Cell Signaling Technology

Product Pathways - Apoptosis

Bim (C34C5) Rabbit mAb (PE Conjugate) #12186

No. Size Price
12186S 100 µl ( 50 tests ) ¥3,986.00 现货查询 购买询价
12186 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
F 1:50 Human,Mouse,Rat, Endogenous Rabbit IgG

Species cross-reactivity is determined by western blot.

Applications Key: F=Flow Cytometry,

Homology

Species predicted to react based on 100% sequence homology: Monkey, Bovine, Dog, Pig,

Specificity / Sensitivity

Bim (C34C5) Rabbit mAb (PE Conjugate) recognizes endogenous levels of total Bim protein (EL, L, and S isoforms).

Bim (C34C5) Rabbit mAb (PE Conjugate)兔单抗能够检测内源水平Bim (EL, L 和S 形式) 总蛋白。

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro25 of Bim protein.

该单克隆抗体是采用合成的人源Bim蛋白Pro25周围残基相对应的肽段免疫动物而制备的。

Description

This Cell Signaling Technology antibody is conjugated to phycoerythrin (PE) and tested in-house for direct flow cytometry analysis in human cells. The antibody is expected to exhibit the same species cross-reactivity as the unconjugated Bim (C34C5) Rabbit mAb #2933.

该CST抗体标记了藻红素(PE),通过了内部测试可以直接用于细胞的流式试验。该抗体与不带标记Bim (C34C5) Rabbit mAb 兔单抗#2933有着相同的种属交叉反应。

Flow Cytometry

Flow Cytometry

Flow cytometric analysis of HeLa cells using Bim (C34C5) Rabbit mAb (PE Conjugate) (green) compared to concentration-matched Rabbit (DA1E) mAb IgG XP® Isotype Control (PE Conjugate) #5742 (red).

流式细胞术检测HeLa细胞,使用的抗体为Bim (C34C5) Rabbit mAb (PE Conjugate) 兔单抗(绿色),浓度匹配的Rabbit (DA1E) mAb IgG XP® Isotype Control (PE Conjugate) #5742(红色)作为对照。

Background

Bim/Bod is a pro-apoptotic protein belonging to the BH3-only group of Bcl-2 family members including Bad, Bid, Bik, Hrk, and Noxa that contain a BH3 domain but lack other conserved BH1 or BH2 domains (1,2). Bim induces apoptosis by binding to and antagonizing anti-apoptotic members of the Bcl-2 family. Interactions have been observed with Bcl-2, Bcl-xL, Mcl-1, Bcl-w, Bfl-1, and BHRF-1 (1,2). Bim functions in regulating apoptosis associated with thymocyte negative selection and following growth factor withdrawal, during which Bim expression is elevated (3-6). Three major isoforms of Bim are generated by alternative splicing: BimEL, BimL, and BimS (1). The shortest form, BimS, is the most cytotoxic and is generally only transiently expressed during apoptosis. The BimEL and BimL isoforms may be sequestered to the dynein motor complex through an interaction with the dynein light chain and released from this complex during apoptosis (7). Apoptotic activity of these longer isoforms may be regulated by phosphorylation (8,9). Environmental stress triggers Bim phosphorylation by JNK and results in its dissociation from the dynein complex and increased apoptotic activity.

Bim/Bod是促凋亡蛋白,属于Bcl-2家族只含有BH3域的成员,此家族还包括Bad、Bid、Bik、Hrk和 Noxa,它们都只包含BH3域,但缺少其它保守的BH1或BH2(1,2)。Bim通过结合并拮抗 Bcl-2家族抗凋亡因子而诱导凋亡。研究发现,其与Bcl-2、Bcl-xL、Mcl-1、Bcl-w、Bfl-1和 BHRF-1存在相互作用 (1,2)。Bim调控凋亡的功能是与胸腺细胞负向选择性有关,并伴随生长因子的撤回,在这期间Bim的表达是上调的(3-6)。Bim通过可变剪切,主要形成三种不同的形式:BimEL、BimL和BimS (1)。BimS是最短的形式,也是毒性最强的,它只在凋亡的瞬间表达。在凋亡过程中,BimEL 和 BimL 形式可能通过与动力蛋白的轻链互作,进而与动力蛋白复合体隔离并从这个复合体上得到释放(7)。这些长剪切形式的凋亡活性是通过磷酸化调控(8,9)。环境的胁迫引起JNK对Bim的磷酸化,并导致其与动力蛋白复合体的解离,从而增加凋亡活性。

  1. O'Connor, L. et al. (1998) EMBO J 17, 384-95.
  2. Hsu, S.Y. et al. (1998) Mol Endocrinol 12, 1432-40.
  3. Bouillet, P. et al. (2002) Nature 415, 922-6.
  4. Whitfield, J. et al. (2001) Neuron 29, 629-43.
  5. Dijkers, P.F. et al. (2000) Curr Biol 10, 1201-4.
  6. Ley, R. et al. (2003) J Biol Chem 278, 18811-6.
  7. Puthalakath, H. et al. (1999) Mol Cell 3, 287-96.
  8. Lei, K. and Davis, R.J. (2003) Proc Natl Acad Sci U S A 100, 2432-7.
  9. Putcha, G.V. et al. (2003) Neuron 38, 899-914.

Application References

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Protocols


For Research Use Only. Not For Use In Diagnostic Procedures.

U.S. Patent No. 5,675,063.

Cell Signaling Technology is a trademark of Cell Signaling Technology, Inc.

Cell Signaling Technology® is a trademark of Cell Signaling Technology, Inc.

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