癌症的基本特征包括细胞增殖、血管生成、迁移、凋亡逃避机制和细胞永生等。找到癌症发生过程中这些通路的关键标记物和对应的抗体用于检测至关重要。
为您推荐一个泛素化位点预测神器——泛素化分析工具，可以为您的蛋白的泛素化位点作出预测和评分。
细胞自噬受体图形绘图工具为你的蛋白的细胞受体结合位点作出预测和评分，识别结合到自噬通路中的蛋白是非常重要的，便于让我们理解自噬在正常生理、病理过程中的作用，如发育、细胞分化、神经退化性疾病、压力条件下、感染和癌症。
CD272/BTLA Rabbit mAb
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- 实验流程
- 背景知识
Application 
| WB, IHC-P, FC, IP |
|---|---|
| Primary Accession | Q7TSA3 |
| Reactivity | Mouse |
| Host | Rabbit |
| Clonality | Monoclonal Antibody |
| Isotype | IgG |
| Conjugate | Unconjugated |
| Purification | Affinity Purified |
| Calculated MW | 34337 Da |
| Gene ID | 208154 |
|---|---|
| Other Names | Btla |
| Dilution | WB~~1:500-1:1000 IHC-P~~1:50~200 FC~~1:200-1:500 IP~~1:20-1:50 |
| Format | Liquid in 50mM Tris-Glycine(pH 7.4), 0.15M NaCl, 40%Glycerol, 0.01% sodium azide and 0.05% BSA. |
| Storage | Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles. |
For Research Use Only. Not For Use In Diagnostic Procedures.
| Name | Btla {ECO:0000303|PubMed:12796776, ECO:0000312|MGI:MGI:2658978} |
|---|---|
| Function | Inhibitory receptor on lymphocytes that negatively regulates antigen receptor signaling via PTPN6/SHP-1 and PTPN11/SHP-2 (PubMed:12796776, PubMed:14652006). May interact in cis (on the same cell) or in trans (on other cells) with TNFRSF14 (PubMed:19915044). In cis interactions, appears to play an immune regulatory role inhibiting in trans interactions in naive T cells to maintain a resting state. In trans interactions, can predominate during adaptive immune response to provide survival signals to effector T cells (PubMed:19915044). |
| Cellular Location | Cell membrane; Single-pass type I membrane protein |
| Tissue Location | Expressed in splenic T- and B-cells as well as lymph node tissues but very weakly in somatic tissues. Also expressed in macrophages, NK cells and dendritic cells. A polymorphic tissue distribution between several strains is seen |
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
CD272, also known as B and T lymphocyte attenuator (BTLA), is an Ig superfamily co-inhitory receptor with structural similarity to programmed cell death 1 (PD-1) and CTLA-4. BTLA is expressed on B cells, T cells, macrophages, dendritic cells, NKT cells, and NK cells. Engagement of BTLA by its ligand herpes virus entry mediator (HVEM) is critical for negatively regulating immune response. The absence of BTLA with HVEM inhibitory interactions leads to increased experimental autoimmune encephalomyelitis severity, enhanced rejection of partially mismatched allografts, an increased CD8+ memory T cell population, increased severity of colitis, and reduced effectiveness of T regulatory cells. BTLA plays an important role in the induction of peripheral tolerance of both CD4+ and CD8+ T cells in vivo. Tolerant T cells have significantly higher expression of BTLA compared with effectors and nave T cells. BTLA may cooperate with CTLA-4 and PD-1 to control T cell tolerance and autoimmunity. It was reported that BTLA may regulate T cell function by binding to B7-H4, but further studies are needed to confirm. The existence of three distinct BTLA alleles has been reported.
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