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mouse monoclonal mcp 1 antibody  (R&D Systems)


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    Structured Review

    R&D Systems mouse monoclonal mcp 1 antibody
    Mouse Monoclonal Mcp 1 Antibody, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 46 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ccl2+antibody/pm41964752-35-10-15?v=R%26D+Systems
    Average 94 stars, based on 46 article reviews
    mouse monoclonal mcp 1 antibody - by Bioz Stars, 2026-07
    94/100 stars

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    METH enhances HIV-1 NL4-3 replication in HBVPs independently of Sigma-1R. A - B Impact of METH (25 µM) on HIV-1 replication as measured by p24 antigen release levels in HBVPs infected with HIV-1 NL4-3 ( A ) or JR-CSF ( B ). Data are means ± SEM ( n = 3). C - D Impact of METH (25 µM) on HIV-1 replication as measured by HIV-1 Gag mRNA expression levels in HBVPs infected with HIV-1 NL4-3 ( C ) or JR-CSF ( D ) ( n = 4–5). E Impact of pretreatment with S1RA (10 µM) for 6 h on NL4-3 HIV-1 replication in the presence and absence of METH ( n = 3–4). F Impact of HBVP pretreatment with the CXCR4 chemokine receptor antagonist AMD070 (5 µM) for 1 h on HIV-1 NL4-3 replication in the presence and absence of METH ( n = 4). G The heat map demonstrating the impact of HIV-1 NL4-3 infection and/or METH treatment for 72 h on gene expression profile of 42 ISGs in HBVPs ( n = 6). Genes with high expression levels are represented in shades of red, while those with low expression levels are shown in shades of green. Gene names are shown on the x axis. Red arrows indicate genes that were significantly differentially regulated in the HIV-1 NL4-3 + METH group compared to the control group, as determined by the RT² Profiler PCR Array ( p < 0.05). H - K RT-qPCR analysis of mRNA expression of <t>CCL2</t> ( H ), MX2 ( I ), IFI30 ( J ), and PRKD2 ( K ) in HBVPs infected with HIV-1 NL4-3 and/or treated with METH ( n = 12). L Impact of blocking endogenous CCL2 with anti-human CCL2 neutralizing antibody on p24 release in HIV-1 NL4-3-infected HBVPs, with or without METH, at 72 h post-infection ( n = 6). M Impact of pretreatment with the CXCR4 chemokine receptor antagonist AMD070 (5 µM) for 1 h on CCL2 release in the presence and absence of METH at 72 h post-infection ( n = 6). Data are means ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001. Abbreviations as in Fig. ; CCL2 - C-C motif chemokine ligand 2
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    Image Search Results


    Positive area-staining by antibody in intranasally-treated GHK-Cu mice of both sexes for (A) Synaptophysin, (B) GFAP, (C) MCP-1, (D) PSD-95, and (E) TGF-β. ** P < 0.01, *** P < 0.001, **** P < 0.0001.

    Journal: bioRxiv

    Article Title: Middle-aged mice treated with GHK-Cu peptide administered intraperitoneally or intranasally show behavioral rescue but divergent hippocampal aging programs

    doi: 10.64898/2026.04.09.717524

    Figure Lengend Snippet: Positive area-staining by antibody in intranasally-treated GHK-Cu mice of both sexes for (A) Synaptophysin, (B) GFAP, (C) MCP-1, (D) PSD-95, and (E) TGF-β. ** P < 0.01, *** P < 0.001, **** P < 0.0001.

    Article Snippet: Following blocking, sections were incubated overnight at 4°C with primary antibodies against synaptophysin (1:250, Invitrogen MA5-16402), PSD95 (1:250, Abcam ab18258), phospho-SMAD2 (1:50, Invitrogen 44-244G), MCP-1 (1:800, Novus NBP1-07035), p21 (1:200, Abcam ab188224), TGF-β (1:50, Abcam ab215715), and GFAP (1:1500, Invitrogen: PA1-10019).

    Techniques: Staining

    Positive area-staining by antibody in intraperitoneally-treated GHK-Cu mice of both sexes for (A) TGF-β, (B) GFAP), (C) MCP-1, (D) p21, (E) Synaptophysin, (F) pSMAD-2, and (G) PSD-95. * P < 0.05, ** P < 0.01, **** P < 0.0001.

    Journal: bioRxiv

    Article Title: Middle-aged mice treated with GHK-Cu peptide administered intraperitoneally or intranasally show behavioral rescue but divergent hippocampal aging programs

    doi: 10.64898/2026.04.09.717524

    Figure Lengend Snippet: Positive area-staining by antibody in intraperitoneally-treated GHK-Cu mice of both sexes for (A) TGF-β, (B) GFAP), (C) MCP-1, (D) p21, (E) Synaptophysin, (F) pSMAD-2, and (G) PSD-95. * P < 0.05, ** P < 0.01, **** P < 0.0001.

    Article Snippet: Following blocking, sections were incubated overnight at 4°C with primary antibodies against synaptophysin (1:250, Invitrogen MA5-16402), PSD95 (1:250, Abcam ab18258), phospho-SMAD2 (1:50, Invitrogen 44-244G), MCP-1 (1:800, Novus NBP1-07035), p21 (1:200, Abcam ab188224), TGF-β (1:50, Abcam ab215715), and GFAP (1:1500, Invitrogen: PA1-10019).

    Techniques: Staining

    METH enhances HIV-1 NL4-3 replication in HBVPs independently of Sigma-1R. A - B Impact of METH (25 µM) on HIV-1 replication as measured by p24 antigen release levels in HBVPs infected with HIV-1 NL4-3 ( A ) or JR-CSF ( B ). Data are means ± SEM ( n = 3). C - D Impact of METH (25 µM) on HIV-1 replication as measured by HIV-1 Gag mRNA expression levels in HBVPs infected with HIV-1 NL4-3 ( C ) or JR-CSF ( D ) ( n = 4–5). E Impact of pretreatment with S1RA (10 µM) for 6 h on NL4-3 HIV-1 replication in the presence and absence of METH ( n = 3–4). F Impact of HBVP pretreatment with the CXCR4 chemokine receptor antagonist AMD070 (5 µM) for 1 h on HIV-1 NL4-3 replication in the presence and absence of METH ( n = 4). G The heat map demonstrating the impact of HIV-1 NL4-3 infection and/or METH treatment for 72 h on gene expression profile of 42 ISGs in HBVPs ( n = 6). Genes with high expression levels are represented in shades of red, while those with low expression levels are shown in shades of green. Gene names are shown on the x axis. Red arrows indicate genes that were significantly differentially regulated in the HIV-1 NL4-3 + METH group compared to the control group, as determined by the RT² Profiler PCR Array ( p < 0.05). H - K RT-qPCR analysis of mRNA expression of CCL2 ( H ), MX2 ( I ), IFI30 ( J ), and PRKD2 ( K ) in HBVPs infected with HIV-1 NL4-3 and/or treated with METH ( n = 12). L Impact of blocking endogenous CCL2 with anti-human CCL2 neutralizing antibody on p24 release in HIV-1 NL4-3-infected HBVPs, with or without METH, at 72 h post-infection ( n = 6). M Impact of pretreatment with the CXCR4 chemokine receptor antagonist AMD070 (5 µM) for 1 h on CCL2 release in the presence and absence of METH at 72 h post-infection ( n = 6). Data are means ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001. Abbreviations as in Fig. ; CCL2 - C-C motif chemokine ligand 2

    Journal: Journal of Neuroinflammation

    Article Title: Sigma-1 receptor regulates HIV-1 and methamphetamine-induced endothelial/pericyte barrier impairment via strain-specific inflammatory responses and mitochondrial dysregulation

    doi: 10.1186/s12974-026-03750-1

    Figure Lengend Snippet: METH enhances HIV-1 NL4-3 replication in HBVPs independently of Sigma-1R. A - B Impact of METH (25 µM) on HIV-1 replication as measured by p24 antigen release levels in HBVPs infected with HIV-1 NL4-3 ( A ) or JR-CSF ( B ). Data are means ± SEM ( n = 3). C - D Impact of METH (25 µM) on HIV-1 replication as measured by HIV-1 Gag mRNA expression levels in HBVPs infected with HIV-1 NL4-3 ( C ) or JR-CSF ( D ) ( n = 4–5). E Impact of pretreatment with S1RA (10 µM) for 6 h on NL4-3 HIV-1 replication in the presence and absence of METH ( n = 3–4). F Impact of HBVP pretreatment with the CXCR4 chemokine receptor antagonist AMD070 (5 µM) for 1 h on HIV-1 NL4-3 replication in the presence and absence of METH ( n = 4). G The heat map demonstrating the impact of HIV-1 NL4-3 infection and/or METH treatment for 72 h on gene expression profile of 42 ISGs in HBVPs ( n = 6). Genes with high expression levels are represented in shades of red, while those with low expression levels are shown in shades of green. Gene names are shown on the x axis. Red arrows indicate genes that were significantly differentially regulated in the HIV-1 NL4-3 + METH group compared to the control group, as determined by the RT² Profiler PCR Array ( p < 0.05). H - K RT-qPCR analysis of mRNA expression of CCL2 ( H ), MX2 ( I ), IFI30 ( J ), and PRKD2 ( K ) in HBVPs infected with HIV-1 NL4-3 and/or treated with METH ( n = 12). L Impact of blocking endogenous CCL2 with anti-human CCL2 neutralizing antibody on p24 release in HIV-1 NL4-3-infected HBVPs, with or without METH, at 72 h post-infection ( n = 6). M Impact of pretreatment with the CXCR4 chemokine receptor antagonist AMD070 (5 µM) for 1 h on CCL2 release in the presence and absence of METH at 72 h post-infection ( n = 6). Data are means ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001. Abbreviations as in Fig. ; CCL2 - C-C motif chemokine ligand 2

    Article Snippet: To neutralize CCL2, cultures were incubated with an anti-human CCL2 neutralizing antibody (8 μg/mL; R&D Systems, Cat# AF-279-NA) or with normal goat IgG as a control (R&D Systems, Cat# AB-108-C).

    Techniques: Infection, Expressing, Gene Expression, Control, Quantitative RT-PCR, Blocking Assay

    Synergistic impact of METH and CXCR4-Tropic HIV-1 on pericyte-dependent endothelial barrier breakdown via CXCR4/CCL2-driven viral replication and Sigma-1R-mediated mitochondrial and inflammatory dysregulation. This proposed model depicts intersecting pathways through which CXCR4-tropic HIV-1 and METH synergistically compromise endothelial barrier integrity via viral replication, Sigma-1R-mediated mitochondrial dysfunction, and modulation of IL6-associated inflammatory response. Notably, METH-enhanced replication of CXCR4-tropic HIV-1 in pericytes appears to occur independently of the Sigma-1R signaling ( www.BioRender.com )

    Journal: Journal of Neuroinflammation

    Article Title: Sigma-1 receptor regulates HIV-1 and methamphetamine-induced endothelial/pericyte barrier impairment via strain-specific inflammatory responses and mitochondrial dysregulation

    doi: 10.1186/s12974-026-03750-1

    Figure Lengend Snippet: Synergistic impact of METH and CXCR4-Tropic HIV-1 on pericyte-dependent endothelial barrier breakdown via CXCR4/CCL2-driven viral replication and Sigma-1R-mediated mitochondrial and inflammatory dysregulation. This proposed model depicts intersecting pathways through which CXCR4-tropic HIV-1 and METH synergistically compromise endothelial barrier integrity via viral replication, Sigma-1R-mediated mitochondrial dysfunction, and modulation of IL6-associated inflammatory response. Notably, METH-enhanced replication of CXCR4-tropic HIV-1 in pericytes appears to occur independently of the Sigma-1R signaling ( www.BioRender.com )

    Article Snippet: To neutralize CCL2, cultures were incubated with an anti-human CCL2 neutralizing antibody (8 μg/mL; R&D Systems, Cat# AF-279-NA) or with normal goat IgG as a control (R&D Systems, Cat# AB-108-C).

    Techniques: