- ￥1712
- BioXcell
- 美国
- BE0015-1-1MG
- 2025年07月10日
- in vivo T cell depletion, in vitro T cell stimulation/activation, Immunofluorescence, Flow cytometry, Western blot
- mouse
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- 详细信息
- 文献和实验
- 技术资料
- 克隆性：
单克隆
- 适应物种：
mouse
- 级别：
体内研究
- 库存：
99
- 供应商：
欣博盛生物
- 应用范围：
in vivo T cell depletion, in vitro T cell stimulation/activation, Immunofluorescence, Flow cytometry, Western blot
- 浓度：
Lot specific,typically between 4-11 mg/ml
- 抗体英文名：
InVivoMab anti-mouse CD28
- 抗体名：
InVivoMab anti-mouse CD28
- 规格：
1 mg
产品描述：
The 37.51 monoclonal antibody reacts with mouse CD28, a 45 kDa costimulatory receptor and a member of the Ig superfamily. CD28 is expressed by thymocytes, most peripheral T cells, and NK cells. CD28 is a receptor for CD80 (B7-1) and CD86 (B7-2). Signaling through CD28 augments IL-2 and IL-2 receptor expression as well as cytotoxicity of CD3-activated T cells. The 37.51 antibody has been shown to stimulate the proliferation and cytokine production by activated T and NK cells and provide a costimulatory signal for CTL induction.
BioXcell InVivoMab anti-mouse CD28 37.51单克隆抗体与小鼠CD28反应，CD28是一种45kDa的共刺激受体，也是Ig超家族的一员。CD28由胸腺细胞，大多数外周T细胞和NK细胞表达。CD28是CD80（B7-1）和CD86（B7-2）的受体。通过CD28的信号传导增强了IL-2和IL-2受体的表达以及CD3活化的T细胞的细胞毒性。37.51抗体已被证明能刺激活化的T细胞和NK细胞的增殖和细胞因子的产生，并为CTL诱导提供共刺激信号。
产品详情：
| 产品名称 |
InVivoMAb anti-mouse CD28 |
| 产品货号 |
BE0015-1 |
| 产品规格 |
1/5/25/50/100mg |
| 反应种属 |
Mouse |
| 克隆号 |
37.51 |
| 同种型 |
Syrian Hamster IgG2 |
| 免疫原 |
C57BL/6 mouse T cell lymphoma EL-4 cells |
| 实验应用 |
in vitro T cell stimulation/activation in vivo CD28 blockade |
| 产品形式 |
PBS, pH 6.0 0.01% Tween,Contains no stabilizers or preservatives |
| 纯度 |
>95%, Determined by SDS-PAGE |
| 无菌处理 |
0.2 µm filtration |
| 纯化方式 |
Protein G |
| RRID |
AB_1107624 |
| 分子量 |
150 kDa |
| 保存条件 |
抗体原液保存在4°C，不能冷冻保存。 |
| 推荐同型对照 |
InVivoMAb polyclonal Syrian hamster IgG（货号BE0087） |
| 推荐抗体稀释液 |
InVivoPure pH 6.0T Dilution Buffer（货号IPT060） |
该产品自上市已被多篇SCI文献引用，品质有保证，以下是部分已发表的文献引用：
| 应用 |
文章 |
| 体外T细胞刺激/激活 (in vitro T cell stimulation/activation) |
1. Lacher, S. M., et al. (2018). 'NF-kappaB inducing kinase (NIK) is an essential post-transcriptional regulator of T-cell activation affecting F-actin dynamics and TCR signaling' J Autoimmun 94: 110-121. 2. Wendland, K., et al. (2018). 'Retinoic Acid Signaling in Thymic Epithelial Cells Regulates Thymopoiesis' J Immunol 201(2): 524-532. 3. Ron-Harel, N., et al. (2016). 'Mitochondrial Biogenesis and Proteome Remodeling Promote One-Carbon Metabolism for T Cell Activation' Cell Metab 24(1): 104-117. 4. Gu, A. D., et al. (2015). 'A critical role for transcription factor Smad4 in T cell function that is independent of transforming growth factor beta receptor signaling' Immunity 42(1): 68-79. 5. Choi, Y. S., et al. (2015). 'LEF-1 and TCF-1 orchestrate TFH differentiation by regulating differentiation circuits upstream of the transcriptional repressor Bcl6' Nat Immunol 16(9): 980-990. |
| 体内CD28阻断 (in vivo CD28 blockade) |
1. Rouhani, S. J., et al. (2015). 'Roles of lymphatic endothelial cells expressing peripheral tissue antigens in CD4 T-cell tolerance induction' Nat Commun 6: 6771. 2. Eberlein, J., et al. (2012). 'Multiple layers of CD80/86-dependent costimulatory activity regulate primary, memory, and secondary lymphocytic-choriomeningitis-virus-specific T cell immunity' J Virol 86(4): 1955-1970. |
更多产品详情请咨询 BioXcell 中国授权代理——欣博盛生物
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文献和实验1. Lacher, S. M., et al. (2018). 'NF-kappaB inducing kinase (NIK) is an essential post-transcriptional regulator of T-cell activation affecting F-actin dynamics and TCR signaling' J Autoimmun 94: 110-121.
2. Wendland, K., et al. (2018). 'Retinoic Acid Signaling in Thymic Epithelial Cells Regulates Thymopoiesis' J Immunol 201(2): 524-532.
3. Ron-Harel, N., et al. (2016). 'Mitochondrial Biogenesis and Proteome Remodeling Promote One-Carbon Metabolism for T Cell Activation' Cell Metab 24(1): 104-117.
4. Gu, A. D., et al. (2015). 'A critical role for transcription factor Smad4 in T cell function that is independent of transforming growth factor beta receptor signaling' Immunity 42(1): 68-79.
5. Choi, Y. S., et al. (2015). 'LEF-1 and TCF-1 orchestrate TFH differentiation by regulating differentiation circuits upstream of the transcriptional repressor Bcl6' Nat Immunol 16(9): 980-990.
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