歡迎您來(lái)到深圳欣博盛生物科技有限公司網(wǎng)站!
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(shù)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)。
SIRPα和CD47參與調(diào)節(jié)由樹(shù)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。
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。
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。如需購(gòu)買BioXcell公司產(chǎn)品,請(qǐng)聯(lián)系代理商欣博盛生物。

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.