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Rabbit Anti-Bid/BF594 Conjugated antibody (bs-1153R-BF594)
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說 明 書: 100ul  
100ul/2980.00元
大包裝/詢價
產(chǎn)品編號 bs-1153R-BF594
英文名稱 Rabbit Anti-Bid/BF594 Conjugated antibody
中文名稱 BF594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)格價格 100ul/2980元 購買        大包裝/詢價
說 明 書 100ul  
研究領(lǐng)域 腫瘤  信號轉(zhuǎn)導(dǎo)  細(xì)胞凋亡  新陳代謝  線粒體  
抗體來源 Rabbit
克隆類型 Polyclonal
交叉反應(yīng) Human, Mouse, Rat, 
產(chǎn)品應(yīng)用 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 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

Entrez Gene: 64625 Rat

Omim: 601997 Human

SwissProt: P55957 Human

SwissProt: P70444 Mouse

SwissProt: Q9JLT6 Rat

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.
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