were performed. n = 3 healthy control lines and 3 batches of a single ALSP patient line, differentiated side-by-side, ** p < 0.01, *** p < 0.001. Scale bar = 100 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\mu m$$\end{document} μ m in ( F ). G Cytokine secretion assessed in cell supernatants following a 24-h treatment with vehicle, LPS (100 ng/mL) or Pam 3 CSK 4 (100 ng/mL). A two-way ANOVA was performed, followed by Tukey’s post hoc test. n = 4 healthy control lines and 4 batches of a single ALSP patient line, differentiated side-by-side, *** p < 0.001, ns = non-significant. H qRT-PCR performed after three hours of Pam 3 CSK 4 (100 ng/mL) vs. vehicle treatment. T-tests were performed. n = 3 healthy control lines and 3 batches of a single ALSP patient line, differentiated side-by-side, * p < 0.05
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    Santa Cruz Biotechnology anti-cluster of differentiation 68 (cd68, cat. #sc-70761)
    Functional phenotype of iMGL derived from the ALSP-CSF1R patient with a c.2350G > A (p.V784M) CSF1R variant. All iMGL were generated using the 2.9 protocol. Quantification ( A ) and images ( B ) of iMGL migratory activity toward ADP assessed by Boyden chamber assay. Cells were concomitantly treated or not with PSB0739. Kruskal–Wallis tests followed by Dunn’s multiple comparison tests were performed. n = 6 healthy control lines and 6 batches of a single ALSP patient line, differentiated side-by-side. White = Hoechst 33342, scale bar = 75 μm in ( B ). Quantification of green fluorescence intensity per cell ( C ) and representative images ( D ) of iMGL exposed to vehicle or pHrodo.™ Green-labelled myelin, opsonized red blood cells (IgG-RBC) or E. coli for three hours and then counterstained with Hoescht 33342. T-tests were performed. n = 3 healthy control lines and 3 batches of a single ALSP patient line, differentiated side-by-side, * p < 0.05. Scale bar = 250 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\mu m$$\end{document} μ m in ( D ). Quantification of mean fluorescence intensities (MFI; E ) and representative images ( F ) of LAMP1, <t>CD68</t> and IBA1 immunostaining of iMGL. T-tests were performed. n = 3 healthy control lines and 3 batches of a single ALSP patient line, differentiated side-by-side, ** p < 0.01, *** p < 0.001. Scale bar = 100 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\mu m$$\end{document} μ m in ( F ). G Cytokine secretion assessed in cell supernatants following a 24-h treatment with vehicle, LPS (100 ng/mL) or Pam 3 CSK 4 (100 ng/mL). A two-way ANOVA was performed, followed by Tukey’s post hoc test. n = 4 healthy control lines and 4 batches of a single ALSP patient line, differentiated side-by-side, *** p < 0.001, ns = non-significant. H qRT-PCR performed after three hours of Pam 3 CSK 4 (100 ng/mL) vs. vehicle treatment. T-tests were performed. n = 3 healthy control lines and 3 batches of a single ALSP patient line, differentiated side-by-side, * p < 0.05
    Anti Cluster Of Differentiation 68 (Cd68, Cat. #Sc 70761), supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/cluster+differentiation+68+(cd68/anti+cd68/pm38278067-46-0-10
    Average 90 stars, based on 1 article reviews
    anti-cluster of differentiation 68 (cd68, cat. #sc-70761) - by Bioz Stars, 2026-10
    90/100 stars
      Buy from Supplier

    90
    Santa Cruz Biotechnology alex fluor 594 anti-cluster of differentiation 68 (cd68)
    Functional phenotype of iMGL derived from the ALSP-CSF1R patient with a c.2350G > A (p.V784M) CSF1R variant. All iMGL were generated using the 2.9 protocol. Quantification ( A ) and images ( B ) of iMGL migratory activity toward ADP assessed by Boyden chamber assay. Cells were concomitantly treated or not with PSB0739. Kruskal–Wallis tests followed by Dunn’s multiple comparison tests were performed. n = 6 healthy control lines and 6 batches of a single ALSP patient line, differentiated side-by-side. White = Hoechst 33342, scale bar = 75 μm in ( B ). Quantification of green fluorescence intensity per cell ( C ) and representative images ( D ) of iMGL exposed to vehicle or pHrodo.™ Green-labelled myelin, opsonized red blood cells (IgG-RBC) or E. coli for three hours and then counterstained with Hoescht 33342. T-tests were performed. n = 3 healthy control lines and 3 batches of a single ALSP patient line, differentiated side-by-side, * p < 0.05. Scale bar = 250 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\mu m$$\end{document} μ m in ( D ). Quantification of mean fluorescence intensities (MFI; E ) and representative images ( F ) of LAMP1, <t>CD68</t> and IBA1 immunostaining of iMGL. T-tests were performed. n = 3 healthy control lines and 3 batches of a single ALSP patient line, differentiated side-by-side, ** p < 0.01, *** p < 0.001. Scale bar = 100 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\mu m$$\end{document} μ m in ( F ). G Cytokine secretion assessed in cell supernatants following a 24-h treatment with vehicle, LPS (100 ng/mL) or Pam 3 CSK 4 (100 ng/mL). A two-way ANOVA was performed, followed by Tukey’s post hoc test. n = 4 healthy control lines and 4 batches of a single ALSP patient line, differentiated side-by-side, *** p < 0.001, ns = non-significant. H qRT-PCR performed after three hours of Pam 3 CSK 4 (100 ng/mL) vs. vehicle treatment. T-tests were performed. n = 3 healthy control lines and 3 batches of a single ALSP patient line, differentiated side-by-side, * p < 0.05
    Alex Fluor 594 Anti Cluster Of Differentiation 68 (Cd68), supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/cluster+differentiation+68+(cd68/anti+cd68/pm38169465-292-5-10
    Average 90 stars, based on 1 article reviews
    alex fluor 594 anti-cluster of differentiation 68 (cd68) - by Bioz Stars, 2026-10
    90/100 stars
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    Image Search Results


    a , b UMAP embedding of 1180 macrophage nuclei from sciatic nerves color-coded by subtype ( a ) or age ( b ). c Dot plot highlighting the marker genes used to identify the macrophage subtypes from A. Marker genes can be found in Table . d Relative percentage of Mϕs subtypes across ages. Steady state epi- and endoneurial Mϕ, circulating-derived phagocytic Mϕ, and chronic-inflammation Mϕ were more prevalent in sciatic nerves from 2-3, 15-16, and 20-30 months old mice, respectively. e Dot plot showing the expression levels of the marker genes used to identify the macrophage clusters, at the different time points. Markers for resident steady state Mϕ ( Cx3cr1, Mrc1, Csf1r ) are more expressed at 2-3 months old, those for circulating-derived phagocytic Mϕ (Cd74, Hspa5, Cd44, C1qa, Grn, Cd68), are more expressed at 15-16 months old, and those belonging to chronic inflammation ( Tgfβr1, Kynu) are more expressed in the 20-30 months old samples. f Representative immunofluorescence images of sciatic nerve samples show increased CD45 + /MRC1 + Mϕs in nerves from 2-3 months old mice, CD68 + /GRN + Mϕs in nerves from 15-16 and 20-30 months old mice, and CD45 + /TGF βR1+ in nerves from 20-30 months old mice. Yellow or pink arrowheads point to CD45 + /MRC1+ or CD68 + /GRN+ or CD45 + / TGF βR1 + cells. g Quantification of the number of CD45+ cells relative to the total number of cells. n = 7 - 9 - 10, biological replicates. h Quantification of the number of CD45 + /MRC1 + cells relative to the total number of CD45 + cells. n = 4 - 4 - 5 biological replicates. i Quantification of the number of CD68 + / GRN+ cells relative to the total number of CD68+ cells. n = 6 - 6 - 5. j Quantification of the number of CD45 + /TGF βR1 + cells relative to the total number of CD45 + cells. n = 3 - 5 - 5, biological replicates. Data are presented as mean values +/− SD. Source data for panels is provided as a Source Data file.

    Journal: Nature Communications

    Article Title: Fibroblast growth factor signaling induces a chondrocyte-like state of peripheral nerve fibroblast during aging

    doi: 10.1038/s41467-025-65297-8

    Figure Lengend Snippet: a , b UMAP embedding of 1180 macrophage nuclei from sciatic nerves color-coded by subtype ( a ) or age ( b ). c Dot plot highlighting the marker genes used to identify the macrophage subtypes from A. Marker genes can be found in Table . d Relative percentage of Mϕs subtypes across ages. Steady state epi- and endoneurial Mϕ, circulating-derived phagocytic Mϕ, and chronic-inflammation Mϕ were more prevalent in sciatic nerves from 2-3, 15-16, and 20-30 months old mice, respectively. e Dot plot showing the expression levels of the marker genes used to identify the macrophage clusters, at the different time points. Markers for resident steady state Mϕ ( Cx3cr1, Mrc1, Csf1r ) are more expressed at 2-3 months old, those for circulating-derived phagocytic Mϕ (Cd74, Hspa5, Cd44, C1qa, Grn, Cd68), are more expressed at 15-16 months old, and those belonging to chronic inflammation ( Tgfβr1, Kynu) are more expressed in the 20-30 months old samples. f Representative immunofluorescence images of sciatic nerve samples show increased CD45 + /MRC1 + Mϕs in nerves from 2-3 months old mice, CD68 + /GRN + Mϕs in nerves from 15-16 and 20-30 months old mice, and CD45 + /TGF βR1+ in nerves from 20-30 months old mice. Yellow or pink arrowheads point to CD45 + /MRC1+ or CD68 + /GRN+ or CD45 + / TGF βR1 + cells. g Quantification of the number of CD45+ cells relative to the total number of cells. n = 7 - 9 - 10, biological replicates. h Quantification of the number of CD45 + /MRC1 + cells relative to the total number of CD45 + cells. n = 4 - 4 - 5 biological replicates. i Quantification of the number of CD68 + / GRN+ cells relative to the total number of CD68+ cells. n = 6 - 6 - 5. j Quantification of the number of CD45 + /TGF βR1 + cells relative to the total number of CD45 + cells. n = 3 - 5 - 5, biological replicates. Data are presented as mean values +/− SD. Source data for panels is provided as a Source Data file.

    Article Snippet: Cluster of differentiation 68 (CD68) 1:250 , Mouse , MCA1957 Biorad Hercules, CA, USA.

    Techniques: Marker, Derivative Assay, Expressing, Immunofluorescence

    A , Immunofluorescent staining depicts IL1RAP (green) alongside VWF (red), SMA (red), and the macrophage marker CD68 (red) within different areas of a human atherosclerotic plaque (in gray). All scalebars=100 μm except for whole plaque images, where the scalebar=1 mm. B , Expression of IL1R1 , IL1RAP , ST2 , and IL36R in human atherosclerotic plaques compared with donor‐matched macroscopically intact carotid tissue (n=32 biological replicates in each group), from the Gene Expression Omnibus database of microarray data. C , Expression of IL1R1, IL1RAP, ST2, and IL36R in human umbilical vein endothelial cells detected by flow cytometry shown as mean fluorescence intensity of fluorophore (APC, PE, A647)‐conjugated antibodies (Ab) towards the receptor components (IL1R1, IL1RAP, ST2, IL36R). CD68 indicates cluster of differentiation 68; DAPI, 4′,6‐diamidino‐2‐phenylindole; FC, fold change; IL‐1, interleukin 1; IL1R1, IL‐1 receptor 1; IL1RAP, interleukin 1 receptor associated protein; IL36R, IL‐36 receptor; SMA, smooth muscle actin; ST2, supression of tumorigenicity 2; and VWF, von Willebrand factor

    Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

    Article Title: IL1RAP Expression in Human Atherosclerosis: A Target of Novel Antibodies to Reduce Vascular Inflammation and Adhesion

    doi: 10.1161/JAHA.124.039557

    Figure Lengend Snippet: A , Immunofluorescent staining depicts IL1RAP (green) alongside VWF (red), SMA (red), and the macrophage marker CD68 (red) within different areas of a human atherosclerotic plaque (in gray). All scalebars=100 μm except for whole plaque images, where the scalebar=1 mm. B , Expression of IL1R1 , IL1RAP , ST2 , and IL36R in human atherosclerotic plaques compared with donor‐matched macroscopically intact carotid tissue (n=32 biological replicates in each group), from the Gene Expression Omnibus database of microarray data. C , Expression of IL1R1, IL1RAP, ST2, and IL36R in human umbilical vein endothelial cells detected by flow cytometry shown as mean fluorescence intensity of fluorophore (APC, PE, A647)‐conjugated antibodies (Ab) towards the receptor components (IL1R1, IL1RAP, ST2, IL36R). CD68 indicates cluster of differentiation 68; DAPI, 4′,6‐diamidino‐2‐phenylindole; FC, fold change; IL‐1, interleukin 1; IL1R1, IL‐1 receptor 1; IL1RAP, interleukin 1 receptor associated protein; IL36R, IL‐36 receptor; SMA, smooth muscle actin; ST2, supression of tumorigenicity 2; and VWF, von Willebrand factor

    Article Snippet: Cellular markers for endothelial cells (anti‐human von Willebrand factor; M0616; Dako, Denmark; 1:200), smooth muscle cells (anti‐human smooth muscle actin; M0851, Dako; 1:150), and macrophages (anti‐CD68 [cluster of differentiation 68]; Novocastra, Leica Biosystems, Newcastle, UK; 1:10) were used in parallel.

    Techniques: Staining, Marker, Expressing, Gene Expression, Microarray, Flow Cytometry, Fluorescence

    Functional phenotype of iMGL derived from the ALSP-CSF1R patient with a c.2350G > A (p.V784M) CSF1R variant. All iMGL were generated using the 2.9 protocol. Quantification ( A ) and images ( B ) of iMGL migratory activity toward ADP assessed by Boyden chamber assay. Cells were concomitantly treated or not with PSB0739. Kruskal–Wallis tests followed by Dunn’s multiple comparison tests were performed. n = 6 healthy control lines and 6 batches of a single ALSP patient line, differentiated side-by-side. White = Hoechst 33342, scale bar = 75 μm in ( B ). Quantification of green fluorescence intensity per cell ( C ) and representative images ( D ) of iMGL exposed to vehicle or pHrodo.™ Green-labelled myelin, opsonized red blood cells (IgG-RBC) or E. coli for three hours and then counterstained with Hoescht 33342. T-tests were performed. n = 3 healthy control lines and 3 batches of a single ALSP patient line, differentiated side-by-side, * p < 0.05. Scale bar = 250 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\mu m$$\end{document} μ m in ( D ). Quantification of mean fluorescence intensities (MFI; E ) and representative images ( F ) of LAMP1, CD68 and IBA1 immunostaining of iMGL. T-tests were performed. n = 3 healthy control lines and 3 batches of a single ALSP patient line, differentiated side-by-side, ** p < 0.01, *** p < 0.001. Scale bar = 100 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\mu m$$\end{document} μ m in ( F ). G Cytokine secretion assessed in cell supernatants following a 24-h treatment with vehicle, LPS (100 ng/mL) or Pam 3 CSK 4 (100 ng/mL). A two-way ANOVA was performed, followed by Tukey’s post hoc test. n = 4 healthy control lines and 4 batches of a single ALSP patient line, differentiated side-by-side, *** p < 0.001, ns = non-significant. H qRT-PCR performed after three hours of Pam 3 CSK 4 (100 ng/mL) vs. vehicle treatment. T-tests were performed. n = 3 healthy control lines and 3 batches of a single ALSP patient line, differentiated side-by-side, * p < 0.05

    Journal: Molecular Neurodegeneration

    Article Title: An adapted protocol to derive microglia from stem cells and its application in the study of CSF1R-related disorders

    doi: 10.1186/s13024-024-00723-x

    Figure Lengend Snippet: Functional phenotype of iMGL derived from the ALSP-CSF1R patient with a c.2350G > A (p.V784M) CSF1R variant. All iMGL were generated using the 2.9 protocol. Quantification ( A ) and images ( B ) of iMGL migratory activity toward ADP assessed by Boyden chamber assay. Cells were concomitantly treated or not with PSB0739. Kruskal–Wallis tests followed by Dunn’s multiple comparison tests were performed. n = 6 healthy control lines and 6 batches of a single ALSP patient line, differentiated side-by-side. White = Hoechst 33342, scale bar = 75 μm in ( B ). Quantification of green fluorescence intensity per cell ( C ) and representative images ( D ) of iMGL exposed to vehicle or pHrodo.™ Green-labelled myelin, opsonized red blood cells (IgG-RBC) or E. coli for three hours and then counterstained with Hoescht 33342. T-tests were performed. n = 3 healthy control lines and 3 batches of a single ALSP patient line, differentiated side-by-side, * p < 0.05. Scale bar = 250 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\mu m$$\end{document} μ m in ( D ). Quantification of mean fluorescence intensities (MFI; E ) and representative images ( F ) of LAMP1, CD68 and IBA1 immunostaining of iMGL. T-tests were performed. n = 3 healthy control lines and 3 batches of a single ALSP patient line, differentiated side-by-side, ** p < 0.01, *** p < 0.001. Scale bar = 100 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\mu m$$\end{document} μ m in ( F ). G Cytokine secretion assessed in cell supernatants following a 24-h treatment with vehicle, LPS (100 ng/mL) or Pam 3 CSK 4 (100 ng/mL). A two-way ANOVA was performed, followed by Tukey’s post hoc test. n = 4 healthy control lines and 4 batches of a single ALSP patient line, differentiated side-by-side, *** p < 0.001, ns = non-significant. H qRT-PCR performed after three hours of Pam 3 CSK 4 (100 ng/mL) vs. vehicle treatment. T-tests were performed. n = 3 healthy control lines and 3 batches of a single ALSP patient line, differentiated side-by-side, * p < 0.05

    Article Snippet: Cells were incubated at 4 °C overnight with primary antibodies against the following targets: ionized calcium binding adaptor molecule 1 (IBA1; #NC9288364, Fujifilm Wako Chemicals at 1:1000), PU.1 (#2258, Cell Signaling at 1:250), Nanog (#ab21624, Abcam at 1:500), Tra-1–60 (#60064, STEMCell Technologies at 1:200), stage-specific embryonic antigen-4 (SSEA-4; #sc-21704, Santa Cruz Biotechnologies at 1:200), octamer-binding transcription factor 3/4 (OCT3/4; #sc-8628, Santa Cruz Biotechnologies at 1:500), Ki67 (#556003, BD Biosciences at 1:200), lysosomal-associated membrane protein 1 (LAMP1; #9091, Cell Signaling at 1:200) or cluster of differentiation 68 (CD68; #M0814, Dako Omnis at 1:200).

    Techniques: Functional Assay, Derivative Assay, Variant Assay, Generated, Activity Assay, Boyden Chamber Assay, Comparison, Fluorescence, Immunostaining, Quantitative RT-PCR