Bcl-2 抗体
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- 抗原 See all Bcl-2 (BCL2) 抗体
- Bcl-2 (BCL2) (B-Cell CLL/lymphoma 2 (BCL2))
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适用
- 小鼠, 大鼠
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宿主
- 小鼠
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克隆类型
- 单克隆
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标记
- This Bcl-2 antibody is un-conjugated
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应用范围
- Flow Cytometry (FACS)
- 纯化方法
- The antibody was purified by affinity chromatography.
- 克隆位点
- BCL-10C4
- 亚型
- IgG1 kappa
- Top Product
- Discover our top product BCL2 Primary Antibody
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- 应用备注
- Optimal working dilution should be determined by the investigator.
- 限制
- 仅限研究用
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- 浓度
- 0.5 mg/mL
- 缓冲液
- phosphate-buffered solution, pH 7.2, containing 0.09 % sodium azide at 0.5 mg/mL.
- 储存液
- Sodium azide
- 注意事项
- This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
- 储存条件
- 4 °C
- 储存方法
- Upon receipt, store undiluted at between 2°C and 8°C.
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- 抗原
- Bcl-2 (BCL2) (B-Cell CLL/lymphoma 2 (BCL2))
- 别名
- Bcl-2 (BCL2 产品)
- 背景
- Bcl-2 (B-cell leukemia 2) is an apoptotic protein and a member of the Bcl-2 family containing BH1-4 domains. Two reported isoforms exist α=25 kD, β=22 kD. The Bcl-2 protein forms homo- or hetero-dimers with other Bcl-2 family members. Bcl-2 is distributed in the outer mitochondrial membrane, the nuclear envelope, and the endoplasmic reticulum. This protein blocks apoptotic death by controlling mitochondrial membrane permeability. Cleavage of Bcl-2 can convert to pro-apoptotic (by cleavage of BH4 domain). Bcl-2 has been reported to regulate cell cycle progression via ROS. This protein is modified by ASK1/JNK1, PKC, ERKs, and stress-activated kinase phosphorylation and can be ubiquitinated. Bcl-2 has been shown to interact with Apaf-1, Raf-1, TP53BP2, caspase-3, and form heterodimers with Bax, Bad, Bak, Bcl-xL, and Bag-1. Clone BCL/10C4 has been shown to be useful for Western blotting, immunoprecipitation, and immunofluorescence of the mouse and rat Bcl-2 protein.
- 途径
- MAPK Pathway, PI3K-Akt Signaling, Apoptosis, Caspase Cascade in Apoptosis, Regulation of Muscle Cell Differentiation, Cell-Cell Junction Organization, Skeletal Muscle Fiber Development, Autophagy, Smooth Muscle Cell Migration, Negative Regulation of intrinsic apoptotic Signaling
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