Cell Signaling Technology

Product Pathways - Cell Cycle / Checkpoint

Bora (D2B9) Rabbit mAb #12109

Applications Reactivity Sensitivity MW (kDa) Isotype
W IP F H Endogenous 80 Rabbit IgG

Applications Key:  W=Western Blotting  IP=Immunoprecipitation  F=Flow Cytometry
Reactivity Key:  H=Human
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

Bora (D2B9) Rabbit mAb recognizes endogenous levels of total Bora protein.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a recombinant protein specific to the carboxy terminus of human Bora protein.

Western Blotting

Western Blotting

Western blot analysis of extracts from various cell lines using Bora (D2B9) Rabbit mAb.

IP

IP

Immunoprecipitation of Bora from Jurkat cell extracts using Bora (D2B9) Rabbit mAb. Western blot detection was performed using the same antibody. Lane 1 is 10% input.

Flow Cytometry

Flow Cytometry

Flow cytometric analysis of Jurkat cells using Bora (D2B9) Rabbit mAb compared to DNA content (Propidium Iodide (PI)/RNase Staining Solution #4087), showing peak bora expression in G2 phase. Anti-rabbit IgG (H+L), F(ab')2 Fragment (Alexa Fluor® 488 Conjugate) #4412 was used as a secondary antibody.


Background

The eukaryotic cell cycle is carefully controlled by protein phosphorylation involving a number of phosphatases, kinases, and co-factors. Cyclin-dependent kinases (CDKs/cdcs), Polo-like kinases (PLKs), and Aurora kinases have been shown to be major regulators of mitotic control (reviewed in 1,2). Protein aurora borealis (Bora), a co-factor of Aurora-A first identified in Drosophila, also plays a key roll in cell cycle progression (3). Bora levels are low in G0/G1, increasing in S-phase and peaking at G2 (4).Found to be conserved from C. elegans to humans, Bora is translocated from the nucleus to the cytoplasm upon activation of cdc2 at the onset of mitosis. Once present in the cytoplasm, Bora binds to and activates Aurora-A and PLK1 (3-5). It has been proposed that the binding of human Bora to PLK1 may lead to a conformational change in the protein that disrupts the autoinhibition by the Polo-Box Domain (PBD). This would allow for Thr210 on PLK1 to become more accessible for phosphorylation by Aurora-A (reviewed in 6). Active PLK1 then initiates the PLK1-cdc25-cdc2 positive feedback loop, leading to mitotic entry and the phosphorylation of Bora. Once phosphorylated in prophase, Bora is degraded allowing for normal mitotic progression (7).

  1. Nigg, E.A. (2001) Nat Rev Mol Cell Biol 2, 21-32.
  2. Archambault, V. and Carmena, M. (2012) Cell Cycle 11, 1490-5.
  3. Hutterer, A. et al. (2006) Dev Cell 11, 147-57.
  4. Seki, A. et al. (2008) Science 320, 1655-8.
  5. Chan, E.H. et al. (2008) Chromosoma 117, 457-69.
  6. Macurek, L. et al. (2009) Cancer Res 69, 4555-8.
  7. Seki, A. et al. (2008) J Cell Biol 181, 65-78.

Application References

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

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