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. 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. Bim functions in regulating apoptosis associated with thymocyte negative selection and following growth factor withdrawal, during which Bim expression is elevated. Three major isoforms of Bim are generated by alternative splicing: bimEL, BimL, and BimS. 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. Apoptotic activity of these longer isoforms may be regulated by phosphorylation. Environmental stress triggers Bim phosphorylation by JNK and results in its dissociation from the dynein complex and increased apoptotic activity.

Classification:

Primary antibody

Alternative names:

BCL2L11; BIM; Bcl-2-like protein 11; Bcl2-L-11; Bcl2-interacting mediator of cell death

Species reactivity:

Human;mouse;rat

Host:

Rabbit

Isotype:

IgG

Immunogen:

The antiserum was produced against synthesized peptide derived from human BIM around the phosphorylation site of Ser59. AA range:31-80

Concentration:

1 mg/ml

Molecular weight:

22171

Applications:

IHC-p, ELISA

Storage:

-20°C for one year

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