| 產(chǎn)品編號(hào) | bs-1153R-PE-Cy5 |
| 英文名稱1 | Rabbit Anti-Bid/PE-Cy5 Conjugated antibody |
| 中文名稱 | PE-Cy5標(biāo)記的BH3結(jié)構(gòu)域凋亡誘導(dǎo)蛋白抗體 |
| 別 名 | Apoptic death agonist; Apoptotic death agonist; Apoptotic death agonist BID; BH3 interacting domain death agonist; BH3 interacting domain death agonist; BH3 interacting domain death agonist p11; BH3 interacting domain death agonist p13; BH3 interacting domain death agonist p15; BH3-interacting domain death agonist p11; BID; BID isoform ES(1b); BID isoform L(2); BID isoform Si6; BID_HUMAN; Desmocollin type 4; FP497; HGNC:1050; Human BID coding sequence; MGC15319; MGC42355; p11 BID; p13 BID; p15 BID; p22 BID. |
| 規(guī)格價(jià)格 | 100ul/2980元 購(gòu)買(mǎi) 大包裝/詢價(jià) |
| 說(shuō) 明 書(shū) | 100ul |
| 研究領(lǐng)域 | 腫瘤 信號(hào)轉(zhuǎn)導(dǎo) 細(xì)胞凋亡 新陳代謝 線粒體 |
| 抗體來(lái)源 | Rabbit |
| 克隆類型 | Polyclonal |
| 交叉反應(yīng) | Human, Mouse, Rat, |
| 產(chǎn)品應(yīng)用 | Flow-Cyt=1:50-200 IF=1:50-200
not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
| 分 子 量 | 21kDa |
| 性 狀 | Lyophilized or Liquid |
| 濃 度 | 1mg/ml |
| 免 疫 原 | KLH conjugated synthetic peptide derived from human Bid |
| 亞 型 | IgG |
| 純化方法 | affinity purified by Protein A |
| 儲(chǔ) 存 液 | 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. |
| 保存條件 | Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. |
| 產(chǎn)品介紹 |
background: Bid, a BH3 domain containing proapoptotic Bcl2 family member, is localized in the cytosolic fraction of cells as an inactive precursor. Its active form is generated upon proteolytic cleavage by caspase 8 in the Fas signaling pathway. Cleaved Bid translocates to mitochondria and releases its potent proapoptotic activity, which in turn induces cytochrome c release and mitochondrial damage. The cytochrome c releasing activity of Bid was antagonized by Bcl2. Mutation in the SH3 domain can diminish the cytochrome c releasing activity. In animal model studies, Bid deficient mice are found resistant to the lethal effects of death factor signals relayed through Fas. Function: The major proteolytic product p15 BID allows the release of cytochrome c. Isoform 1, isoform 2 and isoform 4 induce ICE-like proteases and apoptosis. Isoform 3 does not induce apoptosis. Counters the protective effect of Bcl-2. Subunit: Forms heterodimers either with the pro-apoptotic protein BAX or the anti-apoptotic protein Bcl-2. Subcellular Location: Cytoplasm. Mitochondrion membrane. Note=When uncleaved, it is predominantly cytoplasmic. BH3-interacting domain death agonist p15: Mitochondrion membrane. Note=Translocates to mitochondria as an integral membrane protein. BH3-interacting domain death agonist p13: Mitochondrion membrane. Note=Associated with the mitochondrial membran. Isoform 1: Cytoplasm. Isoform 3: Cytoplasm. Isoform 2: Mitochondrion membrane. Note=A significant proportion of isoform 2 localizes to mitochondria, it may be cleaved constitutively. Tissue Specificity: Isoform 2 and isoform 3 are expressed in spleen, bone marrow, cerebral and cerebellar cortex. Isoform 2 is expressed in spleen, pancreas and placenta (at protein level). Isoform 3 is expressed in lung, pancreas and spleen (at protein level). Isoform 4 is expressed in lung and pancreas (at protein level). Post-translational modifications: TNF-alpha induces a caspase-mediated cleavage of p22 BID into a major p15 and minor p13 and p11 products. Phosphorylated upon DNA damage, probably by ATM or ATR. Database links: Entrez Gene: 637 Human Entrez Gene: 12122 Mouse Omim: 601997 Human SwissProt: P55957 Human SwissProt: P70444 Mouse Unigene: 591054 Human Unigene: 235081 Mouse Unigene: 31142 Rat Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
