Product Pathways - Cell Cycle / Checkpoint
Cyclin D2 (D52F9) Rabbit mAb #3741
PhosphoSitePlus® protein, site, and accession data: CCND2
| Applications | Reactivity | Sensitivity | MW (kDa) | Isotype |
|---|---|---|---|---|
| W IP | H M R | Endogenous | 31 | Rabbit IgG |
Applications Key:
W=Western Blotting
IP=Immunoprecipitation
Reactivity Key:
H=Human
M=Mouse
R=Rat
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.
Protocols
Specificity / Sensitivity
Cyclin D2 (D52F9) Rabbit mAb detects endogenous levels of total cyclin D2 protein. It does not cross-react with other family members.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the amino terminus of cyclin D2.
Background
Activity of the cyclin-dependent kinases CDK4 and CDK6 is regulated by T-loop phosphorylation, by the abundance of their cyclin partners (the D-type cyclins), and by association with CDK inhibitors of the Cip/Kip or INK family of proteins (1). The inactive ternary complex of cyclin D/CDK4 and p27 Kip1 requires extracellular mitogenic stimuli for the release and degradation of p27 concomitant with a rise in cyclin D levels to effect progression through the restriction point and pRb-dependent entry into S-phase (2). The active complex of cyclin D/CDK4 targets the retinoblastoma protein for phosphorylation, allowing the release of E2F transcription factors that activate G1/S-phase gene expression (3). Levels of cyclin D protein drop upon withdrawal of growth factors through downregulation of its protein expression and through phosphorylation-dependent degradation (4).
- Hirai, H. et al. (1995) Mol. Cell. Biol. 15, 2672-2681.
- Sherr, C.J. (1996) Science 274, 1672-1677.
- Lukas, J. et al. (1996) Mol. Cell. Biol. 16, 6917-6925.
- Diehl, J.A. et al. (1997) Genes Dev. 11, 957-972.
Application References
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This product is intended for research purposes only. The product is not intended to be used for therapeutic or diagnostic purposes in humans or animals.