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mouse ccl2 elisa kit  (Proteintech)


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    Proteintech mouse ccl2 elisa kit
    Mouse Ccl2 Elisa Kit, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 14 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mouse+ccl2+elisa+kit/Mouse+CCL5+ELISA+Kit/pm41813910-91-12-16
    Average 94 stars, based on 14 article reviews
    mouse ccl2 elisa kit - by Bioz Stars, 2026-10
    94/100 stars

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    Related Articles

    Enzyme-linked Immunosorbent Assay:

    Article Title: Caffeine upregulates SIRT3 expression to ameliorate astrocytes-mediated HIV-1 Tat neurotoxicity via suppression of EGR1 signaling pathway.
    Article Snippet: 1 Medical Research Center, Affiliated Hospital 2 of Nantong University, No. 666, Shengli Road, Nantong 226001, Jiangsu, People’s Republic of China 2 Jiangsu Provincial Medical Key Discipline (Laboratory) Cultivation Unit, Medical Research Center, Nantong First People’s Hospital, Nantong 226001, People’s Republic of China 3 Nantong Municipal Medical Key Laboratory of Molecular Immunology, Medical Research Center, Nantong First People’s Hospital, Nantong 226001, People’s Republic of China 4 Nantong Municipal Key Laboratory of Metabolic Immunology and Disease Microenvironment, Medical Research Center, Nantong First People’s Hospital, Nantong 226001, People’s Republic of China 5 Disease Prevention and Control Center of Chongchuan District, Nantong 226000, People’s Republic of China 6 Health Commission of Chongchuan District, Nantong 226000, People’s Republic of China 7 Nantong Health College of Jiangsu Province, Nantong 226001, People’s Republic of China Abstract Caffeine is one of the most popular consumed psychostimulants that mitigates several neurodegenerative diseases.. Nevertheless, the roles and molecular mechanisms of caffeine in HIV-associated neurocognitive disorders (HAND) remain largely unclear.. Transactivator of transcription (Tat) is a major contributor to the neuropathogenesis of HAND in the central nervous system.

    Article Title: HIV-1 Nef induces astrocytes proliferation, inflammatory response, A1-like astrocytes polarization and subsequent neuronal apoptosis via NF-κB signaling pathway.
    Article Snippet: 1 Research Center of Molecular Medicine, Ph.D.. Laboratory, Nantong Health College of Jiangsu Province, Nantong 226001, People’s Republic of China 2 Shaanxi Key Laboratory of Research and Utilization of Resource Plants On the Loess Plateau, College of Life Sciences, Yan’an University, No. 580, Shengdi Road, Baota District, Yan’an 716000, Shaanxi, People’s Republic of China 3 Department of Pathogen Biology, Medical College, Nantong University, Nantong 226001, People’s Republic of China 4 Department of Traditional Chinese Medicine, Affiliated Hospital of Jiangsu University, Zhenjiang 212000, People’s Republic of China 5 Medical Research Center, Affiliated Hospital 2 of Nantong University, and First People’s Hospital of Nantong City, No. 666, Shengli Road, Nantong 226001, Jiangsu, People’s Republic of China Abstract Currently, human immunodeficiency virus-1 (HIV-1) spreads around the globe and half of HIV-1-positive individuals suffer from HIV-associated neurocognitive disorder (HAND).. HIV-1 infection of astrocytes leads to neuroinflammation and neuronal injury.



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    Vagotomy promoted Ly6G + cell infiltration into eWAT. Wild‐type mice were subjected to left cervical vagotomy (VX) or sham surgery and tissues were collected at 7 days following surgery. (A) The percentage of non‐adipocyte nuclei of total nuclei per section was quantified using ImageJ ( n = 4) and right panels show representative images of paraffin sections of eWAT stained with H&E in sham and VX animals. (B) <t>CCL2</t> release from eWAT was analyzed by ELISA. The bar shows the CCL2 levels from sham ( n = 4) or VX ( n = 4) mice normalized to eWAT weight: ng/mL per g ± SEM (unpaired Student's t test). (C) eWAT was collected at 1 ( n = 3), 4 ( n = 4 sham, n = 5 VX), and 7 ( n = 15) days following VX or sham surgery and the eWAT SVCs were analyzed by flow cytometry. The bar shows the % ± SEM of CD11b + Ly6G + cells from CD45 + (one‐way ANOVA, Uncorrected Fisher's LSD). (D) Graphs show representative gating for CD11b + Ly6G + cells in sham and VX eWAT at 7 days (concatenated n = 5–6). (E) Representative immunostaining of Ly6G (red) and Perilipin1 (green) in paraffin sections of eWAT. (F–H) Bone marrow neutrophils after sham ( n = 9) or VX ( n = 5) surgery were isolated using negative magnetic beads and analyzed using bulk RNAseq (DESeq2). Heatmap (F), volcano plot (G) of differentially expressed genes, and GO (Gene Ontology) (H) enrichment bar plot. ns = not significant, * p < 0.05. VX, Vagotomy; eWAT, epididymal white adipose tissue; H&E, hematoxylin–eosin; SVCs, stromal vascular cells.
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    Vagotomy promoted Ly6G + cell infiltration into eWAT. Wild‐type mice were subjected to left cervical vagotomy (VX) or sham surgery and tissues were collected at 7 days following surgery. (A) The percentage of non‐adipocyte nuclei of total nuclei per section was quantified using ImageJ ( n = 4) and right panels show representative images of paraffin sections of eWAT stained with H&E in sham and VX animals. (B) <t>CCL2</t> release from eWAT was analyzed by ELISA. The bar shows the CCL2 levels from sham ( n = 4) or VX ( n = 4) mice normalized to eWAT weight: ng/mL per g ± SEM (unpaired Student's t test). (C) eWAT was collected at 1 ( n = 3), 4 ( n = 4 sham, n = 5 VX), and 7 ( n = 15) days following VX or sham surgery and the eWAT SVCs were analyzed by flow cytometry. The bar shows the % ± SEM of CD11b + Ly6G + cells from CD45 + (one‐way ANOVA, Uncorrected Fisher's LSD). (D) Graphs show representative gating for CD11b + Ly6G + cells in sham and VX eWAT at 7 days (concatenated n = 5–6). (E) Representative immunostaining of Ly6G (red) and Perilipin1 (green) in paraffin sections of eWAT. (F–H) Bone marrow neutrophils after sham ( n = 9) or VX ( n = 5) surgery were isolated using negative magnetic beads and analyzed using bulk RNAseq (DESeq2). Heatmap (F), volcano plot (G) of differentially expressed genes, and GO (Gene Ontology) (H) enrichment bar plot. ns = not significant, * p < 0.05. VX, Vagotomy; eWAT, epididymal white adipose tissue; H&E, hematoxylin–eosin; SVCs, stromal vascular cells.
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    Image Search Results


    Vagotomy promoted Ly6G + cell infiltration into eWAT. Wild‐type mice were subjected to left cervical vagotomy (VX) or sham surgery and tissues were collected at 7 days following surgery. (A) The percentage of non‐adipocyte nuclei of total nuclei per section was quantified using ImageJ ( n = 4) and right panels show representative images of paraffin sections of eWAT stained with H&E in sham and VX animals. (B) CCL2 release from eWAT was analyzed by ELISA. The bar shows the CCL2 levels from sham ( n = 4) or VX ( n = 4) mice normalized to eWAT weight: ng/mL per g ± SEM (unpaired Student's t test). (C) eWAT was collected at 1 ( n = 3), 4 ( n = 4 sham, n = 5 VX), and 7 ( n = 15) days following VX or sham surgery and the eWAT SVCs were analyzed by flow cytometry. The bar shows the % ± SEM of CD11b + Ly6G + cells from CD45 + (one‐way ANOVA, Uncorrected Fisher's LSD). (D) Graphs show representative gating for CD11b + Ly6G + cells in sham and VX eWAT at 7 days (concatenated n = 5–6). (E) Representative immunostaining of Ly6G (red) and Perilipin1 (green) in paraffin sections of eWAT. (F–H) Bone marrow neutrophils after sham ( n = 9) or VX ( n = 5) surgery were isolated using negative magnetic beads and analyzed using bulk RNAseq (DESeq2). Heatmap (F), volcano plot (G) of differentially expressed genes, and GO (Gene Ontology) (H) enrichment bar plot. ns = not significant, * p < 0.05. VX, Vagotomy; eWAT, epididymal white adipose tissue; H&E, hematoxylin–eosin; SVCs, stromal vascular cells.

    Journal: The FASEB Journal

    Article Title: Lymphocyte Antigen 6G Mediates Vagotomy‐Associated Reduction in Body Weight

    doi: 10.1096/fj.202600151RR

    Figure Lengend Snippet: Vagotomy promoted Ly6G + cell infiltration into eWAT. Wild‐type mice were subjected to left cervical vagotomy (VX) or sham surgery and tissues were collected at 7 days following surgery. (A) The percentage of non‐adipocyte nuclei of total nuclei per section was quantified using ImageJ ( n = 4) and right panels show representative images of paraffin sections of eWAT stained with H&E in sham and VX animals. (B) CCL2 release from eWAT was analyzed by ELISA. The bar shows the CCL2 levels from sham ( n = 4) or VX ( n = 4) mice normalized to eWAT weight: ng/mL per g ± SEM (unpaired Student's t test). (C) eWAT was collected at 1 ( n = 3), 4 ( n = 4 sham, n = 5 VX), and 7 ( n = 15) days following VX or sham surgery and the eWAT SVCs were analyzed by flow cytometry. The bar shows the % ± SEM of CD11b + Ly6G + cells from CD45 + (one‐way ANOVA, Uncorrected Fisher's LSD). (D) Graphs show representative gating for CD11b + Ly6G + cells in sham and VX eWAT at 7 days (concatenated n = 5–6). (E) Representative immunostaining of Ly6G (red) and Perilipin1 (green) in paraffin sections of eWAT. (F–H) Bone marrow neutrophils after sham ( n = 9) or VX ( n = 5) surgery were isolated using negative magnetic beads and analyzed using bulk RNAseq (DESeq2). Heatmap (F), volcano plot (G) of differentially expressed genes, and GO (Gene Ontology) (H) enrichment bar plot. ns = not significant, * p < 0.05. VX, Vagotomy; eWAT, epididymal white adipose tissue; H&E, hematoxylin–eosin; SVCs, stromal vascular cells.

    Article Snippet: In vitro release rate was calculated as mg NEFAs per mg eWAT tissue per hour. (2) CCL2 levels were quantified using a mouse CCL2 ELISA kit (R&D Systems, #DY497‐05), according to the manufacturer's instructions ( n = 1 experiment).

    Techniques: Staining, Enzyme-linked Immunosorbent Assay, Flow Cytometry, Immunostaining, Isolation, Magnetic Beads, RNA sequencing