Product Pathways - Cell Cycle / Checkpoint
E2F-1 Antibody #3742
| Applications | Reactivity | MW (kDa) | Source |
|---|---|---|---|
| W | H M (R) | 70 | Rabbit |
Applications Key:
W=Western Blotting
Reactivity Key:
H=Human
M=Mouse
R=Rat
Species enclosed in parentheses are predicted to react based on 100% sequence homology. Species cross-reactivity is determined by Western blot.
Specificity / Sensitivity
E2F1 Antibody detects endogenous levels of total E2F1 protein. The antibody does not cross-react with other proteins.
Source / Purification
Polyclonal antibodies are produced by immunizing rabbits with a synthetic peptide (KLH-coupled) corresponding to the carboxy-terminal residues of human E2F1. Antibodies are purified by protein A and peptide affinity chromatography.
Background
The E2F transcription factors are essential for regulation of the cell cycle (1,2). Physiological E2F is a heterodimer composed of an E2F subunit together with a DP subunit (3, 4). Six members of the E2F family have been identified, and each E2F subunit has a DNA binding and a dimerization domain. E2F-1 to -5 activate transcription. E2F-1 to -3 bind pRb, and E2F-4 and -5 bind p107 or p130, and these interactions are under cell cycle control (5-8). E2F-1 has oncogenic properties in vivo and in vitro. E2F-1 can induce apoptosis through p53-dependent and -independent mechanisms. E2F-1 is stress-responsive, and is regulated by a PI3-kinase-like kinase family such as the ATM/ATR kinases (9-11).
- Helin, K. (1998) Curr. Opin. Genet. Dev. 8, 28-35.
- Dyson, N. (1998) Genes Dev. 12, 2245-2262.
- Helin, K. et al. (1993) Genes Dev. 7, 1850-1861.
- Wu, C. et al. (1995) Mol. Cell. Biol. 15, 2536-2546.
- Takahashi, Y. et al. (2000) Genes Dev. 14, 804-816.
- Wu, L. et al. (2001) Nature 414, 457-462.
- Gaubatz, S. et al. (2000) Mol. Cell 6, 729-735.
- Hurford, R. K. et al. (1997) Genes Dev. 11, 1447-1463.
- Tsai, K. Y. et al. (1998) Mol. Cell 2, 293-304.
- Garcia, I. et al. (2000) Cell Growth Differ. 11, 91-98.
- Lin, W. C. et al. (2001) Genes Dev. 15, 1833-1844.
Application References
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