重组抗小鼠CD115单抗(AFS98)流式 | Syd Labs PA007484.r2a

重组抗小鼠CD115单抗流式(AFS98) Syd Labs PA007484.r2a - 武汉多找找科技

重组抗小鼠CD115单抗(AFS98)流式 | Syd Labs PA007484.r2a

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Syd Labs重组抗小鼠CD115单克隆抗体(克隆号AFS98) ,大鼠IgG2a Kappa(货号:PA007484.r2a)是用哺乳动物细胞生产的重组抗体,可用于流式细胞术和免疫组织化学-冷冻等研究,纯度>95%。其不变区为大鼠Rat IgG2a Kappa (rIgG2a或r2a),可与重组大鼠IgG2a同型对照抗体配套使用。样品制备条件和最佳样品稀释度应由研究人员通过实验确定。

SKU: PA007484.r2a 分类: ,

产品参数

货号 PA007484.r2a
产品名称重组抗小鼠CD115单抗(AFS98)流式 | Syd Labs PA007484.r2a
英文名 Recombinant Anti-mouse CD115 Monoclonal Antibody (Clone: AFS98), Rat IgG2a Kappa
供货商名称 Syd Labs, Inc.
品牌名 Syd Labs
别称 集落刺激因子 1 受体,CSF1R,巨噬细胞集落刺激因子受体,M-CSFR
概述 Syd Labs提供重组大鼠IgG2a同型对照抗体。样品制备条件和最佳样品稀释度应由研究人员通过实验确定。
克隆号 AFS98
同种型 大鼠 IgG2a kappa
特异性 该重组 AFS98 抗体与小鼠 CD115 蛋白特异性结合
免疫源 重组抗小鼠CD115单克隆抗体 (克隆:AFS98)在哺乳动物细胞中产生
抗体形式 0.2微米过滤溶液,pH 7.4,含0.09%叠氮化钠
偶联 非偶联
纯度 >95%(在还原条件下通过SDS-PAGE测定)
运输 重组抗小鼠CD115单克隆抗体(克隆号AFS98) ,大鼠IgG2a Kappa用冰袋运输。收到后,请立即将其存放在下面建议的温度下。
稳定性与存储 使用手动除霜冰箱并避免重复冻融循环。 自收到之日起 12个月,保存在2 至 8°C。 请勿冻结。
注意事项 PA007484.r2a Syd Labs提供重组大鼠IgG2a同型对照抗体。样品制备条件和最佳样品稀释度应由研究人员通过实验确定。
产品咨询 Syd Labs在国内只通过代理商销售其产品,不做直销。终端用户咨询价格请联系Syd Labs中国代理商
关于Syd Labs产品如果有任何技术或其它问题,欢迎随时联系Syd Labs国内市场推广合作伙伴:武汉多找找科技有限公司企业微信:duozhaozhao2024 联系电话:18162581039(龙经理)
应用详情 流式细胞术(FC)和免疫组织化学-冷冻(IHC-F)。

文献

重组抗小鼠CD115单克隆抗体(克隆号AFS98) ,大鼠IgG2a Kappa(Recombinant Anti-mouse CD115 Monoclonal Antibody (Clone: AFS98), Rat IgG2a Kappa,货号:PA007484.r2a Syd Labs)

抗小鼠CD115单抗(又称AFS98抗体)是一种特异性识别小鼠CD115分子的单克隆抗体。CD115即巨噬细胞集落刺激因子受体(Macrophage Colony-Stimulating Factor Receptor, M-CSFR 或 CSF-1R),主要表达于单核细胞、巨噬细胞及其祖细胞表面,在调节单核巨噬细胞系的存活、增殖及分化过程中起着决定性作用。在现代免疫学与肿瘤微环境研究中,抗小鼠CD115单抗(AFS98抗体)被广泛应用于流式细胞术中髓系细胞的精准检测与表型分析,以及在体内实验中用于特异性阻断CSF-1R信号通路,从而深入探讨巨噬细胞在组织稳态、炎症反应及肿瘤免疫耐受中的关键调控机制。

作为专业的生命科学试剂供应商,Syd Labs推出的重组抗小鼠CD115单抗(克隆号AFS98)采用高效的哺乳动物细胞表达系统进行重组生产,确保了批次间极高的稳定性与批次一致性。该产品完全达到严格的体内实验级标准,具备超低的内毒素水平,且采用Human IgG1 Fc Silent Kappa格式进行工程化突变改造,能够有效消除Fc段与巨噬细胞或树突状细胞表面Fc受体的非特异性结合干扰。无论是用于流式细胞术检测还是开展高要求的体内巨噬细胞清除与免疫调节干预研究,Syd Labs重组AFS98抗体都能为您提供高特异性与可靠的实验数据支持。

抗小鼠CD115单抗(AFS98)流式部分参考文献:

1. Antibody blockade of c-fms suppresses the progression of inflammation and injury in early diabetic nephropathy in obese db/db mice
Lim, A. K. H., et al. Diabetologia. 2009 Aug;52(8):1669-79. PMID: 19466391
“Periglomerular and interstitial levels of α-SMA were seen in accumulating myofibroblasts in a diabetic kidney from a db/db mouse receiving control mAb; levels were reduced in a diabetic db/db mouse treated with AFS98 mAb. …Additional collagen IV deposition was found in the expanded mesangium and interstitial areas of a diabetic kidney from a diabetic db/db mouse given control mAb; deposition was reduced in a diabetic db/db mouse treated with AFS98 mAb. …Our primary outcome was that AFS98 treatment reduced kidney macrophages in diabetic db/db mice…”

2. Intraperitoneal administration of anti-c-fms monoclonal antibody prevents initial events of atherogenesis but does not reduce the size of advanced lesions in apolipoprotein E-deficient mice
Murayama, T., et al. Circulation. 1999 Apr 6;99(13):1740-6. PMID: 10190885
“To elucidate the central role of macrophage and macrophage-colony stimulating factor (M-CSF) during atherogenesis, we used a new strategy to administer to adult apolipoprotein E (apoE)-deficient mice a monoclonal antibody (AFS98) raised against c-fms, the receptor of M-CSF. …AFS98, a rat monoclonal anti-murine c-fms antibody (IgG2a), which inhibits M-CSF-dependent colony formation and cell growth by blocking the binding of M-CSF to its receptor, has been described previously…”

3. Bone- and cartilage-protective effects of a monoclonal antibody against colony-stimulating factor 1 receptor in experimental arthritis
Bonnefoy, J. Y., et al. Arthritis Rheumatol. 2014 Nov;66(11):2989-3000. PMID: 24623505
“We undertook this study to determine CSF-1R expression in human RA as well as the efficacy of a specific anti-CSF-1R monoclonal antibody (AFS98) in 2 different animal models of RA. …The efficacy of AFS98 was examined by clinical assessment, histology, and bone histomorphometry in collagen-induced arthritis (CIA) and serum-transfer arthritis. …In mice, blockade of CSF-1R abrogated cartilage damage, bone erosion, and systemic bone loss, and this was associated with the depletion of osteoclasts in both models…”