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antihuman fpr2 alx extracellular antibody  (Alomone Labs)


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    Structured Review

    Alomone Labs antihuman fpr2 alx extracellular antibody
    Antihuman Fpr2 Alx Extracellular Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/afr-002/pm40464830-32-1-11?v=Alomone+Labs
    Average 93 stars, based on 2 article reviews
    antihuman fpr2 alx extracellular antibody - by Bioz Stars, 2026-07
    93/100 stars

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    Alomone Labs rabbit anti fpr2 anti bodies
    BML-111 decreased TGF-β1-induced NIH3T3 cell α-SMA expression in a dose-dependent manner. (A) NIH3T3 cells express rs1 and (B) <t>FPR2.</t> Cells were pretreated with a vehicle (0.035% ethanol) or BML-111 (1, 10, 100, 200 and 500 nM) for 30 min and then treated with TGF-β1 (5 ng/ml) for 24 h. (C) The expression of α-SMA was assessed using western blotting and (D) quantified. Similar results were obtained from at least 3 sections. Data are expressed as the mean ± standard deviation. # P<0.05 and ## P<0.01 vs. the vehicle group. * P<0.05 and ** P<0.01 vs. the TGF-β1 group in the absence of BML-111. Magnification, ×200. TGF-β1, Transforming growth factor-β1; α-SMA, smooth muscle α actin; rs1, related sequence 1; FPR2, formyl peptide receptor; marker 1, Trans DNA ladder (Tiangen Biotech, Co., Ltd., Beijing, China).
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    Alomone Labs fpr2 antibody
    Antibodies used in this study
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    BML-111 decreased TGF-β1-induced NIH3T3 cell α-SMA expression in a dose-dependent manner. (A) NIH3T3 cells express rs1 and (B) FPR2. Cells were pretreated with a vehicle (0.035% ethanol) or BML-111 (1, 10, 100, 200 and 500 nM) for 30 min and then treated with TGF-β1 (5 ng/ml) for 24 h. (C) The expression of α-SMA was assessed using western blotting and (D) quantified. Similar results were obtained from at least 3 sections. Data are expressed as the mean ± standard deviation. # P<0.05 and ## P<0.01 vs. the vehicle group. * P<0.05 and ** P<0.01 vs. the TGF-β1 group in the absence of BML-111. Magnification, ×200. TGF-β1, Transforming growth factor-β1; α-SMA, smooth muscle α actin; rs1, related sequence 1; FPR2, formyl peptide receptor; marker 1, Trans DNA ladder (Tiangen Biotech, Co., Ltd., Beijing, China).

    Journal: International Journal of Molecular Medicine

    Article Title: BML-111 suppresses TGF-β1-induced lung fibroblast activation in vitro and decreases experimental pulmonary fibrosis in vivo

    doi: 10.3892/ijmm.2018.3914

    Figure Lengend Snippet: BML-111 decreased TGF-β1-induced NIH3T3 cell α-SMA expression in a dose-dependent manner. (A) NIH3T3 cells express rs1 and (B) FPR2. Cells were pretreated with a vehicle (0.035% ethanol) or BML-111 (1, 10, 100, 200 and 500 nM) for 30 min and then treated with TGF-β1 (5 ng/ml) for 24 h. (C) The expression of α-SMA was assessed using western blotting and (D) quantified. Similar results were obtained from at least 3 sections. Data are expressed as the mean ± standard deviation. # P<0.05 and ## P<0.01 vs. the vehicle group. * P<0.05 and ** P<0.01 vs. the TGF-β1 group in the absence of BML-111. Magnification, ×200. TGF-β1, Transforming growth factor-β1; α-SMA, smooth muscle α actin; rs1, related sequence 1; FPR2, formyl peptide receptor; marker 1, Trans DNA ladder (Tiangen Biotech, Co., Ltd., Beijing, China).

    Article Snippet: Following permeabilization, washing and blocking, the cells were incubated with rabbit anti-FPR2 anti-bodies (1:100; cat. no. AFR-002; Alomone Labs, Jerusalem, Israel) at 4°C overnight and then washed and incubated with a fluorescent-labeled secondary antibody (fluorescein isothiocyanate-labelled goat anti-rabbit immunoglobulin G; 1:50; cat. no. AS1110; Aspen Biological, Wuhan, China) for 45 min at 37°C.

    Techniques: Expressing, Western Blot, Standard Deviation, Sequencing, Marker

    Antibodies used in this study

    Journal: The Journal of Neuroscience

    Article Title: Resolvin D1 Programs Inflammation Resolution by Increasing TGF-β Expression Induced by Dying Cell Clearance in Experimental Autoimmune Neuritis

    doi: 10.1523/JNEUROSCI.0020-16.2016

    Figure Lengend Snippet: Antibodies used in this study

    Article Snippet: The following antibodies were used in this study: ED1 antibody for macrophages (1:100; Serotec), W3/13 antibody for T lymphocytes (1:50; Serotec), OX22 antibody for B cells (1:200; Serotec), ED2 antibody for anti-inflammatory macrophages (1:100; Serotec), or FPR2 antibody for ALX receptor (1:50; Alomone).

    Techniques: Expressing

    Primers used in this study

    Journal: The Journal of Neuroscience

    Article Title: Resolvin D1 Programs Inflammation Resolution by Increasing TGF-β Expression Induced by Dying Cell Clearance in Experimental Autoimmune Neuritis

    doi: 10.1523/JNEUROSCI.0020-16.2016

    Figure Lengend Snippet: Primers used in this study

    Article Snippet: The following antibodies were used in this study: ED1 antibody for macrophages (1:100; Serotec), W3/13 antibody for T lymphocytes (1:50; Serotec), OX22 antibody for B cells (1:200; Serotec), ED2 antibody for anti-inflammatory macrophages (1:100; Serotec), or FPR2 antibody for ALX receptor (1:50; Alomone).

    Techniques: