研發(fā)背景：
P84單克隆抗體，也被稱為CD172a抗體，可與信號(hào)調(diào)節(jié)蛋白α(SIRPα)反應(yīng)。SIRPα蛋白是I型跨膜糖蛋白，在單核細(xì)胞、巨噬細(xì)胞和樹突狀細(xì)胞均有表達(dá)。此外，在神經(jīng)元和中樞神經(jīng)系統(tǒng)的一些其他組織也發(fā)現(xiàn)有SIRPα蛋白的表達(dá)。其配體CD47在多種細(xì)胞均有表達(dá)。
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SIRPα和CD47參與調(diào)節(jié)由樹突狀細(xì)胞介導(dǎo)的T細(xì)胞的活化、中性粒細(xì)胞遷移和吞噬等過(guò)程。SIRPα蛋白可在巨噬細(xì)胞的細(xì)胞膜上進(jìn)行橫向擴(kuò)散并在吞噬性突觸中積累，與CD47結(jié)合后，抑制巨噬細(xì)胞的吞噬作用。
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研究結(jié)果表明，使用anti-SIRPα抗體阻斷SIRPα與CD47相互作用，可抑制小鼠體內(nèi)腫瘤的形成。此外，P84（CD172a）單克隆抗體在體內(nèi)和體外均具有中和活性。
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BioXcell最新推出InVivoMAb anti-mouse CD172a (SIRPα)單克隆抗體，助力腫瘤免疫檢查點(diǎn)研究。
產(chǎn)品信息：
| 產(chǎn)品貨號(hào) | BE0322 |
| 產(chǎn)品名稱 | InVivoMAb anti-mouse CD172a (SIRPα) |
| 規(guī)格 | 1mg,5mg,25mg, 50mg, 100mg |
| 克隆號(hào) | P84 |
| 同種型(Isotype) | Rat IgG1, κ |
| 免疫原(Immunogen) | Mouse brain membrane protein |
| 成分(Formulation) | PBS, pH 7.0?? |
| Contains no stabilizers or preservatives |
| 內(nèi)毒素(Endotoxin) | <2EU/mg (<0.002EU/μg) |
| Determined by LAL gel clotting assay |
| 純度(Purity) | >95% |
| Determined by SDS-PAGE |
| 無(wú)菌(Sterility) | 0.2 μM filtered |
| 生產(chǎn)(Production) | Purified from tissue culture supernatant in an animal free facility |
| 純化(Purification) | Protein A |
| 保存(Storage) | Undiluted at 4°C in the dark |
| 應(yīng)用(Reported Applications) | In vivo?SIRPα blocking |
| In vitro?SIRPα blocking |
| Western blot |
Application References:
Yanagita, T., et al. (2017). 'Anti-SIRPalpha antibodies as a potential new tool for cancer immunotherapy.'?JCI Insight?2(1): e89140.?
Koskinen, C., et al. (2013). 'Lack of CD47 impairs bone cell differentiation and results in an osteopenic phenotype in vivo due to impaired signal regulatory protein alpha (SIRPalpha) signaling.'?J Biol Chem?288(41): 29333-29344.?
Teraoka, Y., et al. (2013). 'Expression of recipient CD47 on rat insulinoma cell xenografts prevents macrophage-mediated rejection through SIRPalpha inhibitory signaling in mice.'?PLoS One?8(3): e58359.?
Zen, K., et al. (2013). 'Inflammation-induced proteolytic processing of the SIRPalpha cytoplasmic ITIM in neutrophils propagates a proinflammatory state.'?Nat Commun?4: 2436.
Lundberg, P., et al. (2007). 'Osteoclast formation is strongly reduced both in vivo and in vitro in the absence of CD47/SIRPalpha-interaction.'?Biochem Biophys Res Commun?352(2): 444-448.?
Oldenborg, P. A., et al. (2001). 'CD47-signal regulatory protein alpha (SIRPalpha) regulates Fcgamma and complement receptor-mediated phagocytosis.'?J Exp Med?193(7): 855-862.
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