Bax (phospho Thr167) Polyclonal Antibody
活动价:
市场价:¥880.00
- 50μL
- 100μL
FAB2611946
- 产品信息
商品描述
靶点-Target
Bax
反应性
Human,Mouse,Rat
应用
IF,ELISA
宿主物种-Host Species
Rabbit
同种型-Isotype
IgG
修饰-Modification
Phospho
MW(Calculated)
21kD
推荐稀释比
IF 1:200-1:1000;ELISA 1:40000;Not yet tested in other applications;
组成
Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
纯化工艺
The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
储存
-15°C to -25°C/1 year(Do not lower than -25°C)
浓度
1 mg/ml
克隆性
Polyclonal
免疫原
The antiserum was produced against synthesized peptide derived from human Bax around the phosphorylation site of Thr167. AA range:133-182
特异性
Phospho-Bax (T167) Polyclonal Antibody detects endogenous levels of Bax protein only when phosphorylated at T167.
基因名称
BAX
蛋白名称
Apoptosis regulator BAX
别名
BAX;BCL2L4;Apoptosis regulator BAX;Bcl-2-like protein 4;Bcl2-L-4
Organism-1
Human
基因ID-1
581
SwissProt-1
Q07812
Organism-2
Mouse
基因ID-2
12028
SwissProt-2
Q07813
Organism-3
Rat
SwissProt-3
Q63690
背景
The protein encoded by BAX (BCL2 associated X, apoptosis regulator) belongs to the BCL2 protein family. BCL2 family members form hetero- or homodimers and act as anti- or pro-apoptotic regulators that are involved in a wide variety of cellular activities. This protein forms a heterodimer with BCL2, and functions as an apoptotic activator. This protein is reported to interact with, and increase the opening of, the mitochondrial voltage-dependent anion channel (VDAC), which leads to the loss in membrane potential and the release of cytochrome c. The expression of this gene is regulated by the tumor suppressor P53 and has been shown to be involved in P53-mediated apoptosis. Multiple alternatively spliced transcript variants, which encode different isoforms, have been reported for BAX.
细胞定位
[Isoform Alpha]: Mitochondrion outer membrane ; Single-pass membrane protein . Cytoplasm . Colocalizes with 14-3-3 proteins in the cytoplasm. Under stress conditions, undergoes a conformation change that causes release from JNK-phosphorylated 14-3-3 proteins and translocation to the mitochondrion membrane. Upon Sendai virus infection, recruited to the mitochondrion through interaction with IRF3 (PubMed:25609812). .; [Isoform Beta]: Cytoplasm.; [Isoform Gamma]: Cytoplasm.; [Isoform Delta]: Cytoplasm .





