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anti ccl2 antibody  (R&D Systems)


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    Structured Review

    R&D Systems anti ccl2 antibody
    Anti Ccl2 Antibody, supplied by R&D Systems, used in various techniques. Bioz Stars score: 90/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+ccl2+antibody/Canine+CCL2%2FJE%2FMCP-1+Antibody/pm41910735-67-17-19
    Average 90 stars, based on 8 article reviews
    anti ccl2 antibody - by Bioz Stars, 2026-09
    90/100 stars

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    Related Articles

    other:

    Article Title: B cells mediate lung ischemia/reperfusion injury by recruiting classical monocytes via synergistic B cell receptor/TLR4 signaling
    Article Snippet: For selected experiments, mice were treated with 25 ng anti-CCL7 antibody (AF-456-NA, R&D Systems) or 25 ng anti-CCL2 antibody (AF-479NA, R&D Systems) i.v. 24 hours prior to hilar clamp.

    Article Title: B cells mediate lung ischemia/reperfusion injury by recruiting classical monocytes via synergistic B cell receptor/TLR4 signaling
    Article Snippet: For selected experiments, mice were treated with 25 ng anti-CCL7 antibody (AF-456-NA, R&D Systems) or 25 ng anti-CCL2 antibody (AF-479-NA, R&D Systems) i.v. 24 hours prior to hilar clamp.

    Recombinant:

    Article Title: Human 3D Ovarian Cancer Models Reveal Malignant Cell–Intrinsic and –Extrinsic Factors That Influence CAR T-cell Activity
    Article Snippet: .. Target cell and CAR T-cell cultures were treated with 0 to 25 μg/mL of pembrolizumab (Merck), 1 μmol/L of birinapant TL32711 (Selleckchem, Cat. S7015), 5 ng/mL recombinant CCL2 (R&D Systems, Cat. 279-MC-010), 5 μg/mL anti-CCL2 antibody (R&D Systems, Cat. MAB679), or 5 μg/mL anti-TNFα antibody (Thermo Fisher Scientific, Cat. AMC3012). .. Enzyme-linked immunosorbent assay (ELISA) was performed using human IFNα Quantikine kit (R&D Systems, Cat. DIF50C), human TNFα QuantiGlo kit (R&D Systems, Cat. QTA00C), human CCL2/MCP1 Quantikine kit (R&D Systems, Cat. DCP00), and human TGFβ1 Quantikine kit (R&D Systems, Cat. DB100C) according to manufacturer’s instructions.

    In Vivo:

    Article Title: Repolarization of Immunosuppressive Macrophages by Targeting SLAMF7-Regulated CCL2 Signaling Sensitizes Hepatocellular Carcinoma to Immunotherapy
    Article Snippet: 1 Repolarization of immunosuppressive macrophages by targeting SLAMF7regulated CCL2 signaling sensitizes hepatocellular carcinoma to immunotherapy Jialei Weng 1,2,† , Zheng Wang 3,† , Zhiqiu Hu 4,5,† , Wenxin Xu 1 , Jia-Lei Sun 6 , Fu Wang 6 , Qiang Zhou 1,2 , Shaoqing Liu 1,2 , Min Xu 1,2 , Minghao Xu 1,2 , Dongmei Gao 1 , Ying-Hao Shen 1 , Yong Yi 1 , Yi Shi 7 , Qiongzhu Dong 2,4 , Chenhao Zhou 1,2,* , and Ning Ren 1,2,4,* 1 Department of Liver Surgery and Transplantation, Liver Cancer Institute, Zhongshan Hospital, Fudan University, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Shanghai, 200032, P.R.. China.. 2 Key Laboratory of Whole-Period Monitoring and Precise Intervention of Digestive Cancer of Shanghai Municipal Health Commission, Shanghai, 201199, P.R.

    Injection:

    Article Title: Repolarization of Immunosuppressive Macrophages by Targeting SLAMF7-Regulated CCL2 Signaling Sensitizes Hepatocellular Carcinoma to Immunotherapy
    Article Snippet: 1 Repolarization of immunosuppressive macrophages by targeting SLAMF7regulated CCL2 signaling sensitizes hepatocellular carcinoma to immunotherapy Jialei Weng 1,2,† , Zheng Wang 3,† , Zhiqiu Hu 4,5,† , Wenxin Xu 1 , Jia-Lei Sun 6 , Fu Wang 6 , Qiang Zhou 1,2 , Shaoqing Liu 1,2 , Min Xu 1,2 , Minghao Xu 1,2 , Dongmei Gao 1 , Ying-Hao Shen 1 , Yong Yi 1 , Yi Shi 7 , Qiongzhu Dong 2,4 , Chenhao Zhou 1,2,* , and Ning Ren 1,2,4,* 1 Department of Liver Surgery and Transplantation, Liver Cancer Institute, Zhongshan Hospital, Fudan University, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Shanghai, 200032, P.R.. China.. 2 Key Laboratory of Whole-Period Monitoring and Precise Intervention of Digestive Cancer of Shanghai Municipal Health Commission, Shanghai, 201199, P.R.

    Control:

    Article Title: Repolarization of Immunosuppressive Macrophages by Targeting SLAMF7-Regulated CCL2 Signaling Sensitizes Hepatocellular Carcinoma to Immunotherapy
    Article Snippet: 1 Repolarization of immunosuppressive macrophages by targeting SLAMF7regulated CCL2 signaling sensitizes hepatocellular carcinoma to immunotherapy Jialei Weng 1,2,† , Zheng Wang 3,† , Zhiqiu Hu 4,5,† , Wenxin Xu 1 , Jia-Lei Sun 6 , Fu Wang 6 , Qiang Zhou 1,2 , Shaoqing Liu 1,2 , Min Xu 1,2 , Minghao Xu 1,2 , Dongmei Gao 1 , Ying-Hao Shen 1 , Yong Yi 1 , Yi Shi 7 , Qiongzhu Dong 2,4 , Chenhao Zhou 1,2,* , and Ning Ren 1,2,4,* 1 Department of Liver Surgery and Transplantation, Liver Cancer Institute, Zhongshan Hospital, Fudan University, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Shanghai, 200032, P.R.. China.. 2 Key Laboratory of Whole-Period Monitoring and Precise Intervention of Digestive Cancer of Shanghai Municipal Health Commission, Shanghai, 201199, P.R.

    Concentration Assay:

    Article Title: ALKBH5 facilitates Srgn stability via m6A demethylation to disrupt blood-testis barrier integrity in the high-fat diet mice.
    Article Snippet: Cells were transfected with plasmids or siRNAs using Lipofectamine 3000 reagent (Invitrogen; Thermo Fisher Scientific, Inc.) following the manufacturer's instructions after being seeded in a dish and cultured for 24 h. The transfection efficiency was evaluated after 24–72 h. The siRNA sequences used in this study were as follows: siAlkbh5-1: 5′ - CACCGCGAUUGGAAACAAATT- 3′, siAlkbh5-2: 5′- GCUGCAAGUUCCAGUUCATT - 3′; siSrgn-1: 5′ - GGATCTTCAGTGCAAGGTT - 3′, siSrgn-2: 5′ - GACCACAGTTTGACCTAAT - 3′, siSrgn-3: 5′ - CCAACAGATGAAAGCAATA - 3′. .. Following the instructions provided in the reagent manual, the TM4 and primary Sertoli cells were treated with anti-CCL2 antibody (R&D Systems, AF479-SP) at a concentration of 2 μg/mL and anti-TNF-α antibody (R&D Systems, AF-410-SP) at 10 ng/mL. .. Cells treated with Anti-IgG antibody (R&D Systems, AB-108-C) were used as the control.

    Blocking Assay:

    Article Title: Hydrophobic surface induced pro-metastatic cancer cells for in vitro extravasation models
    Article Snippet: After processing the images with ZEN (Carl Zeiss) or ImageJ software, the fully-extravasated or non-extravasated SKOV3 cells were counted over the entire chip and the extravasation percentage was quantified. .. For blocking CCL2-CCR2 binding interactions, the cancer cell suspensions were supplemented with anti-CCL2 antibody (R&D Systems, 2.5 μg/mL) and then introduced into one of the microfluidic chip reservoirs that connected to the intravascular region. ..

    Article Title: Cooperation between ZEB2 and SP1 upregulates PD-L1 and CCL2 to promote the immunosuppressive activity of tumor cells
    Article Snippet: .. The cells were allowed to migrate for 24 h. Where indicated, an anti-CCL2 antibody (5 μ g/ml; MAB679, R&D systems) was added to block the activity of CCL2. ..

    Binding Assay:

    Article Title: Hydrophobic surface induced pro-metastatic cancer cells for in vitro extravasation models
    Article Snippet: After processing the images with ZEN (Carl Zeiss) or ImageJ software, the fully-extravasated or non-extravasated SKOV3 cells were counted over the entire chip and the extravasation percentage was quantified. .. For blocking CCL2-CCR2 binding interactions, the cancer cell suspensions were supplemented with anti-CCL2 antibody (R&D Systems, 2.5 μg/mL) and then introduced into one of the microfluidic chip reservoirs that connected to the intravascular region. ..

    Activity Assay:

    Article Title: Cooperation between ZEB2 and SP1 upregulates PD-L1 and CCL2 to promote the immunosuppressive activity of tumor cells
    Article Snippet: .. The cells were allowed to migrate for 24 h. Where indicated, an anti-CCL2 antibody (5 μ g/ml; MAB679, R&D systems) was added to block the activity of CCL2. ..



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    Positive area-staining by antibody in intranasally-treated GHK-Cu mice of both sexes for (A) Synaptophysin, (B) GFAP, (C) <t>MCP-1,</t> (D) PSD-95, and (E) TGF-β. ** P < 0.01, *** P < 0.001, **** P < 0.0001.
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    R&D Systems anti human ccl2 neutralizing antibody
    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: