E2F-1 Antibody #3742
- WB
- ChIP
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 70 |
| SOURCE | Rabbit |
Application Key:
- WB-Western Blotting
- ChIP-Chromatin Immunoprecipitation
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
For optimal ChIP results, use 5 μl of antibody and 10 μg of chromatin (approximately 4 x 106 cells) per IP. This antibody has been validated using SimpleChIP® Enzymatic Chromatin IP Kits.
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Chromatin IP | 1:100 |
Storage
Protocol
Specificity / Sensitivity
Species Reactivity:
The antigen sequence used to produce this antibody shares 100% sequence homology with the species listed here, but reactivity has not been tested or confirmed to work by CST. Use of this product with these species is not covered under our Product Performance Guarantee.
Species predicted to react based on 100% sequence homology:
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide 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.
限制使用
除非 CST 的合法授书代表以书面形式书行明确同意，否书以下条款适用于 CST、其关书方或分书商提供的书品。 任何书充本条款或与本条款不同的客书条款和条件，除非书 CST 的合法授书代表以书面形式书独接受， 否书均被拒书，并且无效。
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