Cell Signaling Technology

Product Pathways - Apoptosis / Autophagy

Bim (C34C5) Rabbit mAb #2933

Applications Reactivity MW (kDa) Source Isotype
W IP IHC-P F H M R (Mk) (B) (Dg) 12,15,23 Rabbit IgG

Applications Key:  W=Western Blotting  IP=Immunoprecipitation  IHC-P=Immunohistochemistry (Paraffin)  F=Flow Cytometry
Reactivity Key:  H=Human  M=Mouse  R=Rat  Mk=Monkey  B=Bovine  Dg=Dog
Species enclosed in parentheses are predicted to react based on 100% sequence homology. Species cross-reactivity is determined by Western blot.

Specificity / Sensitivity

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

Source / Purification

Rabbit monoclonal antibody is produced by immunizing rabbits with a synthetic peptide (KLH-coupled) corresponding to residues surrounding Pro25 of Bim.

Western Blotting

Western Blotting

Western blot analysis of extracts from Raji, A20 and RL-7 cells using Bim (C34C5) Rabbit mAb.

IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded human lung carincoma using Bim (C34C5) Rabbit mAb.

IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded human lymphoma using Bim (C34C5) Rabbit mAb.


IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded human breast carcinoma using Bim (C34C5) Rabbit mAb in the presence of control peptide (left) or antigen specific peptide (right).

Flow Cytometry

Flow Cytometry

Flow cytometric analysis of Raji cells using Bim (C34C5) Rabbit mAb (blue) compared to a nonspecific negative control antibody (red).

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.

  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.

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