製品# | サイズ | 数量 | 価格 | 在庫 |
---|---|---|---|---|
17229T | 1 Kit (7 x 20 microliters) |
|
Product Includes | Quantity | Applications | Reactivity | MW(kDa) | Isotype |
---|---|---|---|---|---|
Bcl-2 (D55G8) Rabbit mAb 4223 | 20 µl |
|
H | 26 | Rabbit IgG |
Phospho-Bcl-2 (Ser70) (5H2) Rabbit mAb 2827 | 20 µl |
|
H | 28 | Rabbit IgG |
Mcl-1 (D2W9E) Rabbit mAb 94296 | 20 µl |
|
H M R | 40 (human), 35 (rodent) | Rabbit IgG |
Phospho-Mcl-1 (Thr163) (D5M9D) Rabbit mAb 14765 | 20 µl |
|
H | 40 | Rabbit IgG |
Bcl-xL (54H6) Rabbit mAb 2764 | 20 µl |
|
H M R Mk | 30 | Rabbit IgG |
A1/Bfl-1 (D1A1C) Rabbit mAb 14093 | 20 µl |
|
H | 18 | Rabbit IgG |
Bcl-w (31H4) Rabbit mAb 2724 | 20 µl |
|
H M R | 18 | Rabbit IgG |
Anti-rabbit IgG, HRP-linked Antibody 7074 | 100 µl |
|
Rab | Goat |
製品情報
Rabbit monoclonal antibodies are produced by immunizing animals with synthetic peptides corresponding to residues surrounding Gly47 of human Bcl-2, Asp61 of human Bcl-xL, Pro60 of mouse Mcl-1, Gly29 of human A1/Bfl-1, and Ala39 of human Bcl-w. Phospho-specific rabbit monoclonal antibodies are produced by immunizing animlars with synthetic phospho-peptides correspoding to residues surrounding Ser70 of human Bcl-2 and Thr163 of human Mcl-1.
The Bcl-2 family consists of a number of evolutionarily conserved proteins containing Bcl-2 homology domains (BH) that regulate apoptosis through control of mitochondrial membrane permeability and release of cytochrome c (1-3). Four BH domains have been identified (BH1-4) that mediate protein interactions. The family can be separated into three groups based upon function and sequence homology: pro-survival members include Bcl-2, Bcl-xL, Mcl-1, A1 and Bcl-w; pro-apoptotic proteins include Bax, Bak and Bok; and "BH3 only" proteins Bad, Bik, Bid, Puma, Bim, Bmf, Noxa and Hrk. Interactions between death-promoting and death-suppressing Bcl-2 family members has led to a rheostat model in which the ratio of pro-apoptotic and anti-apoptotic proteins controls cell fate (4). Thus, pro-survival members exert their behavior by binding to and antagonizing death-promoting members. In general, the "BH3-only members" can bind to and antagonize the pro-survival proteins leading to increased apoptosis (5). While some redundancy of this system likely exists, tissue specificity, transcriptional and post-translational regulation of many of these family members can account for distinct physiological roles.
Several phosphorylation sites have been identified within Bcl-2 including Thr56, Ser70, Thr74 and Ser87 (6). These phosphorylation sites may be targets of the ASK1/MKK7/JNK1 pathway, and phosphorylation of Bcl-2 may be a marker for mitotic events (7,8). Mutation of Bcl-2 at Thr56 or Ser87 inhibits its anti-apoptotic activity during glucocorticoid-induced apoptosis of T lymphocytes (9). Interleukin 3 and JNK-induced Bcl-2 phosphorylation at Ser70 may be required for its enhanced antiapoptotic functions (10).
Mcl-1 is phosphorylated in response to treatment with phorbol ester, microtubule-damaging agents, oxidative stress, and cytokine withdrawal (11-14). Phosphorylation at Thr163, the conserved MAP kinase/ERK site located within the PEST region, slows Mcl-1 protein turnover (13) but may prime the GSK-3 mediated phosphorylation at Ser159 that leads to Mcl-1 destabilization (14).
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