phospho-Bad (Ser118) Rabbit pAb (一抗) | Bioss

bs-5216R

磷酸化抗体、KO/KD Validated、宠物抗体、农牧业/家禽抗体

phospho-Bad (Ser118) Rabbit pAb

磷酸化相关死亡促进因子抗体

BBC2; BCL2L8; Bad_v1; Bad_v2; BAD_HUMAN; BAD; Bcl-2-binding component 6; Bcl-2-like protein 8 (Bcl2-L-8); Bcl-xL/Bcl-2-associated death promoter; Bcl2 antagonist of cell death; BBC6; BAD_MOUSE; BAD_RAT; BCL2 associated agonist of cell death; Bad (phospho-S118); p-BAD; phospho-BAD; Bad (phospho-Ser118)

Rabbit

KLH conjugated Synthesised phosphopeptide derived from human BAD around the phosphorylation site of Ser118: RM(p-S)DE

IgG

Liquid

affinity purified by Protein G

Polyclonal

22 kDa

22 kDa

1mg/ml

0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol.

Shipped at 4℃. Store at -20℃ for one year. Avoid repeated freeze/thaw cycles.

This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.

BAD是BCL2/BAX、BCL-XL/BAX异二聚体的负调节基因。BAD是BCL2/BCL-XL相关死亡促进因子，作为BCL2、 bCL-XL异二聚体伴分子而促进细胞凋亡。
有学者认为：BAD缺乏典型的羧基端跨膜结构，提示其并非一完整膜蛋白。与同BCL2作用相比，BAD与BCL-XL的结合更强，BAD以浓度依赖性方式替换BCL-XL/BAX、BCL2/BAX异二聚体中的BAX，使BAX游离而促进细胞凋亡。当一细胞系的所有细胞内异二聚体（BCL-XL/BAX和BCL2/BAX）的含量≥50%时，则细胞耐受凋亡；而当细胞内BAX同二聚体＞80%时且在适当信号诱导下则细胞出现凋亡。这表明BAD通过调节BAX同二聚体与异二聚体量的比值而介导凋亡。

Bad is a member of the Bcl2 family and acts to promote apoptosis by forming heterodimers with the survival proteins Bcl2 and BclxL, thus preventing them from binding with BAX. Bad is found on the outer mitochondrial membrane and, once phosphorylated in response to growth stimuli, translocates to the cytoplasm. The phosphorylation status of Bad represents a key checkpoint for death or cell survival. JNK-induced phosphorylation of BAD serine 128 promotes the apoptotic role of Bad by opposing the inhibitory effect of growth factor on Bad-mediated apoptosis. Cdc2-induced phosphorylation of Bad serine 128 has an inhibitory effect on its interaction with 14-3-3 proteins. The latter interaction is critical for Bad phosphorylation at serine 155, a site within the BH3 domain that leads to the release of BclxL and the promotion of cell survival. Alternative splicing of this gene results in two transcript variants which encode the same isoform.

BAD

Bcl2-associated agonist of cell death

Forms heterodimers with the anti-apoptotic proteins, Bcl-X(L), Bcl-2 and Bcl-W. Also binds protein S100A10 (By similarity). The Ser-75/Ser-99 phosphorylated form binds 14-3-3 proteins (By similarity). Interacts with AKT1 and PIM3.

Mitochondrion outer membrane. Cytoplasm. Note=Upon phosphorylation, locates to the cytoplasm.

Expressed in a wide variety of tissues.

Phosphorylated on one or more of Ser-75, Ser-99, Ser-118 and Ser-134 in response to survival stimuli, which blocks its pro-apoptotic activity.
Phosphorylation on Ser-99 or Ser-75 promotes heterodimerization with 14-3-3 proteins. This interaction then facilitates the phosphorylation at Ser-118, a site within the BH3 motif, leading to the release of Bcl-X(L) and the promotion of cell survival. Ser-99 is the major site of AKT/PKB phosphorylation, Ser-118 the major site of protein kinase A (CAPK) phosphorylation. Ser-75 is phosphorylated by AKT/PKB, protein kinase A and PIM2.

Belongs to the Bcl-2 family.

Promotes cell death. Successfully competes for the binding to Bcl-X(L), Bcl-2 and Bcl-W, thereby affecting the level of heterodimerization of these proteins with BAX. Can reverse the death repressor activity of Bcl-X(L), but not that of Bcl-2 (By similarity). Appears to act as a link between growth factor receptor signaling and the apoptotic pathways.