BioXCell熱銷產(chǎn)品--RecombiMAb anti-mouse PD-L1 (B7-H1) (D265A)
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產(chǎn)品描述：
10F.9G2?-CP001單克隆抗體是原始10F.9G2?單克隆抗體的重組嵌合型抗體?？勺兘Y(jié)構(gòu)域序列與原始10F.9G2?克隆號相同，但是恒定區(qū)序列已經(jīng)從大鼠IgG2b變?yōu)樾∈驣gG1。10F.9G2?-CP001單克隆抗體在Fc片段中也含有D265A突變，使其無法與內(nèi)源性Fcγ受體結(jié)合。
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10F.9G2?-CP001單克隆抗體與小鼠PD-L1（程序性死亡配體1，也稱為B7-H1或CD274）反應(yīng)。PD-L1是屬于Ig超家族的B7家族的I型跨膜蛋白，分子量為40kDa。PD-L1在T淋巴細(xì)胞、B淋巴細(xì)胞、NK細(xì)胞、樹突狀細(xì)胞以及IFNγ刺激的單核細(xì)胞、上皮細(xì)胞和內(nèi)皮細(xì)胞上表達。PD-L1與CD4和CD8胸腺細(xì)胞以及活化的T和B淋巴細(xì)胞和骨髓細(xì)胞上的受體PD-1結(jié)合。PD-L1與PD-1的結(jié)合導(dǎo)致抑制TCR介導(dǎo)的T細(xì)胞增殖和細(xì)胞因子產(chǎn)生。PD-L1被認(rèn)為在腫瘤免疫逃逸中起著重要作用。誘導(dǎo)的PD-L1表達在許多腫瘤中很常見，并導(dǎo)致腫瘤細(xì)胞對CD8+?T細(xì)胞介導(dǎo)的裂解的抗性增加。在黑色素瘤的小鼠模型中，可以通過用阻斷PD-L1和PD-1之間相互作用的抗體進行治療，暫時抑制腫瘤生長。10F.9G2?單克隆抗體已被證明可以阻斷PD-L1和PD-1之間以及PD-L1和B7-1之間的相互作用（CD80）。
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產(chǎn)品詳情：
產(chǎn)品名稱 | RecombiMAb anti-mouse PD-L1 (B7-H1) (D265A) |
產(chǎn)品貨號 | CP001 |
產(chǎn)品規(guī)格 | 1mg |
反應(yīng)種屬 | Mouse |
克隆號 | 10F.9G2?-CP001 |
同種型 | Mouse IgG1(switched from rat IgG2b) |
免疫原 | Mouse CD274 |
實驗應(yīng)用 | in vivo PD-L1 blockade* Immunofluorescence* Immunohistochemistry (frozen)* Flow cytometry* Western blot* *Reported for the original rat IgG2b 10F.9G2 antibody |
產(chǎn)品形式 | PBS, pH 7.0,Contains no stabilizers or preservatives |
純度 | >95%, Determined by SDS-PAGE |
聚合 | <5%, Determined by SEC |
無菌處理 | 0.2 μm filtration |
純化方式 | Protein A |
分子量 | 150 kDa |
小鼠病原檢測 | Ectromelia/Mousepox Virus: Negative Hantavirus: Negative K Virus: Negative Lactate Dehydrogenase-Elevating Virus: Negative Lymphocytic Choriomeningitis virus: Negative Mouse Adenovirus: Negative Mouse Cytomegalovirus: Negative Mouse Hepatitis Virus: Negative Mouse Minute Virus: Negative Mouse Norovirus: Negative Mouse Parvovirus: Negative Mouse Rotavirus: Negative Mycoplasma Pulmonis: Negative Pneumonia Virus of Mice: Negative Polyoma Virus: Negative Reovirus Screen: Negative Sendai Virus: Negative Theiler’s Murine Encephalomyelitis: Negative |
保存條件 | 抗體原液保存在4°C，不能冷凍保存。 |
推薦抗體稀釋液 | InVivoPure pH 7.0 Dilution Buffer（貨號IP0070） |
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該產(chǎn)品自上市已被多篇SCI文獻引用，品質(zhì)有保證，以下是部分已發(fā)表的文獻引用：
應(yīng)用 | 文章 |
體內(nèi)PD-L1阻斷 (in vivo PD-L1 blockade) | 1.?Grasselly, C., et al. (2018). 'The Antitumor Activity of Combinations of Cytotoxic? Chemotherapy and Immune Checkpoint Inhibitors Is Model-Dependent' Front? Immunol 9: 2100.
2.?Stathopoulou, C., et al. (2018). 'PD-1 Inhibitory Receptor Downregulates Asparaginyl? Endopeptidase and Maintains Foxp3 Transcription Factor Stability in Induced Regulatory? T Cells' Immunity 49(2): 247-263 e247.
3.?Jaworska, K., et al. (2015). 'Both PD-1 ligands protect the kidney from ischemia? reperfusion injury' J Immunol 194(1): 325-333.
4.?Kim, J., et al. (2015). 'Memory programming in CD8(+) T-cell differentiation is? intrinsic and is not determined by CD4 help' Nat Commun 6: 7994.
5.?Zander, R. A., et al. (2015). 'PD-1 Co-inhibitory and OX40 Co-stimulatory Crosstalk? Regulates Helper T Cell Differentiation and Anti-Plasmodium Humoral Immunity' Cell? Host Microbe 17(5): 628-641. |
體內(nèi)PD-L1阻斷，流式細(xì)胞術(shù) (in vivo PD-L1 blockade, Flow? Cytometry) | 1.?Aloulou, M., et al. (2016). 'Follicular regulatory T cells can be specific for the? immunizing antigen and derive from naive T cells' Nat Commun 7: 10579.
2.?Ngiow, S. F., et al. (2015). 'A Threshold Level of Intratumor CD8+ T-cell PD1? Expression Dictates Therapeutic Response to Anti-PD1' Cancer Res 75(18): 3800-3811.
3.?Rutigliano, J. A., et al. (2014). 'Highly pathological influenza A virus infection is? associated with augmented expression of PD-1 by functionally compromised? virus-specific CD8+ T cells' J Virol 88(3): 1636-1651. |
體內(nèi)PD-L1阻斷，免疫熒光 (in vivo PD-L1 blockade,? Immunofluorescence) | 1.Willimsky, G., et al. (2013). 'Virus-induced hepatocellular carcinomas cause? antigen-specific local tolerance' J Clin Invest 123(3): 1032-1043. |
免疫組織化學(xué)（冷凍），免疫熒光 (Immunohistochemistry (frozen),? Immunofluorescence) | 1.Riella, L. V., et al. (2011). 'Essential role of PDL1 expression on nonhematopoietic? donor cells in acquired tolerance to vascularized cardiac allografts' Am J Transplant? 11(4): 832-840. |
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